Cells in the body that store FATS, usually in the form of TRIGLYCERIDES. WHITE ADIPOCYTES are the predominant type and found mostly in the abdominal cavity and subcutaneous tissue. BROWN ADIPOCYTES are thermogenic cells that can be found in newborns of some species and hibernating mammals.
Fat cells with light coloration and few MITOCHONDRIA. They contain a scant ring of CYTOPLASM surrounding a single large lipid droplet or vacuole.
A continuous cell line that is a substrain of SWISS 3T3 CELLS developed though clonal isolation. The mouse fibroblast cells undergo an adipose-like conversion as they move to a confluent and contact-inhibited state.
Specialized connective tissue composed of fat cells (ADIPOCYTES). It is the site of stored FATS, usually in the form of TRIGLYCERIDES. In mammals, there are two types of adipose tissue, the WHITE FAT and the BROWN FAT. Their relative distributions vary in different species with most adipose tissue being white.
The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
A glucose transport protein found in mature MUSCLE CELLS and ADIPOCYTES. It promotes transport of glucose from the BLOOD into target TISSUES. The inactive form of the protein is localized in CYTOPLASMIC VESICLES. In response to INSULIN, it is translocated to the PLASMA MEMBRANE where it facilitates glucose uptake.
The differentiation of pre-adipocytes into mature ADIPOCYTES.
Cell lines whose original growing procedure consisted being transferred (T) every 3 days and plated at 300,000 cells per plate (J Cell Biol 17:299-313, 1963). Lines have been developed using several different strains of mice. Tissues are usually fibroblasts derived from mouse embryos but other types and sources have been developed as well. The 3T3 lines are valuable in vitro host systems for oncogenic virus transformation studies, since 3T3 cells possess a high sensitivity to CONTACT INHIBITION.
A large group of membrane transport proteins that shuttle MONOSACCHARIDES across CELL MEMBRANES.
A thermogenic form of adipose tissue composed of BROWN ADIPOCYTES. It is found in newborns of many species including humans, and in hibernating mammals. Brown fat is richly vascularized, innervated, and densely packed with MITOCHONDRIA which can generate heat directly from the stored lipids.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
Fatty tissue composed of WHITE ADIPOCYTES and generally found directly under the skin (SUBCUTANEOUS FAT) and around the internal organs (ABDOMINAL FAT). It has less vascularization and less coloration than the BROWN FAT. White fat provides heat insulation, mechanical cushion, and source of energy.
A nuclear transcription factor. Heterodimerization with RETINOID X RECEPTOR ALPHA is important in regulation of GLUCOSE metabolism and CELL GROWTH PROCESSES. It is a target of THIAZOLIDINEDIONES for control of DIABETES MELLITUS.
2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
A cell surface receptor for INSULIN. It comprises a tetramer of two alpha and two beta subunits which are derived from cleavage of a single precursor protein. The receptor contains an intrinsic TYROSINE KINASE domain that is located within the beta subunit. Activation of the receptor by INSULIN results in numerous metabolic changes including increased uptake of GLUCOSE into the liver, muscle, and ADIPOSE TISSUE.
A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.
A 30-kDa COMPLEMENT C1Q-related protein, the most abundant gene product secreted by FAT CELLS of the white ADIPOSE TISSUE. Adiponectin modulates several physiological processes, such as metabolism of GLUCOSE and FATTY ACIDS, and immune responses. Decreased plasma adiponectin levels are associated with INSULIN RESISTANCE; TYPE 2 DIABETES MELLITUS; OBESITY; and ATHEROSCLEROSIS.
A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).
An enzyme that catalyzes the hydrolysis of CHOLESTEROL ESTERS and some other sterol esters, to liberate cholesterol plus a fatty acid anion.
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The beta-3 adrenergic receptors are the predominant beta-adrenergic receptor type expressed in white and brown ADIPOCYTES and are involved in modulating ENERGY METABOLISM and THERMOGENESIS.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
Mutant mice exhibiting a marked obesity coupled with overeating, hyperglycemia, hyperinsulinemia, marked insulin resistance, and infertility when in a homozygous state. They may be inbred or hybrid.
A structurally-related group of signaling proteins that are phosphorylated by the INSULIN RECEPTOR PROTEIN-TYROSINE KINASE. The proteins share in common an N-terminal PHOSPHOLIPID-binding domain, a phosphotyrosine-binding domain that interacts with the phosphorylated INSULIN RECEPTOR, and a C-terminal TYROSINE-rich domain. Upon tyrosine phosphorylation insulin receptor substrate proteins interact with specific SH2 DOMAIN-containing proteins that are involved in insulin receptor signaling.
A non-metabolizable glucose analogue that is not phosphorylated by hexokinase. 3-O-Methylglucose is used as a marker to assess glucose transport by evaluating its uptake within various cells and organ systems. (J Neurochem 1993;60(4):1498-504)
A ubiquitously expressed glucose transporter that is important for constitutive, basal GLUCOSE transport. It is predominately expressed in ENDOTHELIAL CELLS and ERYTHROCYTES at the BLOOD-BRAIN BARRIER and is responsible for GLUCOSE entry into the BRAIN.
The convoluted cordlike structure attached to the posterior of the TESTIS. Epididymis consists of the head (caput), the body (corpus), and the tail (cauda). A network of ducts leaving the testis joins into a common epididymal tubule proper which provides the transport, storage, and maturation of SPERMATOZOA.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
THIAZOLES with two keto oxygens. Members are insulin-sensitizing agents which overcome INSULIN RESISTANCE by activation of the peroxisome proliferator activated receptor gamma (PPAR-gamma).
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.
Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.
N-Isopropyl-N-phenyl-adenosine. Antilipemic agent. Synonym: TH 162.
Substances which lower blood glucose levels.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Fatty tissue under the SKIN through out the body.
Polypeptides produced by the ADIPOCYTES. They include LEPTIN; ADIPONECTIN; RESISTIN; and many cytokines of the immune system, such as TUMOR NECROSIS FACTOR-ALPHA; INTERLEUKIN-6; and COMPLEMENT FACTOR D (also known as ADIPSIN). They have potent autocrine, paracrine, and endocrine functions.
Compounds which inhibit or antagonize the biosynthesis or action of insulin.
Transport proteins that carry specific substances in the blood or across cell membranes.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A CCAAT-enhancer-binding protein found in LIVER; ADIPOSE TISSUE; INTESTINES; LUNG; ADRENAL GLANDS; PLACENTA; OVARY and peripheral blood mononuclear cells (LEUKOCYTES, MONONUCLEAR). Experiments with knock-out mice have demonstrated that CCAAT-enhancer binding protein-alpha is essential for the functioning and differentiation of HEPATOCYTES and ADIPOCYTES.
A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent.
Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)
A zinc-containing sialoglycoprotein that is used to study aminopeptidase activity in the pathogenesis of hypertension. EC 3.4.11.3.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
LIPOLYSIS of stored LIPIDS in the ADIPOSE TISSUE to release FREE FATTY ACIDS. Mobilization of stored lipids is under the regulation of lipolytic signals (CATECHOLAMINES) or anti-lipolytic signals (INSULIN) via their actions on the hormone-sensitive LIPASE. This concept does not include lipid transport.
Proteins encoded by the mitochondrial genome or proteins encoded by the nuclear genome that are imported to and resident in the MITOCHONDRIA.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
Intracellular proteins that reversibly bind hydrophobic ligands including: saturated and unsaturated FATTY ACIDS; EICOSANOIDS; and RETINOIDS. They are considered a highly conserved and ubiquitously expressed family of proteins that may play a role in the metabolism of LIPIDS.
The generation of heat in order to maintain body temperature. The uncoupled oxidation of fatty acids contained within brown adipose tissue and SHIVERING are examples of thermogenesis in MAMMALS.
Drugs that selectively bind to and activate beta-adrenergic receptors.
A potent cyclic nucleotide phosphodiesterase inhibitor; due to this action, the compound increases cyclic AMP and cyclic GMP in tissue and thereby activates CYCLIC NUCLEOTIDE-REGULATED PROTEIN KINASES
Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.
The rate dynamics in chemical or physical systems.
Compounds that bind to and activate ADRENERGIC BETA-3 RECEPTORS.
A double-layered fold of peritoneum that attaches the STOMACH to other organs in the ABDOMINAL CAVITY.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
A 12-kDa cysteine-rich polypeptide hormone secreted by FAT CELLS in the ADIPOSE TISSUE. It is the founding member of the resistin-like molecule (RELM) hormone family. Resistin suppresses the ability of INSULIN to stimulate cellular GLUCOSE uptake.
A cyclic nucleotide phosphodiesterase subfamily that is inhibited by the binding of CYCLIC GMP to an allosteric domain found on the enzyme and through phosphorylation by regulatory kinases such as PROTEIN KINASE A and PROTEIN KINASE B. The two members of this family are referred to as type 3A, and type 3B, and are each product of a distinct gene. In addition multiple enzyme variants of each subtype can be produced due to multiple alternative mRNA splicing.
One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)
Hormones released from neoplasms or from other cells that are not the usual sources of hormones.
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3.
FATTY ACIDS found in the plasma that are complexed with SERUM ALBUMIN for transport. These fatty acids are not in glycerol ester form.
Enzymes that catalyze the synthesis of FATTY ACIDS from acetyl-CoA and malonyl-CoA derivatives.
Two populations of Zucker rats have been cited in research--the "fatty" or obese and the lean. The "fatty" rat (Rattus norvegicus) appeared as a spontaneous mutant. The obese condition appears to be due to a single recessive gene.
A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.
Derivatives of the steroid androstane having two double bonds at any site in any of the rings.
Gated, ion-selective glycoproteins that traverse membranes. The stimulus for ION CHANNEL GATING can be due to a variety of stimuli such as LIGANDS, a TRANSMEMBRANE POTENTIAL DIFFERENCE, mechanical deformation or through INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS.
Bone-marrow-derived, non-hematopoietic cells that support HEMATOPOETIC STEM CELLS. They have also been isolated from other organs and tissues such as UMBILICAL CORD BLOOD, umbilical vein subendothelium, and WHARTON JELLY. These cells are considered to be a source of multipotent stem cells because they include subpopulations of mesenchymal stem cells.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Established cell cultures that have the potential to propagate indefinitely.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
An anti-inflammatory 9-fluoro-glucocorticoid.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
Consumption of excessive DIETARY FATS.
The relationship between the dose of an administered drug and the response of the organism to the drug.
The process of moving proteins from one cellular compartment (including extracellular) to another by various sorting and transport mechanisms such as gated transport, protein translocation, and vesicular transport.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
Intracellular receptors that can be found in the cytoplasm or in the nucleus. They bind to extracellular signaling molecules that migrate through or are transported across the CELL MEMBRANE. Many members of this class of receptors occur in the cytoplasm and are transported to the CELL NUCLEUS upon ligand-binding where they signal via DNA-binding and transcription regulation. Also included in this category are receptors found on INTRACELLULAR MEMBRANES that act via mechanisms similar to CELL SURFACE RECEPTORS.
An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
A class of proteins that were originally identified by their ability to bind the DNA sequence CCAAT. The typical CCAAT-enhancer binding protein forms dimers and consists of an activation domain, a DNA-binding basic region, and a leucine-rich dimerization domain (LEUCINE ZIPPERS). CCAAT-BINDING FACTOR is structurally distinct type of CCAAT-enhancer binding protein consisting of a trimer of three different subunits.
Fatty tissue inside the ABDOMINAL CAVITY, including visceral fat and retroperitoneal fat. It is the most metabolically active fat in the body and easily accessible for LIPOLYSIS. Increased visceral fat is associated with metabolic complications of OBESITY.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
De novo fat synthesis in the body. This includes the synthetic processes of FATTY ACIDS and subsequent TRIGLYCERIDES in the LIVER and the ADIPOSE TISSUE. Lipogenesis is regulated by numerous factors, including nutritional, hormonal, and genetic elements.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
Components of a cell produced by various separation techniques which, though they disrupt the delicate anatomy of a cell, preserve the structure and physiology of its functioning constituents for biochemical and ultrastructural analysis. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p163)
A sterol regulatory element binding protein that regulates expression of GENES involved in FATTY ACIDS metabolism and LIPOGENESIS. Two major isoforms of the protein exist due to ALTERNATIVE SPLICING.
An enzyme that catalyzes the formation of nicotinamide mononucleotide (NMN) from nicotinamide and 5-phosphoribosyl-1-pyrophosphate, the rate-limiting step in the biosynthesis of the NAD coenzyme. It is also known as a growth factor for early B-LYMPHOCYTES, or an ADIPOKINE with insulin-mimetic effects (visfatin).
A common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids.
Enzymes that catalyze the hydrolysis of CYCLIC AMP to form adenosine 5'-phosphate. The enzymes are widely distributed in animal tissue and control the level of intracellular cyclic AMP. Many specific enzymes classified under this heading demonstrate additional spcificity for 3',5'-cyclic IMP and CYCLIC GMP.
Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.
Benzopyrans saturated in the 2 and 3 positions.
Elements of limited time intervals, contributing to particular results or situations.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed)
The chemical reactions involved in the production and utilization of various forms of energy in cells.
A serum protein which is important in the ALTERNATIVE COMPLEMENT ACTIVATION PATHWAY. This enzyme cleaves the COMPLEMENT C3B-bound COMPLEMENT FACTOR B to form C3bBb which is ALTERNATIVE PATHWAY C3 CONVERTASE.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
The quantity of volume or surface area of CELLS.
A genetically related subfamily of RAB GTP-BINDING PROTEINS involved in recycling of proteins such as cell surface receptors from early endosomes to the cell surface. This enzyme was formerly listed as EC 3.6.1.47.
Potent activator of the adenylate cyclase system and the biosynthesis of cyclic AMP. From the plant COLEUS FORSKOHLII. Has antihypertensive, positive inotropic, platelet aggregation inhibitory, and smooth muscle relaxant activities; also lowers intraocular pressure and promotes release of hormones from the pituitary gland.
An enzyme that catalyzes the hydrolysis of ADENOSINE to INOSINE with the elimination of AMMONIA.
Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.
An enzyme that catalyzes the acyl group transfer of ACYL COA to 1-acyl-sn-glycerol 3-phosphate to generate 1,2-diacyl-sn-glycerol 3-phosphate. This enzyme has alpha, beta, gamma, delta and epsilon subunits.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.
The amount of fat or lipid deposit at a site or an organ in the body, an indicator of body fat status.
Regulatory proteins and peptides that are signaling molecules involved in the process of PARACRINE COMMUNICATION. They are generally considered factors that are expressed by one cell and are responded to by receptors on another nearby cell. They are distinguished from HORMONES in that their actions are local rather than distal.
A cytokine that stimulates the growth and differentiation of B-LYMPHOCYTES and is also a growth factor for HYBRIDOMAS and plasmacytomas. It is produced by many different cells including T-LYMPHOCYTES; MONOCYTES; and FIBROBLASTS.
Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.
Endocytic/exocytic CELL MEMBRANE STRUCTURES rich in glycosphingolipids, cholesterol, and lipid-anchored membrane proteins that function in ENDOCYTOSIS (potocytosis), transcytosis, and SIGNAL TRANSDUCTION. Caveolae assume various shapes from open pits to closed vesicles. Caveolar coats are composed of CAVEOLINS.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A tyrosine phosphoprotein that plays an essential role in CAVEOLAE formation. It binds CHOLESTEROL and is involved in LIPIDS transport, membrane traffic, and SIGNAL TRANSDUCTION.
A CCAAT-enhancer-binding protein found in LIVER; INTESTINES; LUNG and ADIPOSE TISSUE. It is an important mediator of INTERLEUKIN-6 signaling.
Fatty tissue under the SKIN in the region of the ABDOMEN.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
The smaller fragment generated from the cleavage of complement C3 by C3 CONVERTASE. C3a, a 77-amino acid peptide, is a mediator of local inflammatory process. It induces smooth MUSCLE CONTRACTION, and HISTAMINE RELEASE from MAST CELLS and LEUKOCYTES. C3a is considered an anaphylatoxin along with COMPLEMENT C4A; COMPLEMENT C5A; and COMPLEMENT C5A, DES-ARGININE.
Cell surface receptors for obesity factor (LEPTIN), a hormone secreted by the WHITE ADIPOCYTES. Upon leptin-receptor interaction, the signal is mediated through the JAK2/STAT3 pathway to regulate food intake, energy balance and fat storage.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A broad category of membrane transport proteins that specifically transport FREE FATTY ACIDS across cellular membranes. They play an important role in LIPID METABOLISM in CELLS that utilize free fatty acids as an energy source.
A cyclic nucleotide derivative that mimics the action of endogenous CYCLIC AMP and is capable of permeating the cell membrane. It has vasodilator properties and is used as a cardiac stimulant. (From Merck Index, 11th ed)
Connective tissue cells of an organ found in the loose connective tissue. These are most often associated with the uterine mucosa and the ovary as well as the hematopoietic system and elsewhere.
A partitioning within cells due to the selectively permeable membranes which enclose each of the separate parts, e.g., mitochondria, lysosomes, etc.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.

DEF-1, a novel Src SH3 binding protein that promotes adipogenesis in fibroblastic cell lines. (1/5446)

The Src homology 3 (SH3) motif is found in numerous signal transduction proteins involved in cellular growth and differentiation. We have purified and cloned a novel protein, DEF-1 (differentiation-enhancing factor), from bovine brain by using a Src SH3 affinity column. Ectopic expression of DEF-1 in fibroblasts resulted in the differentiation of a significant fraction of the culture into adipocytes. This phenotype appears to be related to the induction of the transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma), since DEF-1 NIH 3T3 cells demonstrated augmented levels of PPARgamma mRNA and, when treated with activating PPARgamma ligands, efficient induction of differentiation. Further evidence for a role for DEF-1 in adipogenesis was provided by heightened expression of DEF-1 mRNA in adipose tissue isolated from obese and diabetes mice compared to that in tissue isolated from wild-type mice. However, DEF-1 mRNA was detected in multiple tissues, suggesting that the signal transduction pathway(s) in which DEF-1 is involved is not limited to adipogenesis. These results suggest that DEF-1 is an important component of a signal transduction process that is involved in the differentiation of fibroblasts and possibly of other types of cells.  (+info)

Novel peroxisome proliferator-activated receptor (PPAR) gamma and PPARdelta ligands produce distinct biological effects. (2/5446)

The peroxisome proliferator-activated receptors (PPARs) include three receptor subtypes encoded by separate genes: PPARalpha, PPARdelta, and PPARgamma. PPARgamma has been implicated as a mediator of adipocyte differentiation and the mechanism by which thiazolidinedione drugs exert in vivo insulin sensitization. Here we characterized novel, non-thiazolidinedione agonists for PPARgamma and PPARdelta that were identified by radioligand binding assays. In transient transactivation assays these ligands were agonists of the receptors to which they bind. Protease protection studies showed that ligand binding produced specific alterations in receptor conformation. Both PPARgamma and PPARdelta directly interacted with a nuclear receptor co-activator (CREB-binding protein) in an agonist-dependent manner. Only the PPARgamma agonists were able to promote differentiation of 3T3-L1 preadipocytes. In diabetic db/db mice all PPARgamma agonists were orally active insulin-sensitizing agents producing reductions of elevated plasma glucose and triglyceride concentrations. In contrast, selective in vivo activation of PPARdelta did not significantly affect these parameters. In vivo PPARalpha activation with WY-14653 resulted in reductions in elevated triglyceride levels with minimal effect on hyperglycemia. We conclude that: 1) synthetic non-thiazolidinediones can serve as ligands of PPARgamma and PPARdelta; 2) ligand-dependent activation of PPARdelta involves an apparent conformational change and association of the receptor ligand binding domain with CREB-binding protein; 3) PPARgamma activation (but not PPARdelta or PPARalpha activation) is sufficient to potentiate preadipocyte differentiation; 4) non-thiazolidinedione PPARgamma agonists improve hyperglycemia and hypertriglyceridemia in vivo; 5) although PPARalpha activation is sufficient to affect triglyceride metabolism, PPARdelta activation does not appear to modulate glucose or triglyceride levels.  (+info)

Tumor necrosis factor alpha stimulates lipolysis in adipocytes by decreasing Gi protein concentrations. (3/5446)

Prolonged treatment (12-24 h) of adipocytes with tumor necrosis factor alpha (TNFalpha) stimulates lipolysis. We have investigated the hypothesis that TNFalpha stimulates lipolysis by blocking the action of endogenous adenosine. Adipocytes were incubated for 48 h with TNFalpha, and lipolysis was measured in the absence or presence of adenosine deaminase. Without adenosine deaminase, the rate of glycerol release was 2-3-fold higher in the TNFalpha-treated cells, but with adenosine deaminase lipolysis increased in the controls to approximately that in the TNFalpha-treated cells. This suggests that TNFalpha blocks adenosine release or prevents its antilipolytic effect. Both N6-phenylisopropyl adenosine and nicotinic acid were less potent and efficacious inhibitors of lipolysis in treated cells. A decrease in the concentration of alpha-subunits of all three Gi subtypes was detected by Western blotting without a change in Gs proteins or beta-subunits. Gi2alpha was about 50% of control, whereas Gi1alpha and Gi3alpha were about 20 and 40% of control values, respectively. The time course of Gi down-regulation correlated with the stimulation of lipolysis. Furthermore, down-regulation of Gi by an alternative approach (prolonged incubation with N6-phenylisopropyl adenosine) stimulated lipolysis. These findings indicate that TNFalpha stimulates lipolysis by blunting endogenous inhibition of lipolysis. The mechanism appears to be a Gi protein down-regulation.  (+info)

Transgenic UCP1 in white adipocytes modulates mitochondrial membrane potential. (4/5446)

To test if mitochondrial uncoupling in white adipocytes is responsible for obesity resistance of the aP2-Ucp transgenic mice expressing ectopic uncoupling protein 1 (UCPI) in white fat, mitochondrial membrane potential (delta psi(m)) was estimated by flow cytometry in adipocytes isolated from gonadal fat. Ectopic UCP1 (approximately 0.8 mol UCP1/mol respiratory chain) decreased the delta psi(m) and rendered the potential sensitive to GDP and fatty acids. These ligands of UCP1 had no effect on delta psi(m) in white adipocytes from non-transgenic mice, suggesting that the function of endogenous UCP2 in adipocytes was not affected. The results support the hypothesis that mitochondrial uncoupling in white fat may prevent development of obesity.  (+info)

SNAP-23 participates in SNARE complex assembly in rat adipose cells. (5/5446)

SNARE proteins are required for vesicle docking and fusion in eukaryotic cells in processes as diverse as homotypic membrane fusion and synaptic vesicle exocytosis [SNARE stands for SNAP receptor, where SNAP is soluble NSF attachment protein]. The SNARE proteins syntaxin 4 and vesicle-associated membrane protein (VAMP) 2/3 also participate in the insulin-stimulated translocation of GLUT4 from intracellular vesicles to the plasma membrane in adipose cells. We now report the molecular cloning and characterization of rat SNAP-23, a ubiquitously expressed homologue of the essential neuronal SNARE protein SNAP-25 (synaptosomal-associated protein of 25 kDa). Rat SNAP-23 is 86% and 98% identical respectively to human and mouse SNAP-23. Southern blot analysis reveals that the rat, mouse and human SNAP-23 genes encode species-specific isoforms of the same protein. Co-immunoprecipitation of syntaxin 4 and SNAP-23 shows association of these two proteins in rat adipose cell plasma membranes, and insulin stimulation does not alter the SNAP-23/syntaxin 4 complex. In addition, we demonstrate for the first time the participation of SNAP-23, along with syntaxin 4 and VAMP2/3, in the formation of 20S SNARE complexes prepared using rat adipose cell membranes and recombinant alpha-SNAP and NSF proteins. The stoichiometry of the SNARE complexes formed is essentially identical using membranes from either unstimulated or insulin-stimulated adipose cells. These data demonstrate that rat SNAP-23 associates with syntaxin 4 before insulin stimulation and is present in the SNARE complexes known to mediate the translocation of GLUT4 from intracellular vesicles to the plasma membrane of rat adipose cells.  (+info)

Regulation of fatty acid homeostasis in cells: novel role of leptin. (6/5446)

It is proposed that an important function of leptin is to confine the storage of triglycerides (TG) to the adipocytes, while limiting TG storage in nonadipocytes, thus protecting them from lipotoxicity. The fact that TG content in nonadipocytes normally remains within a narrow range, while that of adipocytes varies enormously with food intake, is consistent with a system of TG homeostasis in normal nonadipocytes. The facts that when leptin receptors are dysfunctional, TG content in nonadipocytes such as islets can increase 100-fold, and that constitutively expressed ectopic hyperleptinemia depletes TG, suggest that leptin controls the homeostatic system for intracellular TG. The fact that the function and viability of nonadipocytes is compromised when their TG content rises above or falls below the normal range suggests that normal homeostasis of their intracellular TG is critical for optimal function and to prevent lipoapoptosis. Thus far, lipotoxic diabetes of fa/fa Zucker diabetic fatty rats is the only proven lipodegenerative disease, but the possibility of lipotoxic disease of skeletal and/or cardiac muscle may require investigation, as does the possible influence of the intracellular TG content on autoimmune and neoplastic processes.  (+info)

Reversing adipocyte differentiation: implications for treatment of obesity. (7/5446)

Conventional treatment of obesity reduces fat in mature adipocytes but leaves them with lipogenic enzymes capable of rapid resynthesis of fat, a likely factor in treatment failure. Adenovirus-induced hyperleptinemia in normal rats results in rapid nonketotic fat loss that persists after hyperleptinemia disappears, whereas pair-fed controls regain their weight in 2 weeks. We report here that the hyperleptinemia depletes adipocyte fat while profoundly down-regulating lipogenic enzymes and their transcription factor, peroxisome proliferator-activated receptor (PPAR)gamma in epididymal fat; enzymes of fatty acid oxidation and their transcription factor, PPARalpha, normally low in adipocytes, are up-regulated, as are uncoupling proteins 1 and 2. This transformation of adipocytes from cells that store triglycerides to fatty acid-oxidizing cells is accompanied by loss of the adipocyte markers, adipocyte fatty acid-binding protein 2, tumor necrosis factor alpha, and leptin, and by the appearance of the preadipocyte marker Pref-1. These findings suggest a strategy for the treatment of obesity by alteration of the adipocyte phenotype.  (+info)

Caloric restriction leads to regional specialisation of adipocyte function in the rat. (8/5446)

The study analysed the responses of three metabolic parameters in five distinct adipose tissue depots to caloric restriction (4 weeks) in the rat. The aims were to evaluate whether specific adipose tissue depots were recruited for triacylglycerol (TAG) storage and/or mobilisation, and to determine to what extent specific adipose tissue depots exhibited preferences for the source of fatty acid (FA) for TAG storage. Caloric restriction led to a general enhancement of the response of lipoprotein lipase (LPL), FA synthesis and glucose utilisation to a meal. Effects were particularly marked in the parametrial, perirenal and interscapular depots compared with mesenteric and subcutaneous depots. There was no evidence that individual depots selectively expressed a preference for the pathways concerned with the generation of FA for storage (the exogenous (LPL) and the endogenous (synthesis) pathway). However, the temporal sequence of activation of these pathways differed in a manner consistent with a switch from preponderant use of FA produced via de novo synthesis during the very early phase of feeding towards later use of FA derived from circulating TAG. The overall excursions in insulin levels observed in the calorie-restricted rats were comparable to those found in free-feeding rats, but the magnitude and the rapidity of the individual metabolic responses of the adipocyte were augmented. The data are consistent with a general enhancement of insulin sensitivity and responsiveness in adipose tissue of calorie-restricted rats, together with adaptive regional specialisation of adipocyte function. These adaptations would be predicted to facilitate the immediate conservation of dietary nutrients by promoting their storage as the FA or glycerol moieties of adipose tissue TAG and thereby to ensure the regulated release of FA and glycerol from adipose tissue in accordance with the requirement for glucose conservation and/or production.  (+info)

Amine oxidase substrates mimic several of the insulin effects on adipocyte differentiation in 3T3 F442A cells. Biochem J. 2001 Jun 15; 356(Pt 3):769-77 ...
Horowitz MC, Berry R, Holtrup B, Sebo Z, Nelson T, Fretz JA, Lindskog D, Kaplan JL, Ables GP, Rodeheffer MS, Rosen CJ.. Adipocyte. 2017 Jul 3;6(3):193-204.. PMID: 28872979. Adipocytes were identified in human bone marrow more than a century ago, yet until recently little has been known about their origin, development, function or interactions with other cells in the bone marrow. Little functional significance has been attributed to these cells, a paradigm that still persists today. However, we now know that marrow adipose tissue increases with age and in response to a variety of physiologic induction signals. Bone marrow adipocytes have recently been shown to influence other cell populations within the marrow and can affect whole body metabolism by the secretion of a defined set of adipokines. Recent research shows that marrow adipocytes are distinct from white, brown and beige adipocytes, indicating that the bone marrow is a distinct adipose depot. This review will highlight recent data ...
Gerin I, Bommer GT, McCoin CS, Sousa KM, Krishnan V, MacDougald OA. Roles for miRNA-378/378* in adipocyte gene expression and lipogenesis. Am J Physiol Endocrinol Metab 299: E198-E206, 2010. First published May 18, 2010; doi:10.1152/ajpendo.00179.2010.-In this study, we explored the roles of microRNAs in adipocyte differentiation and metabolism. We first knocked down Argonaute2 (Ago2), a key enzyme in the processing of micro-RNAs (miRNAs), to investigate a potential role for miRNAs in adipocyte differentiation and/or metabolism. Although we did not observe dramatic differences in adipogenesis between Ago2 knock-down and control 3T3-L1 cells, incorporation of [C-14] glucose or acetate into triacylglycerol, and steady-state levels of triacyglycerol were all reduced, suggesting a role for miRNAs in adipocyte metabolism. To study roles of specific miRNAs in adipocyte biology, we screened for miRNAs that are differentially expressed between preadipocytes and adipocytes for the 3T3-L1 and ST2 cell ...
The mechanism of activation for protein kinase B (PKB), an important target for insulin signaling, has been scarcely investigated in primary cells. In this study, we have characterized the insulin-induced phosphorylation and activation of PKB beta in primary rat adipocytes. Insulin stimulation resulted in a translocation of PKB beta from cytosol to membranes, and phosphorylation and activation of PKB beta. Phosphoamino acid analysis and phosphopeptide mapping demonstrated that the phosphorylation occurred mainly on serines, also when using calyculin A, and that these were localized within one major phosphopeptide. Radiosequencing showed that the radioactivity was released in Cycle No. 7. In addition, the peptide was specifically immunoprecipitated from a tryptic digest of PKB beta using the anti-phospho-PKB (Ser-473) antibody. Taken together, these results show that rat adipocyte PKB beta mainly is phosphorylated on Ser-474 in response to insulin stimulation, in contrast to previous studies in ...
Several studies in mice indicate a role for apolipoprotein E (APOE) in lipid accumulation and adipogenic differentiation in adipose tissue. However, little is yet known if APOE functions in a similar manner in human adipocytes. This prompted us to compare lipid loading and expression of adipocyte differentiation markers in APOE-deficient and control adipocytes using the differentiated human mesenchymal stem cell line hMSC-Tert as well as primary human and mouse adipocytes as model systems. Differentiated hMSC-Tert were stably transduced with or without siRNA targeting APOE while murine adipocytes were isolated from wild type and Apoe knockout mice. Human APOE knockdown hMSC-Tert adipocytes accumulated markedly less triglycerides compared to control cells. This correlated with strongly decreased gene expression levels of adipocyte markers such as adiponectin (ADIPOQ) and fatty acid binding protein 4 (FABP4) as well as the key transcription factor driving adipocyte differentiation, peroxisome ...
One of the major findings in the current report is that PIKE-A is critical for adipocyte differentiation. Several lines of evidence support the role of PIKE-A in terminal adipocyte differentiation instead of preadipocyte formation. First, the mature adipocyte marker aP2 is significantly decreased during in vitro adipocyte differentiation in PIKE−/− MEFs, indicating PIKE-A is important for adipocyte differentiation (Fig. 3B and C). Second, PIKE-A expression is increased in fat tissue development of HFD-fed and ob/ob mice, which highlights its function in the process (Fig. 2H). Lastly, HFD induced comparable preadipocyte marker Pref-1 expression in both wild-type and PIKE−/− mice, indicating that formation of new adipocytes is normal in PIKE-null adipose tissue (Fig. 3A). Interestingly, we found a small portion of PIKE−/− MEFs was able to differentiate into mature adipocytes (Fig. 3B), and quantitative analysis revealed a small but statistically significant increment of lipid ...
AIMS/HYPOTHESIS: Salt-inducible kinase 2 (SIK2) is downregulated in adipose tissue from obese or insulin-resistant individuals and inhibition of SIK isoforms results in reduced glucose uptake and insulin signalling in adipocytes. However, the regulation of SIK2 itself in response to insulin in adipocytes has not been studied in detail. The aim of our work was to investigate effects of insulin on various aspects of SIK2 function in adipocytes.. METHODS: Primary adipocytes were isolated from human subcutaneous and rat epididymal adipose tissue. Insulin-induced phosphorylation of SIK2 and HDAC4 was analyzed using phosphospecific antibodies and changes in the catalytic activity of SIK2 with in vitro kinase assay. SIK2 protein levels were analyzed in primary adipocytes treated with the proteasome inhibitor MG132.. RESULTS: We have identified a novel regulatory pathway of SIK2 in adipocytes, which involves insulin-induced phosphorylation at Thr484. This phosphorylation is impaired in individuals with ...
The Ca2+-insensitive protein kinase C (PKC) isoforms ε, η, δ and ζ are possible direct downstream targets of phosphatidylinositol 3-kinase (PI3-K), and might therefore be involved in insulin signalling. Although isoform-specific changes in PKC expression have been reported for skeletal muscle and liver in insulin-resistant states, little is known about these isoforms in adipocytes. Therefore we studied (1) expression and subcellular localization of these isoforms in murine adipocytes, (2) translocation of specific isoforms to membranes in response to treatment with insulin and phorbol 12-myristate 13-acetate (PMA) and (3) regulation of expression in insulin-resistant states. The PKC isoforms ε, η, δ and ζ are expressed in adipocytes. Immunoreactivity for all isoforms is higher in the membranes than in the cytosol, but subcellular fractionation by differential centrifugation shows an isoform-specific distribution within the membrane fractions. PMA treatment of adipocytes induces ...
TY - JOUR. T1 - Beta-mecaptoethanol suppresses inflammation and induces adipogenic differentiation in 3T3-F442A murine preadipocytes. AU - Guo, Wen. AU - Li, Yahui. AU - Liang, Wentao. AU - Wong, Siu. AU - Apovian, Caroline. AU - Kirkland, James L.. AU - Corkey, Barbara E.. PY - 2012/7/23. Y1 - 2012/7/23. N2 - Preadipocytes are present in adipose tissues throughout adult life that can proliferate and differentiate into mature adipocytes in response to environmental cues. Abnormal increase in adipocyte number or size leads to fat tissue expansion. However, it is now recognized that adipocyte hypertrophy is a greater risk factor for metabolic syndrome whereas fat tissue that continues to produce newer and smaller fat cells through preadipocyte differentiation is metabolically healthy. Because adipocyte hypertrophy is often associated with increased oxidant stress and low grade inflammation, both are linked to disturbed cellular redox, we tested how preadipocyte differentiation may be regulated ...
The retinoblastoma protein (RB) has previously been shown to facilitate adipocyte differentiation by inducing cell cycle arrest and enhancing the transactivation by the adipogenic CCAAT/enhancer binding proteins (C/EBP). We show here that the peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear receptor pivotal for adipogenesis, promotes adipocyte differentiation more efficiently in the absence of RB. PPARgamma and RB were shown to coimmunoprecipitate, and this PPARgamma-RB complex also contains the histone deacetylase HDAC3, thereby attenuating PPARgammas capacity to drive gene expression and adipocyte differentiation. Dissociation of the PPARgamma-RB-HDAC3 complex by RB phosphorylation or by inhibition of HDAC activity stimulates adipocyte differentiation. These observations underscore an important function of both RB and HDAC3 in fine-tuning PPARgamma activity and adipocyte differentiation.. Keywords: Thiazolidinediones. ...
Uncoupling protein 1 (UCP-1), the specific marker of brown adipose tissue, is transcriptionally activated in response to adrenergic stimuli and thyroid hormones are necessary for its full expression. We describe differences in the regulation of UCP-1 mRNA expression between rat and mouse brown adipocytes in culture, using norepinephrine (NE), triiodothyronine (T3), insulin and retinoic acid (RA). Results: NE and cAMP-elevating agents strongly increase UCP-1 mRNA levels in cultures of mouse adipocytes, but increases are low in those from rat. In rat adipocytes NE poorly increases UCP-1 mRNA expression and T3 markedly increases the adrenergic response of UCP-1, an effect not observed in mouse adipocytes. In the absence of insulin, T3 itself increases UCP-1 mRNA in rat adipocytes and enhances the response to NE, while in mouse adipocytes no effect of T3 is observed. RA by itself stimulates UCP-1 mRNA in mouse adipocytes, but not in those from rat. In rat cultures, RA requires the presence of NE ...
TY - JOUR. T1 - Regulation of gene expression during adipocyte differentiation. T2 - a review.. AU - Gaskins, H. R.. AU - Hausman, G. J.. AU - Martin, R. J.. PY - 1989/9. Y1 - 1989/9. N2 - The differentiation of adipose precursor cells is accompanied by the acquisition of adipocyte-specific messenger (m) RNAs allowing characteristic changes in protein composition. The development of methods for cloning and characterizing individual genes has provided the opportunity to study selective gene expression by adipocytes at the molecular level. In this review, the information obtained to date regarding transcriptional and post-transcriptional regulatory mechanisms utilized by adipocytes is summarized. Included are descriptions of conserved DNA sequences found in noncoding regions of adipose genes and of how protein-DNA interactions at these regions are thought to regulate the initiation of transcription. Among the transcription factors implemented in regulation of adipocyte-specific gene expression are ...
Tumor necrosis factor (TNF)-alpha is postulated to play a major role in the pathogenesis of obesity-linked insulin resistance, probably resulting from an interaction with insulin signaling pathways. This cross talk has now been investigated in human adipocytes at the level of phosphatidylinositol (PI) 3-kinase, and the TNF receptors (TNFRs) mediating these processes have been identified. Equilibrium binding studies using human adipocytes from mammary tissue indicated the presence of two populations of TNFR with apparent affinity constants of 13 pmol/l and 1.6 nmol/l, respectively. Interaction of TNF-alpha with insulin signaling was determined by quantification of insulin receptor substrate (IRS)-1-associated PI 3-kinase activity. Under control conditions, PI 3-kinase was activated about 10-fold in response to insulin (10[-7] mol/l, 5 min). Preincubation of adipocytes with 5 nmol/l TNF-alpha for 15 min resulted in a 60-70% reduction of insulin action, reaching a stable inhibition (40%) after ...
In contrast to the published studies, which demonstrated associations between average adipocyte size and serum levels or secretion, our study is unique because it investigated the secretory capacity of adipocyte fractions from the same individual separated by cell size. The results obtained by the technique clearly suggest that only the very large adipocytes are dysregulated. Adipocyte hypertrophy appears to cause a differentially impaired secretion between pro- and antiinflammatory adipokines shifting the immunological balance toward the expression of proinflammatory proteins. Thisabnormal function of adipocytes may play an important role in the development of a chronic low-grade proinflammatory state in obesity, which is considered to build the common soil for the development of insulin resistance, type 2 diabetes, and atherosclerosis (5, 68 ...
Oct 17, 2019 , Publications. Sebo ZL, Rendina-Ruedy E, Ables GP, Lindskog DM, Rodeheffer MS, Fazeli PK, Horowitz MC.. Endocr Rev. 2019 Oct 1;40(5):1187-1206. PMID: 31127816. The presence of adipocytes in mammalian bone marrow (BM) has been recognized histologically for decades, yet, until recently, these cells have received little attention from the research community. Advancements in mouse transgenics and imaging methods, particularly in the last 10 years, have permitted more detailed examinations of marrow adipocytes than ever before and yielded data that show these cells are critical regulators of the BM microenvironment and whole-body metabolism. Indeed, marrow adipocytes are anatomically and functionally separate from brown, beige, and classic white adipocytes. Thus, areas of BM space populated by adipocytes can be considered distinct fat depots and are collectively referred to as marrow adipose tissue (MAT) in this review. In the proceeding text, we focus on the developmental origin and ...
There is a physiologic limit to adipocyte cell size. Adipocytes in the mouse inguinal and epididymal fat pads can increase in size three- and seven-fold, respectively, during 12 weeks of HFF (62). Cell size correlates strongly with the frequency of adipocyte death. The percentage of dead epididymal adipocytes increases progressively from 0.1% at one week to as much as 16% at 12 weeks of HFF (62). Independent of how adipocytes die - from necrosis or apoptosis - the reaction of AT to adipocyte death can be likened to the initiation of a wound healing response, triggering a considerable increase in immune cell infiltration. Monocyte recruitment and differentiation to proinflammatory macrophages are of particular importance. These macrophages surround the dead adipocytes, forming what is described histologically as crown-like structures (62-64). Concomitantly, activated myofibroblasts in the area secrete collagen to maintain the integrity of the damaged tissue (65). As macrophages and neutrophils ...
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Dermal adipose tissue (also known as dermal white adipose tissue and herein referred to as dWAT) has been the focus of much discussion in recent years. However, dWAT remains poorly characterized. The fate of the mature dermal adipocytes and the origin of the rapidly reappearing dermal adipocytes at different stages remain unclear. Here, we isolated dermal adipocytes and characterized dermal fat at the cellular and molecular level. Together with dWATs dynamic responses to external stimuli, we established that dermal adipocytes are a distinct class of white adipocytes with high plasticity. By combining pulse-chase lineage tracing and single-cell RNA sequencing, we observed that mature dermal adipocytes undergo dedifferentiation and redifferentiation under physiological and pathophysiological conditions. Upon various challenges, the dedifferentiated cells proliferate and redifferentiate into adipocytes. In addition, manipulation of dWAT highlighted an important role for mature dermal adipocytes ...
It is a desirable goal to stimulate fuel oxidation in adipocytes and shift the balance toward less fuel storage and more burning. To understand this regulatory process, respiration was measured in primary rat adipocytes, mitochondria, and fat-fed mice. Maximum O(2) consumption, in vitro, was determi …
Adipocytes play an important role in energy storage and metabolism. Adipocyte differentiation is a developmental process that is critical for metabolic homeostasis and nutrient signaling. It is controlled by complex actions involving gene expression and signal transduction. Preadipocytes are present throughout adult life in adipose tissues and can proliferate and differentiate into mature adipocytes according to the energy balance. The proliferation and differentiation of these preadipocytes contribute to increases in adipose tissue mass. In vitro study indicates that different tissue-derived preadipocytes exhibit differently in lipid accumulation, adipogenic transcription factor expression, and TNF?-induced apoptosis. It has also been demonstrated that there is a close relationship between adipocyte differentiation and many physiological and pathological processes including fat metabolism, energy balance, obesity, diabetes, hyperlipidemia and breast cancer. HPA-s from Bioarray Research ...
In a previous study designed to understand the role of Myo1c in GLUT4 trafficking and membrane dynamics, we observed that Myo1c overexpression induced dramatic cortical actin remodeling (membrane ruffling) in 3T3-L1 adipocytes, in a serum- and insulin-independent manner (4). This observation suggested that Myo1c might mediate the effect of insulin on membrane ruffling in 3T3-L1 adipocytes, which is supported by our observation that Myo1c depletion in 3T3-L1 adipocytes does indeed attenuate insulin-induced membrane ruffling (data not shown). Interestingly, expression of Myo1c in cultured adipocytes induces membrane ruffling even in the presence of wortmannin, suggesting that Myo1c may function downstream or independent of PI3K in activating membrane ruffling. Our studies here suggest that formation and maintenance of the Rictor-Myo1c complex are not dependent on insulin, rapamycin, or wortmannin (Fig. 1, 2, and 4). Therefore, to determine the functional relevance of Rictors association with ...
CEBPA [ENSP00000427514]. CCAAT/enhancer binding protein (C/EBP), alpha; Transcription factor that coordinates proliferation arrest and the differentiation of myeloid progenitors, adipocytes, hepatocytes, and cells of the lung and the placenta. Binds directly to the consensus DNA sequence 5-T[TG]NNGNAA[TG]-3 acting as an activator on distinct target genes. During early embryogenesis, plays essential and redundant functions with CEBPB. Essential for the transition from common myeloid progenitors (CMP) to granulocyte/monocyte progenitors (GMP). Critical for the proper development of the liver and the lung (By similarity). Necessary for terminal adipocyte differentiation, is required for postnatal maintenance of systemic energy homeostasis and lipid storage (By similarity). To regulate these different processes at the proper moment and tissue, interplays with other transcription factors and modulators. Downregulates the expression of genes that maintain cells in an undifferentiated and ...
Obesity is an increasing health problem worldwide, and nonsurgical strategies to treat obesity have remained rather inefficient. We here show that acute loss of TGF-β-activated kinase 1 (TAK1) in adipocytes results in an increased rate of apoptotic adipocyte death and increased numbers of M2 macrophages in white adipose tissue. Mice with adipocyte-specific TAK1 deficiency have reduced adipocyte numbers and are resistant to obesity induced by a high-fat diet or leptin deficiency. In addition, adipocyte-specific TAK1-deficient mice under a high-fat diet showed increased energy expenditure, which was accompanied by enhanced expression of the uncoupling protein UCP1. Interestingly, acute induction of adipocyte-specific TAK1 deficiency in mice already under a high-fat diet was able to stop further weight gain and improved glucose tolerance. Thus, loss of TAK1 in adipocytes reduces the total number of adipocytes, increases browning of white adipose tissue, and may be an attractive strategy to treat ...
Introduction: Renin-Angiotensin System (RAS) induces oxidative stress and contributes to various pathological conditions including insulin resistance and the metabolic syndrome. Recent studies have shown the role of PPARδ-agonist in attenuation of Angiotensin II induced oxidative stress.The aim of this study was to explore the effectiveness of a PPARδ-agonist in the prevention of Ang II-induced vascular and adipocyte dysfunction and the possible interaction between PPARδ and HO-1 system in a model of enhanced oxidative stress, the Goldblatt 2K1C model.. Methods: We first established a direct stimulatory effect of the PPARδ-agonist (GW 501516) on the HO-1 gene by demonstrating increased luciferase activity in COS-7 cells transfected with a luciferase-HO-1 promoter construct. SD rats were divided in 4 groups: sham operated animals, 2K1C rats and 2K1C rats treated with GW 501516, in the absence or presence of the HO activity inhibitor, stannous mesoporphyrin (SnMP).. Results: 2K1C animals had ...
In our studies, we initially focused on protein kinase G (PKG/cGK), which is expressed both in white and brown adipocytes. Using gain- and loss-of-function models, we found that PKG is the major receptor for cGMP in brown adipocytes. We investigated the downstream targets of PKG and found a novel negative feedback loop that regulates cGMP levels. Importantly, in the presence of increased cGMP levels, we found an enhanced development of brown-like adipocytes, so-called beige or brite (brown in white) cells both in vitro and in vivo. These data indicate that cGMP not only enhances development of classical brown adipocytes, but also promotes development of beige cells.. Therefore, we studied the effect of cGMP in white adipocytes in more detail. Lentiviral overexpression of PKG enhanced differentiation of white adipocytes. Moreover, PKG induced the expression of a brown-like adipogenic program in white fat cells. Treatment of mice with the PDE inhibitor sildenafil for only 7 days promoted ...
Chemerin is a leukocyte chemoattractant and adipokine with important immune and metabolic roles. Chemerin, secreted in an inactive form prochemerin, undergoes C-terminal proteolytic cleavage to generate active chemerin, a ligand for the chemokine-like receptor-1 (CMKLR1). We previously identified that adipocytes secrete and activate chemerin. Following treatment with the obesity-associated inflammatory mediator TNF alpha, unknown adipocyte mechanisms are altered resulting in an increased ratio of active to total chemerin production. Based on these findings we hypothesized adipocytes produce proteases capable of modifying chemerin and its ability to activate CMKRL1. 3T3-L1 adipocytes expressed mRNA of immunocyte and fibrinolytic proteases known to activate chemerin in vitro. Following treatment with a general protease inhibitor cocktail (PIC), the TNF alpha-stimulated increase in apparent active chemerin concentration in adipocyte media was amplified 10-fold, as measured by CMKLR1 activation. ...
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The number of overweight and obese individuals continues to increase in both the U.S. and worldwide. This increase has led to a significant increase in obesity-related medical problems including diabetes mellitus, cardiovascular disease and cancer. In obesity, the differentiation of adipocytes is suppressed. Although adipocyte differentiation is associated with changes in glucose metabolism, little is known about the potential of enzymes involved in glucose metabolism to modulate this process. Pyruvate kinase (PK) mediates the rate-limiting step of glycolysis. The M2 isoform of PK (PKM2) is expressed in adipocytes but its role in adipogenesis is unknown. Here we demonstrate that PKM2 regulates the differentiation of both human and mouse adipocytes. Silencing of PKM2 in preadipocytes led to increased lipid accumulation, enhanced expression of markers (FABP4, PPARgamma, C/EBPBeta) of adipocyte differentiation and caused a shift in the pattern of enzymes involved in glucose metabolism favoring the ...
Occurrence of hyperplasia (negative morphology value) or hypertrophy (positive morphology value) was independent of sex and body weight but correlated with fasting plasma insulin levels and insulin sensitivity, independent of adipocyte volume (β-coefficient = 0.3, P , 0.0001). Total adipocyte number and morphology were negatively related (r = −0.66); i.e., the total adipocyte number was greatest in pronounced hyperplasia and smallest in pronounced hypertrophy. The absolute number of new adipocytes generated each year was 70% lower (P , 0.001) in hypertrophy than in hyperplasia, and individual values for adipocyte generation and morphology were strongly related (r = 0.7, P , 0.001). The relative death rate (∼10% per year) or mean age of adipocytes (∼10 years) was not correlated with morphology. ...
Interestingly, the protein levels of GLUT4, PPARg and Leptin are independent of insulin. It would thus appear that insulin controls the translocation of GLUT4 to the cell surface, not the amount of GLUT4 in an adipocyte. The results of the PPARg and leptin also fly in the face of what I have blogged on before, even small adipocytes contain the same amount of leptin as large adipocytes. And PPARg does not appear to predict adipocyte size in this data set. ( I would of expected larger adipocytes to have higher PPARg, and vice versa for the small adipocytes. *shrug ...
Using a subtraction method, we have isolated genes that are induced early in the differentiation of mouse 3T3-L1 preadipocyte cells into adipocytes. These include the genes encoding transcription factors and signalling proteins, as well as unknown genes. Bach1, a transcription factor, and ARA70, a cofactor, were rapidly induced during differentiation. The induction of these two genes was observed only in growth-arrested 3T3-L1 cells, and not in proliferating cells. In NIH-3T3 cells, no induction was observed under either set of conditions. These results strongly indicate that Bach1 and ARA70 have valuable roles at the onset of adipocyte differentiation.. ...
The study on PDE3B phosphorylation shows that PDE3B is multisite phosphorylated in response to both insulin and catecholamines. We were able to identify six phosphorylation sites on PDE3B namely; 273, S296, S421, S424/5, S474 and S536. From the studies on PDE3B localization we conclude that PDE3B is localized to caveolae and endoplasmic reticulum (ER) in adipocytes and that caveolae localized PDE3B is specifically activated by catecholamines while PDE3B in ER is specifically activated by insulin. Finally, the studies on PDE3B interactions demonstrate that insulin and catecholamines stimulate the recruitment of PDE3B into large macromolecular complexes in adipocytes. The recruitment is dependent on caveolin-1 especially in response to insulin and the constituents of the PDE3B macromolecular complexes are dependent on the stimuli used. After insulin stimulation insulin signaling molecules such as protein kinase B (PKB) are associated with PDE3B in the large complex while after catecholamine ...
Much of the research into obesity and diabetes is carried out using transgenic animal models. FRAMEs experience and that of many others is that such animal models are of little use when trying to study human diseases and responses to potential therapies. The FRAME Alternatives Laboratory cultures primary human adipocytes and skeletal muscle myotubes to study the effects of increased fat and carbohydrate levels on the metabolism and gene expression of human fat and muscle tissue.. ...
article{5d70646d-8df7-4e0f-a397-fb9a3b72cc4f, author = {Ridderstråle, Martin and Amstrup, J and Hilton, D J and Billestrup, N and Tornqvist, H}, issn = {1439-4286}, language = {eng}, number = {3}, pages = {169--177}, publisher = {Georg Thieme Verlag}, series = {Hormone and Metabolic Research}, title = {SOCS-3 is Involved in the Downregulation of the Acute Insulin-Like Effects of Growth Hormone in Rat Adipocytes by Inhibition of Jak2/IRS-1 Signaling.}, url = {http://dx.doi.org/10.1055/s-2003-39077}, volume = {35}, year = {2003 ...
Stimulation of lipogenesis in rat adipocytes by ATP, a ligand for P2-receptors.: The activation of P2-receptors has a wide range of diverse effects in many tiss
Adipocytes are key cells in metabolic homeostasis. They are very useful for creating models for studying metabolic diseases such as obesity and diabetes.
Obesity has spread worldwide and become a common health problem in modern society. One typical feature of obesity is the excessive accumulation of fat in adipocytes, which occurs through the following two physiological phenomena: hyperplasia (increase in quantity) and hypertrophy (increase in size) of adipocytes. In clinical and scientific research, the accurate quantification of the number and diameter of adipocytes is necessary for assessing obesity. In this study, we present a new automatic adipocyte counting system, AdipoCount, which is based on image processing algorithms. Comparing with other existing adipocyte counting tools, AdipoCount is more accurate and supports further manual correction. AdipoCount counts adipose cells by the following three-step process: 1) It detects the image edges, which are used to segment the membrane of adipose cells; 2) It uses a watershed-based algorithm to re-segment the missing dyed membrane; and 3) It applies a domain connectivity analysis to count the cells. The
Background Middle age weight problems is recognized as a risk factor for Alzheimers disease (AD) although a mechanistic linkage remains unclear. stimulation-dependent changes in macrophage and adipocyte culture phenotype were examined for comparison to the changes. CYT997 Conclusions/Significance Adipose brain and tissue from fat rich diet given pets demonstrated increased TNF- and microglial and macrophage activation. Both brains and adipose cells got raised APP amounts localizing to neurons and macrophage/adipocytes also, respectively. APP agonist antibody excitement of macrophage ethnicities improved particular cytokine secretion without obvious results on adipocyte tradition phenotype. These data support the hypothesis that high fats diet-dependent weight problems leads to concomitant pro-inflammatory adjustments in mind and adipose cells thats characterized, partly, by improved degrees of APP which may be adding specifically to inflammatory changes that occur. Introduction Obesity, ...
A major effort in the laboratory focuses on STAT proteins. These proteins are signaling molecules and transcription factors, which means they control the gene expression in a tissue specific manner. Our laboratory studies the activation and function of STAT proteins in adipocytes. We study adipocytes because this cell type has several functions and if any one of these function is disrupted than Type 2 Diabetes can develop. To date, one of our notable observations is that STAT5 can regulate fat cell development both in vitro and in vivo. We have also identified STAT5 target genes in adipocytes. These genes play a role in insulin action, lipid metabolism and the endocrine properties of fat cells. All of our studies demonstrate that STAT5 is an important transcription factor in adipocytes and can regulate genes associated with Type 2 Diabetes. To further understand the biology of this multifunctional protein, we are identifying other proteins that associate with STAT5 and are studying a mouse model ...
Volume 156, Issue 1, January 16, 2014. There has been an upsurge of interest in the adipocyte coincident with the onset of the obesity epidemic and the realization that adipose tissue plays a major role in the regulation of metabolic function. The past few years, in particular, have seen significant changes in the way that we classify adipocytes and how we view adipose development and differentiation. We have new perspective on the roles played by adipocytes in a variety of homeostatic processes and on the mechanisms used by adipocytes to communicate with other tissues. Finally, there has been significant progress in understanding how these relationships are altered during metabolic disease and how they might be manipulated to restore metabolic health.. To view the publication, please click here.. ...
By stimulating the synthesis of AQP8 into adipocytes, Actiporine 8G maintains mitochondrial homeostasis and reactivates lipolysis by adipocytes. This action allows the decrease of adipocytes volume.
A combination of cellular, biochemical, genetic and genomic techniques have revealed a new molecular player in the production of fat cells in mice, which could improve our understanding of obesity.
Exposure of cultures of 3T3-L1 preadipose cells to nitrogen for 16 hours kills almost all of the cells, but after exposure to 5% oxygen for 16 hours most of the cells survive, and recover when culture is continued in 20 ...
The broad area of research that I am interested in is obesity and cardiovascular disease (CVD). My group is particularly focused on deciphering the cellular events and the molecular mechanisms regulating adipocyte energy dissipation in response to oxidative stress. The overreaching goal of our research is to understand the basic regulation of adipocyte function and to identify factors that can be used to reprogram these cells into energetically more active cells for the treatment of obesity.
Description - Human interleukin 1 receptor antagonist (IL1RN, IL1F3, IL1RA, IRAP; Gene ID: 3557) is a protein that is produced in at least two forms, one that stays inside the cell and one that is secreted. This assay is for the secreted version. IL-1RA is secreted by various cell types including epithelial cells, monocytes, and adipocytes. It binds to the IL-1 receptor thus preventing signaling by both IL-1α and IL 1β cytokines ...
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Comments, concepts and statistics about Pancreatic Lipase Inhibitory Gallotannins from Galla Rhois with Inhibitory Effects on Adipocyte Differentiation in 3T3-L1 Cells.
ERRERA, Flavia I.V. et al. COL18A1 is highly expressed during human adipocyte differentiation and the SNP c.1136C , T in its frizzled motif is associated with obesity in diabetes type 2 patients. An. Acad. Bras. Ciênc. [online]. 2008, vol.80, n.1, pp.167-177. ISSN 1678-2690. http://dx.doi.org/10.1590/S0001-37652008000100012.. Collagen XVIII can generate two fragments, NC11-728 containing a frizzled motif which possibly acts in Wnt signaling and Endostatin, which is cleaved from the NC1 and is a potent inhibitor of angiogenesis. Collagen XVIII and Wnt signaling have recently been associated with adipogenic differentiation and obesity in some animal models, but not in humans. In the present report, we have shown that COL18A1 expression increases during human adipogenic differentiation. We also tested if polymorphisms in the Frizzled (c.1136C,T; Thr379Met) and Endostatin (c.4349G,A; Asp1437Asn) regions contribute towards susceptibility to obesity in patients with type 2 diabetes (113 obese, BMI ...
TY - JOUR. T1 - microRNA-320/RUNX2 axis regulates adipocytic differentiation of human mesenchymal (skeletal) stem cells. AU - Hamam, D. AU - Ali, D. AU - Vishnubalaji, R. AU - Hamam, R. AU - Al-Nbaheen, M. AU - Chen, L. AU - Kassem, M. AU - Aldahmash, A. AU - Alajez, N M. PY - 2014. Y1 - 2014. N2 - The molecular mechanisms promoting lineage-specific commitment of human mesenchymal (skeletal or stromal) stem cells (hMSCs) into adipocytes (ADs) are not fully understood. Thus, we performed global microRNA (miRNA) and gene expression profiling during adipocytic differentiation of hMSC, and utilized bioinformatics as well as functional and biochemical assays, and identified several novel miRNAs differentially expressed during adipogenesis. Among these, miR-320 family (miR-320a, 320b, 320c, 320d and 320e) were ~2.2-3.0-fold upregulated. Overexpression of miR-320c in hMSC enhanced adipocytic differentiation and accelerated formation of mature ADs in ex vivo cultures. Integrated analysis of ...
The primary function of adipose tissue is to store energy in the form of triacylglycerol, which is hydrolyzed to fatty acids to supply other tissues with energy. While insulin promotes the storage of triacylglycerol, catecholamines stimulate its hydrolysis. The development of type II diabetes is strongly associated with obesity, indicating a role of triacylglycerol metabolism in the pathogenesis of diabetes. Caveolae are plasma membrane invaginations found in most cells but are highly abundant in adipocytes. Insulin receptors are localized in caveolae and their function depends on intact caveolae structures. In the present thesis work, mass spectrometry-based methodology allowed identification of a number of new proteins and their posttranslational modifications in caveolae of human adipocytes. Variable N-terminal acetylation and phosphorylation of caveolin-1α and caveolin-1β were identified, which might regulate the function of caveolae. The transcription regulator protein PTRF was identified ...
BioVendor - BioVendor Research and Diagnostic Products is a developer and manufacturer of immunoassays, recombinant proteins, antibodies and endotoxin-removal products.
Stem cells are cells that can self-renew and differentiate into a variety of cell types under certain conditions. Stem cells have great potential in regenerative medicine and cell therapy for the treatment of certain diseases. To deliver knowledge about this frontier in science and technology to medical undergraduate students, we designed an innovative practical experiment for freshmen in their second semester. The lab exercise focused on rat bone marrow mesenchymal stem cell (BMSC) isolation, cell culture and differentiation, and it aimed to help students master the aseptic techniques for cell culture, the basic methods and procedures for the primary culture and passage of BMSCs, the basic procedure for the directional differentiation of BMSCs into adipocytes and their subsequent identification by oil-red-O staining ...
TY - JOUR. T1 - Effects of gut microbiota manipulation on ex vivo lipolysis in human abdominal subcutaneous adipocytes. AU - Jocken, Johan W. E.. AU - Reijnders, Dorien. AU - Canfora, Emanuel E.. AU - Boekschoten, Mark V.. AU - Plat, Joghum. AU - Goossens, Gijs H.. AU - Blaak, Ellen E.. PY - 2018/1/1. Y1 - 2018/1/1. KW - Microbiota. KW - Lipolysis. KW - Fatty acid metabolism. KW - Adipose Tissue. KW - Obesity. KW - Insulin resistance. KW - HORMONE-SENSITIVE LIPASE. KW - ADIPOSE TRIGLYCERIDE LIPASE. KW - DIET-INDUCED OBESITY. KW - FREE FATTY-ACIDS. KW - PROPIONIC-ACID. KW - ACETATE. KW - PROTEIN. KW - PHOSPHORYLATION. KW - DIFFERENTIATION. KW - EXPRESSION. U2 - 10.1080/21623945.2018.1464366. DO - 10.1080/21623945.2018.1464366. M3 - Article. VL - 7. SP - 106. EP - 112. JO - Adipocyte. JF - Adipocyte. SN - 2162-3945. IS - 2. ER - ...
TY - JOUR. T1 - Peroxisome proliferator-activated receptor γ and its role in adipocyte homeostasis and thiazolidinedione-mediated insulin sensitization. AU - Wang, Qiong A.. AU - Zhang, Fang. AU - Jiang, Lei. AU - Ye, Risheng. AU - An, Yu. AU - Shao, Mengle. AU - Tao, Caroline. AU - Gupta, Rana K. AU - Scherer, Philipp E. PY - 2018/5/1. Y1 - 2018/5/1. N2 - Adipose tissue is a dynamic organ that makes critical contributions to whole-body metabolic homeostasis. Although recent studies have revealed that different fat depots have distinct molecular signatures, metabolic functions and adipogenic mechanisms, peroxisome proliferator-activated receptor γ (PPARγ) is still widely viewed as the master regulator of adipogenesis and critical for maintaining mature adipocyte function. Using an inducible, adipocyte-specific knockout system, we explored the role of PPARγ in mature adipocytes in vivo. Short-term PPARγ deficiency in adipocytes reduces whole-body insulin sensitivity, but adipocytes are ...
Preadipocyte factor-1 (Pref-1) is a transmembrane protein highly expressed in preadipocytes. Pref-1 expression is, however, completely abolished in adipocytes. The extracellular domain of Pref-1 undergoes two proteolytic cleavage events that generate 50 and 25 kDa soluble products. To understand the function of Pref-1, we generated transgenic mice that express the full ectodomain corresponding to the large cleavage product of Pref-1 fused to human immunoglobulin-γ constant region. Mice expressing the Pref-1/hFc transgene in adipose tissue, driven by the adipocyte fatty acid-binding protein (aP2, also known as aFABP) promoter, showed a substantial decrease in total fat pad weight. Moreover, adipose tissue from transgenic mice showed reduced expression of adipocyte markers and adipocyte-secreted factors, including leptin and adiponectin, whereas the preadipocyte marker Pref-1 was increased. Pref-1 transgenic mice with a substantial, but not complete, loss of adipose tissue exhibited ...
TY - JOUR. T1 - Tumor necrosis factor increases the rate of lipolysis in primary cultures of adipocytes without altering levels of hormone-sensitive lipase. AU - Green, Allan. AU - Dobias, Susan B.. AU - Walters, Diedra J.A.. AU - Brasier, Allan R.. PY - 1994/6. Y1 - 1994/6. N2 - To investigate the effects of cytokines on adipocyte lipolysis, a macrophage cell line (RAW 264.7) was treated with Escherichia coli lipopolysaccharide (1 μg/ml) for 18 h to induce cytokine release. Conditioned medium (5%, vol/vol) from these cells was added to rat epididymal adipocytes isolated and incubated under sterile conditions. After incubation, the adipocytes were washed, and the rate of lipolysis (glycerol release) was determined after a further 1-h incubation. The conditioned medium caused an approximately 2.7-fold increase in lipolysis, detectable after 6-12 h, maximal by 24 h, and reversible by 48 h after washing the cells. The effect of conditioned medium was reversed by a neutralizing antibody to mouse ...
Saturated fatty acids have been shown to cause insulin resistance and low-grade chronic inflammation, whereas unsaturated fatty acids suppress inflammation via G-protein coupled receptor 120 (GPR120) in macrophages. However, the anti-inflammatory effects of unsaturated fatty acids in adipocytes have yet to be elucidated. Hence, the aims of the present study were to evaluate the anti-inflammatory effects of eicosapentaenoic acid (EPA) via GPR120 in adipocytes. We used 250 μM palmitate as a representative saturated fatty acid. 3T3-L1 adipocytes were used for in vitro studies. We further evaluated the effect of EPA supplementation in a high-fat/high-sucrose (HFHS) diet-induced adipose tissue inflammatory mouse model. EPA attenuated palmitate-induced increases in inflammatory gene expression and NF-κB phosphorylation in 3T3-L1 adipocytes. Silencing of GPR120 abolished the anti-inflammatory effects of EPA. In GPR120 downstream signal analysis, EPA was found to decrease palmitate-induced increases in TAK1
The epidemic of obesity and diabetes has markedly spurred the research interest in adipocyte biology. Brown adipocytes are specialized for energy expenditure and of therapeutic interest for treatment of metabolic diseases, but how brown adipocytes are distinguished from white adipocytes at the level of translational regulation remains poorly understood. To systemically determine the translational control of gene expression in adipose tissue, we performed ribosome profiling and RNA-seq in parallel to depict the translatome and transcriptome changes during primary brown and white adipogenesis, and between brown and white adipose tissue. The most prominent layer of translational regulation was the increased translation efficiency of genes encoding mitochondria components in brown adipocytes relative to white. Systemic analysis of the regulatory interactions between microRNAs and their targets revealed that microRNAs were more active in repressing targets mRNA abundance and translation in brown ...
Intramuscular fat or marbling is critical for the palatability of beef. In mice, very recent studies show that adipocytes and fibroblasts share a common pool of progenitor cells, with Zinc finger protein 423 (Zfp423) as a key initiator of adipogenic differentiation. To evaluate the role of Zfp423 in intramuscular adipogenesis and marbling in beef cattle, we sampled beef muscle for separation of stromal vascular cells. These cells were immortalized with pCI neo-hEST2 and individual clones were selected by G418. A total of 288 clones (3×96 well plates) were isolated and induced to adipogenesis. The presence of adipocytes was assessed by Oil-Red-O staining. Three clones with high and low adipogenic potential respectively were selected for further analyses. In addition, fibro/adipogenic progenitor cells were selected using a surface marker, platelet derived growth factor receptor (PDGFR) α. The expression of Zfp423 was much higher (307.4±61.9%, P|0.05) in high adipogenic cells, while transforming growth
TY - JOUR. T1 - Zinc-α2-glycoprotein, a lipid mobilizing factor, is expressed in adipocytes and is up-regulated in mice with cancer cachexia. AU - Bing, Chen. AU - Bao, Yi. AU - Jenkins, John. AU - Sanders, Paul. AU - Manieri, Monia. AU - Cinti, Saverio. AU - Tisdale, Michael J.. AU - Trayhurn, Paul. PY - 2004/2/24. Y1 - 2004/2/24. N2 - Zinc-α2-glycoprotein (ZAG), a 43-kDa protein, is overexpressed in certain human malignant tumors and acts as a lipid-mobilizing factor to stimulate lipolysis in adipocytes leading to cachexia in mice implanted with ZAG-producing tumors. Because white adipose tissue (WAT) is an endocrine organ secreting a wide range of protein factors, including those involved in lipid metabolism, we have investigated whether ZAG is produced locally by adipocytes. ZAG mRNA was detected by RT-PCR in the mouse WAT depots examined (epididymal, perirenal, s.c., and mammary gland) and in interscapular brown fat. In WAT, ZAG gene expression was evident in mature adipocytes and in ...
Our findings presented herein have uncovered a previously unappreciated transcription factor pathway, mediated by HIF-2 in adipocytes, that plays a critical role in the regulation of adipocyte functions. Chronic activation of HIF-2, but not HIF-1, in adipocytes leads to adipose inflammation and pathological hypertrophy in the heart. The hypertrophic heart conditions presented by our mouse models are reminiscent of the cardiac hypertrophy observed in severely obese persons.2 Our solid genetic evidence strongly suggests that adipose hypoxia, observed under the condition of pathological obesity,5-7 may facilitate the development of obesity-related cardiac hypertrophy via sustained activation of HIF-2 in adipocytes.. Our findings demonstrate that HIF activation in adipocytes exerts its cardiac effects in a manner distinct from other purported mechanisms linked to obesity-associated cardiomyopathy. The pathological cardiomegaly observed herein occurs in the absence of lipid accumulation in blood ...
High fat diet-induced endotoxaemia triggers low-grade inflammation and lipid release from adipose tissue. This study aims to unravel the cellular mechanisms leading to the lipopolysaccharide (LPS) effects in human adipocytes. Subcutaneous pre-adipocytes surgically isolated from patients were differentiated into mature adipocytes in vitro. Lipolysis was assessed by measurement of glycerol release and mRNA expression of pro-inflammatory cytokines were evaluated by real-time PCR. Treatment with LPS for 24 h induced a dose-dependent increase in interleukin (IL)-6 and IL-8 mRNA expression. At 1?µg/ml LPS, IL-6 and IL-8 were induced to 19.5?±?1.8-fold and 662.7?±?91.5-fold (P?,?0.01 vs basal), respectively. From 100?ng/ml to 1?µg/ml, LPS-induced lipolysis increased to a plateau of 3.1-fold above basal level (P?,?0.001 vs basal). Co-treatment with inhibitors of inhibitory kappa B kinase kinase beta (IKK?) or NF-?B inhibited LPS-induced glycerol release. Co-treatment with the protein kinase A (PKA) ...
Preadipocyte factor-1 (Pref-1) is a transmembrane protein highly expressed in preadipocytes. Pref-1 expression is, however, completely abolished in adipocytes. The extracellular domain of Pref-1 undergoes two proteolytic cleavage events that generate 50 and 25 kDa soluble products. To understand the function of Pref-1, we generated transgenic mice that express the full ectodomain corresponding to the large cleavage product of Pref-1 fused to human immunoglobulin-γ constant region. Mice expressing the Pref-1/hFc transgene in adipose tissue, driven by the adipocyte fatty acid-binding protein (aP2, also known as aFABP) promoter, showed a substantial decrease in total fat pad weight. Moreover, adipose tissue from transgenic mice showed reduced expression of adipocyte markers and adipocyte-secreted factors, including leptin and adiponectin, whereas the preadipocyte marker Pref-1 was increased. Pref-1 transgenic mice with a substantial, but not complete, loss of adipose tissue exhibited ...
TY - JOUR. T1 - Differential regulation of gene expression and insulin-induced activation of phosphodiesterase 3B in adipocytes of lean insulin-resistant IRS-1 (-/-) mice. AU - Hasegawa, Masaaki. AU - Tang, Yan. AU - Osawa, Haruhiko. AU - Onuma, Hiroshi. AU - Nishimiya, Tatsuya. AU - Ochi, Masaaki. AU - Terauchi, Yasuo. AU - Kadowaki, Takashi. AU - Makino, Hideichi. PY - 2002/11/1. Y1 - 2002/11/1. N2 - Phosphodiesterase (PDE) 3B, a major isoform of PDE in adipocytes, mediates the antilipolytic action of insulin. PDE3B gene expression is generally reduced in adipocytes of either monogenic or polygenic rodent models of obese, insulin-resistance. An increased fat cell size, a common feature of obesity, could account for this reduction. Insulin receptor substrate-1 (IRS-1) (-/-) mice are lean with a reduced fat cell size and have insulin resistance due to a primary defect of insulin signaling. To determine whether the regulation of PDE3B gene expression is correlated with fat cell size, we examined ...
Although numerous works have focused on adipocyte differentiation and function as well as alterations under pathophysiological conditions, only a few studies have considered the importance of mitochondrial activity in these situations [11]. In fact, mitochondria play important roles in adipocyte differentiation and function. Pre-adipocytes mature in two steps: differentiation and then hypertrophy. During the early maturation stage, an increased number of mitochondria are required [11] and 12 E.H. Koh et al., Essential role of mitochondrial function in adiponectin synthesis in adipocytes, Diabetes 56 (2007), pp. 2973-2981.[12], resulting in small adipocytes, which are highly sensitive to insulin and that secrete high levels of adiponectin [12]. By contrast, older adipocytes increase in size (hypertrophy), lose their functional activities and become resistant to insulin. They exhibit decreased numbers of mitochondria with impaired functions and secrete less adiponectin [12]. In addition, ...
Compared to standard 2D culture systems, new methods for 3D cell culture of adipocytes could provide more physiologically accurate data and a deeper understanding of metabolic diseases such as diabetes. By resuspending living cells in a bioink of nanocellulose and hyaluronic acid, we were able to print 3D scaffolds with uniform cell distribution. After one week in culture, cell viability was 95%, and after two weeks the cells displayed a more mature phenotype with larger lipid droplets than standard 2D cultured cells. Unlike cells in 2D culture, the 3D bioprinted cells did not detach upon lipid accumulation. After two weeks, the gene expression of the adipogenic marker genes PPAR. and FABP4 was increased 2.0- and 2.2-fold, respectively, for cells in 3D bioprinted constructs compared with 2D cultured cells. Our 3D bioprinted culture system produces better adipogenic differentiation of mesenchymal stem cells and a more mature cell phenotype than conventional
1 reference with editorial concern (retraction etc.) - Supporting: 851, Disputing: 88, Mentioning: 38647 - Accumulating data have indicated a fundamental role of eosinophils in regulating adipose tissue homeostasis. Here, we performed whole-genome RNA sequencing of the small intestinal tract, which suggested the presence of impaired lipid metabolism in eosinophil-deficient ΔdblGATA mice. ΔdblGATA mice fed a high-fat diet (HFD) showed reduced body fat mass, impaired enlargement of adipocytes, decreased expression of adipogenic genes, and developed glucose intolerance. HFD induced accumulation of eosinophils in the perigonadal white adipose tissue. Concordantly, adipocyte-differentiated 3T3-L1 cells promoted the migration of eosinophils through the expression of CCL11 (eotaxin-1) and likely promoted their survival through the expression of interleukin (IL)-3, IL-5, and granulocyte-macrophage colony-stimulating factor. HFD-fed ΔdblGATA mice showed increased infiltration of macrophages, CD4+ T-cells, and
TY - JOUR. T1 - Esterification of free fatty acids in adipocytes. T2 - A comparison between octanoate and oleate. AU - Guo, Wen. AU - Choi, Ji Kyung. AU - Kirkland, James L.. AU - Corkey, Barbara E.. AU - Hamilton, James A.. PY - 2000/7/15. Y1 - 2000/7/15. N2 - Medium-chain triacylglycerols (MCT) are present in milk, coconut oil and other foods, and are used therapeutically in special diets for certain disorders of lipid and glucose utilization. Recently, it has become apparent that MCT are not only oxidized in the liver, but are also present in lymph and fat tissue, particularly after chronic treatment. To evaluate the influence of MCT on metabolism in fat cells, we compared incorporation of octanoate and oleate into cellular triacylglycerols of 3T3-L1 adipocytes as well as their effects on preadipocyte differentiation. We found that less octanoate than oleate was stored and that more octanoate than oleate was oxidized. Octanoate was esterified to a greater extent at the sn-1,3 position of ...
Obesity is associated with a state of chronic, low-grade inflammation. Recent studies have demonstrated that obese adipose tissue is characterized by increased infiltration of macrophages, suggesting that they are an important source of inflammation in the adipose tissue.13-15,24 It is, therefore, important to elucidate the signals that attract macrophages to the adipose tissue and to dissect the molecular mechanisms whereby adipocytes and macrophages communicate within the adipose tissue. Here we developed an in vitro coculture system composed of differentiated 3T3-L1 adipocytes and the macrophage cell line RAW264. The data herein suggest that our coculture system provides the unique in vitro experimental model system to investigate the functional interaction between adipocytes and macrophages within the adipose tissue.. This study demonstrates for the first time that the coculture of 3T3-L1 and RAW264 results in marked upregulation of proinflammatory cytokines, such as MCP-1, IL-6, and TNF-α, ...
Over the past decade, great progress has been made in understanding the complexity of adipose tissue biology and its role in metabolism. This includes new insights into the multiple layers of adipose tissue heterogeneity, not only differences between white and brown adipocytes, but also differences in white adipose tissue at the depot level and even heterogeneity of white adipocytes within a single depot. These inter- and intra-depot differences in adipocytes are developmentally programmed and contribute to the wide range of effects observed in disorders with fat excess (overweight/obesity) or fat loss (lipodystrophy). Recent studies also highlight the underappreciated dynamic nature of adipose tissue, including potential to undergo rapid turnover and dedifferentiation and as a source of stem cells. Finally, we explore the rapidly expanding field of adipose tissue as an endocrine organ, and how adipose tissue communicates with other tissues to regulate systemic metabolism both centrally and ...
TY - JOUR. T1 - CXCL3 positively regulates adipogenic differentiation. AU - Kusuyama, Joji. AU - Komorizono, Anna. AU - Bandow, Kenjiro. AU - Ohnishi, Tomokazu. AU - Matsuguchi, Tetsuya. PY - 2016/10. Y1 - 2016/10. N2 - Chemokines are a family of cytokines inducing cell migration and inflammation. Recent reports have implicated the roles of chemokines in cell differentiation. However, little is known about the functional roles of chemokines in adipocytes. Here, we explored gene expression levels of chemokines and chemokine receptors during adipogenic differentiation. We have found that two chemokines, chemokine (C-X-C motif) ligand 3 (CXCL3) and CXCL13, as well as CXC chemokine receptor 2(CXCR2), a CXCL3 receptor, are highly expressed in mature adipocytes. When 3T3-L1 cells and ST2 cells were induced to differentiate, both the number of lipid droplets and the expression levels of adipogenic markers were significantly promoted by the addition of CXCL3, but not CXCL13. Conversely, gene knockdown ...
Phosphodiesterase 3B (PDE3B) is an important component of insulin and cAMP-dependent signalling pathways. In order to study phosphorylation of PDE3B, we have used an adenoviral system to express recombinant flag-tagged PDE3B in primary rat adipocytes and H4IIE hepatoma cells. Phosphorylation of PDE3B after treatment of cells with insulin, cAMP-increasing agents, or the phosphatase inhibitor, calyculin A was analyzed by two-dimensional tryptic phosphopeptide mapping and mass spectrometry. We found that PDE3B is multisite phosphorylated in adipocytes and H4IIE hepatoma cells in response to all these stimuli. Several sites were identified; serine (S)273, S296, S421, S424/5, S474 and S536 were phosphorylated in adipocyte as well as H4IIE hepatoma cells whereas S277 and S507 were phosphorylated in hepatoma cells only. Several of the sites were phosphorylated by insulin as well as cAMP-increasing hormones indicating integration of the two signalling pathways upstream of PDE3B, maybe at the level of ...
The present results provide direct evidence for a regulatory role of mechanical stress in adipocyte differentiation, mediated through the activation of the ERK/MAPK system. Controversial observations concerning the role of ERK/MAPK in adipocyte differentiation have been reported by several laboratories - the activation of the ERK/MAPK pathway has been shown to be involved in both the inhibition (Font de Mora et al., 1997; Hu et al., 1996; Kim et al., 2001; Shimba et al., 2001) and the promotion (Bost et al., 2002; Klemm et al., 2001; Machinal-Quelin et al., 2002; Prusty et al., 2002; Zhang et al., 1996) of adipocyte differentiation. Along these lines, Prusty et al. recently suggested that stimulation of the ERK/MAPK pathway might have opposing effects in the process of adipogenesis, depending on the time of activation during the differentiation process (Prusty et al., 2002). In the present study, the activated state of ERK1/2 was more prolonged during the induction period in response to the ...
Obesity and specifically central obesity is related to insulin resistance, type 2 diabetes and other components of the so-called metabolic syndrome. The aim of this study was to elucidate the interplay between hormones, nutrients and adipose depots in normal and insulin-resistant fat cell metabolism.. High levels of free fatty acids (FFAs) induce insulin resistance in muscle and liver in vivo. In the present study, rat adipocytes were treated with high physiological levels of oleic or palmitic acid in vitro for 4-24 h. This treatment had no effect on basal or insulin-stimulated glucose uptake capacity in these cells, neither did it affect the levels of the insulin signalling proteins; insulin receptor substrate (IRS)-1 or -2, phosphatidylinositol 3-kinase (PI3-K), protein kinase B (PKB) or glucose transporter (GLUT) 4, or the regulation of lipolysis rate.. Visceral adiposity is considered to be more harmful than peripheral adiposity with respect to metabolic and cardiovascular complications. In ...
Adipose tissue is a highly specialized compartment of cells actively involved in maintaining global metabolic homeostasis through lipid synthesis and storage, adipokine secretion, and insulin responsiveness (1). Adipocytes compose the majority of cells in adipose tissue and play a critical role in normal physiology, but their dysfunction is also at the center of a diverse range of diseases, including obesity, diabetes, and lipodystrophies (2). Furthermore, primary preadipocytes and adipose-derived stem cells have shown promise in treating multiple conditions (3-5). Therefore, it is critical to understand the process by which spindly fibroblastic precursor cells undergo conversion into round lipid-laden fat cells.. In vitro models of adipogenesis, such as the extensively studied committed preadipocyte cell line 3T3-L1 cells, have elucidated two major phases of adipogenesis: commitment and terminal differentiation (6, 7). Terminal differentiation is characterized by the induction of metabolic ...
The activation of beige adipocyte thermogenesis by cold temperatures and β3-adrenergic receptor agonists induce beige adipocyte formation, function and perdurance.
Induction of brown-like adipocytes (beige/brite cells) in white adipose tissue (WAT) suggests a new approach for preventing and treating obesity via induction of thermogenesis associated with uncoupling protein 1 (UCP1). However, whether diet-derived factors can directly induce browning of white adipocytes has not been well established. In addition, the underlying mechanism of induction of brown-like adipocytes by diet-derived factors has been unclear. Here, we demonstrate that artepillin C (ArtC), which is a typical Brazilian propolis-derived component, significantly induces brown-like adipocytes in murine C3H10T1/2 cells and primary inguinal WAT (iWAT)-derived adipocytes. This significant induction is due to activation of peroxisome proliferator-activated receptor γ and stabilization of PRD1-BF-1-RIZ1 homologous domain-containing protein-16 (PRDM16). Furthermore, the oral administration of ArtC (10 mg/kg) for 4 weeks significantly induced brown-like adipocytes accompanied by significant ...
Regional differences in free fatty acid (FFA) handling contribute to diseases associated with particular fat distributions. As cultured rat preadipocytes became differentiated, FFA transfer into preadipocytes increased and was more rapid in single pe
Adipocytes are now recognized as endocrine cells secreting adipocytokines, regulating multiple metabolic pathways. In this study, we addressed secretion of microvesicles by 3T3-L1 adipocytes. We found that MFG-E8, one of the exosomal proteins, was present in the microvesicles and was distributed in …
Adipocytes arise from mesodermal stem cells, which have the capacity to differentiate into a variety of other cell types, including myocytes (1). Once committed to the adipocyte lineage, preadipocytes can remain quiescent, multiply, or undergo differentiation and become adipocytes. 3T3-L1 and 3T3-F442A cells are established mouse preadipocyte models. Both cell lines can be induced to differentiate in cell culture, but 3T3-F442A cells are thought to be arrested at a later point in development (2). Studies of these cellular models have revealed some of the molecular events that orchestrate adipogenesis, including the role of C/EBPs and PPARγ in mediating the expression of adipocyte-specific genes (3, 4).. Wnts are a family of paracrine and autocrine factors that regulate cell growth and cell fate (5). Signaling is initiated when Wnt ligands bind to transmembrane receptors of the Frizzled family. In the canonical Wnt signaling pathway, Frizzleds signal through Dishevelled to inhibit the kinase ...
As we age, however, the body gradually gets less efficient in using brown adipose tissue - which you may have experienced in the form of slower metabolism that comes with age.. Compounding matters is the issue with sugary foods, preservatives, and a sedentary lifestyle that plagues most Americans. This, unfortunately, leads to a buildup of white adipose tissue, or fat.. Different from white adipocytes that store fat, the brown or beige adipocytes are considered a metabolic sink for fat, glucose and other metabolites, Wang said. Beige adipocytes can take up and burn excessive glucose and fat to liberate heat; therefore, they are promising targets for the treatment of obesity and its related metabolic disorders, including insulin resistance, dyslipidemia and cardiovascular disease.. Previously, researchers targeted reservatol - a nutrient found in the skin of red grapes and some berries - as a means to combat obesity and enhance fat burning. The problem, however, is that reservatol proved ...
Evidence from both human and animal models suggests that estrogens play an important role in adipose tissue development. Most of the actions of estrogens are mediated by two types of ER (α and β). Different roles have been assigned to ER-α and ER-β in mediating estrogen effects in adipose tissue. This was suggested by the observations that ER-α gene knockout mice develop obesity, whereas ER-β knockout mice have a normal amount of adipose tissue (19, 30). Up to now, few studies aimed to characterize ER subtypes in human adipose tissue, and they have led to discrepant results. In this work, we have studied the expression of both ER-α and ER-β subtypes in cultured preadipocytes and isolated mature adipocytes from subcutaneous and intra-abdominal fat deposits from both men and women by using real-time PCR and Western blotting techniques. Moreover, we have investigated the effects of E2 in vitro on ER expression in these cells.. In mature adipocytes both ER-α and ER-β subtypes are ...
The size distribution of adipocytes in a suspension, after collagenase digestion of adipose tissue, can be determined by computerized image analysis. Free lipid, forming droplets, in such suspensions implicates a bias since droplets present in the images may be identified as adipocytes. This problem is not always adjusted for and some reports state that distinguishing droplets and cells is a considerable problem. In addition, if the droplets originate mainly from rupture of large adipocytes, as often described, this will also bias size analysis. We here confirm that our ordinary manual means of distinguishing droplets and adipocytes in the images ensure correct and rapid identification before exclusion of the droplets. Further, in our suspensions, prepared with focus on gentle handling of tissue and cells, we find no association between the amount of free lipid and mean adipocyte size or proportion of large adipocytes. ...
Modulator of adipocyte lipid metabolism. Coats lipid storage droplets to protect them from breakdown by hormone-sensitive lipase (HSL). Its absence may result in leanness (By similarity). Plays a role in unilocular lipid droplet formation by activating CIDEC. Their interaction promotes lipid droplet enlargement and directional net neutral lipid transfer. May modulate lipolysis and triglyceride levels.
Dr. Rayalam has worked in the areas of obesity, body weight regulation, phytochemicals and adipocyte biochemistry for over 8 years. Her research interests include: 1) to study the adipocyte life cycle and to understand the interaction of adipocytes with other cell types as an approach to address several problems associated with obesity; 2) to develop novel treatment strategies for obesity by inducing transdifferentiation of white to beige adipocytes and to inhibit lipid accumulation in white adipocytes; and 3) to identify combinations of phytochemicals and vitamins that have synergistic anti-adipogenic effects with an ultimate goal of developing pharmaceuticals or nutraceuticals for prevention and treatment of obesity and associated disorders. Aging is accompanied by an accumulation of adipocytes in bone marrow and Dr. Rayalams other interest is to understand the fat-bone interaction and to identify molecular targets for the prevention of weight gain and bone loss associated with aging. Dr. ...
In the nucleus HuR binds to mRNAs containing adenylate-uridylate rich elements in the 3?- untranslated region. HuR may influence expression of its ligand mRNA through regulation of polyadenylation, translocation of the message to the cytosol, stabilization of the mRNA and/or altering its translational efficiency. Suppression of HuR using siRNA resulted in an attenuation of the 3T3-L1 differentiation program, consistent with HuR control of the expression of mRNA ligand (s) critical to the differentiation process. In the current study we begin to identify mRNA ligands of HuR whose regulated expression is necessary for adipogenesis. Originally published in Biochemical and Biophysiological Research Communications Vol. 383, No. 2 2009 ...
What initiates the reprogramming of immune cells in obese AT toward proinflammatory subtypes? The answer is likely a combination of different endogenous and exogenous danger signals. In terms of endogenous signals, saturated fatty acids directly activate TLR4 and TLR2 in macrophages, and even in adipocytes themselves, resulting in proinflammatory cytokine production (35, 36). Saturated fatty acids, specifically palmitate, can also activate the NLRP3 inflammasome, causing maturation and release of IL-1β by macrophages (37). In addition to dietary sources, fatty acids are also released from adipocytes during lipolysis, a process that occurs at an increased rate in obese AT (38). Because macrophages surround adipocytes (12, 13), they would be one of the first immune cell types to encounter fatty acids and other endogenous danger signals, such as ATP, that may be released by dying adipocytes. Notably, TNF-α secreted by stimulated macrophages can further stimulate lipolysis (39), resulting in a ...
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The present study indicates that EERP enhance differentiation of 3T3-L1 adipocytes in part by its potency of PPARγ activation and are capable of reversing inhibitory effects of TNF-α on adipocyte differentiation and adiponectin expression. These results suggest the value of EERP as a diet supplement for prevention and treatment of obesity and obesity-associated disorders ...
Effect on adipocytesEdit. In adipocytes, the succinate-activated GPR91 signaling cascade inhibits lipolysis.[30] ...
Adipocytes. Role in development[edit]. Ferroportin-1 plays an important role in neural tube closure and forebrain patterning.[ ...
In adipocytes and hepatocytesEdit. Adrenaline and glucagon affect the activity of protein kinase A by changing the levels of ...
Bone marrow adipocytes secrete factors that promote HSC renewal in most bones. Hematopoietic cells (also known as blood cells) ... The marrow adipocytes originate from mesenchymal stem cell (MSC) progenitors that also give rise to osteoblasts, among other ... MAT, by its "specific marrow location, and its adipocyte origin from at least LepR+ marrow MSC is separated from non-bone fat ... Marrow adipocytes are difficult to isolate and quantify because they are interspersed with bony and hematopoietic elements. ...
Both adipocytes and brown adipocyte may be derived from pericytes, the cells which surround the blood vessels that run through ... In contrast to white adipocytes, which contain a single lipid droplet, brown adipocytes contain numerous smaller droplets and a ... The second develops from white adipocytes that are stimulated by the sympathetic nervous system. These adipocytes are found ... UCP1-containing adipocytes molecularly distinct from classic brown adipocytes". J Biol Chem. 285 (10): 7153-64. doi:10.1074/jbc ...
Erickson HP (October 2013). "Irisin and FNDC5 in retrospect: An exercise hormone or a transmembrane receptor?". Adipocyte. 2 (4 ...
"Quantitative assessment of adipocyte differentiation in cell culture". Adipocyte. 5 (4): 351-358. doi:10.1080/21623945.2016. ...
Within adipose tissue, presence of dead adipocytes is a hallmark of obesity. Macrophages surrounding dying or dead adipocytes ... Adipocyte. 2: 176-83. doi:10.4161/adip.24472. Wagner, M; Dudley, AC (2013). "A three-party alliance in solid tumors: Adipocytes ... 2005). "Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans". J Lipid Res. ... Adipocyte cell death observed within pathologically expanding adipose tissue is one of the factors. Macrophages are specialized ...
Zhang X, Heckmann BL, Liu J (2013-01-01). Yang P, Li H (eds.). "Studying lipolysis in adipocytes by combining siRNA knockdown ... Villena JA, Roy S, Sarkadi-Nagy E, Kim KH, Sul HS (November 2004). "Desnutrin, an adipocyte gene encoding a novel patatin ... "Entrez Gene: PNPLA2 patatin-like phospholipase domain containing 2". Ojha S, Budge H, Symonds ME (2014). "Adipocytes in Normal ... Steinberg GR, Kemp BE, Watt MJ (October 2007). "Adipocyte triglyceride lipase expression in human obesity". American Journal of ...
It is used to mobilize stored energy during fasting or exercise, and usually occurs in fat adipocytes. Lipolysis is induced by ... Insulin counter-regulates this increase in lipolysis when it binds to insulin receptors on the adipocyte cell membrane. Insulin ... Catecholamines bind to 7TM receptors (G protein-coupled receptors) on the adipocyte cell membrane, which activate adenylate ... Frühbeck, G; Méndez-Giménez, L; Fernández-Formoso, JA; Fernández, S; Rodríguez, A (June 2014). "Regulation of adipocyte ...
Adipocytes also have an external lamina. Wheater's Functional Histology, 5th ed. Young, Lowe, Stevens and Heath. v t e. ...
Terminal differentiation is that preadipocytes differentiate into mature adipocytes. Adipocytes can arise either from ... Adipocytes play a vital role in energy homeostasis and process the largest energy reserve as triglycerol in the body of animals ... Adipocytes stay in a dynamic state, they start expanding when the energy intake is higher than the expenditure and undergo ... These genes include adipocyte protein (aP2), insulin receptor, glycerophosphate dehydrogenase, fatty acid synthase, acetyl CoA ...
Infante, Marco; Armani, Andrea; Marzolla, Vincenzo; Fabbri, Andrea; Caprio, Massimiliano (2019). "Adipocyte Mineralocorticoid ...
Adipocytes generate TNF-α and other interleukins. Cytokines derived from adipose tissue serve as remote regulators such as ... Obesity leaves an excess of nutrients for the body, thereby causing adipocytes to release more proinflammatory cytokines. ...
... -12 expression induces apoptosis of adipocytes. Galectin-3 has been shown to be the only galectin with anti-apoptotic ...
2003). Human adipocytes secrete mineralocorticoid-releasing factors. In: Proceedings of the National Academy of Sciences. doi: ...
Fatty acids are normally stored in adipocytes as triglycerides. However, as triglycerides accumulate in adipocytes, fatty acids ... Adipocytes (fat cells) secrete proteins and signaling molecules known as adipokines. Certain adipokines have been implicated in ... In obesity, the greater number of adipocytes release greater amounts of leptin. These higher levels of leptin have been ... Leptin is a satiety adipokine released from adipocytes. Normally, leptin interacts with leptin receptors (LEPRs) in the brain ...
MSCs can differentiate into osteoblasts, chondrocytes, and adipocytes. In biology, oligopotency is the ability of progenitor ...
For example, insulin is known to activate LPL in adipocytes and its placement in the capillary endothelium. By contrast, ... Vannier C, Ailhaud G (August 1989). "Biosynthesis of lipoprotein lipase in cultured mouse adipocytes. II. Processing, subunit ... they responded with an increase in adipose tissue LPL activity per adipocyte, or a decrease in skeletal muscle LPL activity per ... "The role of glucose and glycosylation in the regulation of lipoprotein lipase synthesis and secretion in rat adipocytes". J. ...
... , body fat, or simply fat is a loose connective tissue composed mostly of adipocytes. In addition to adipocytes, ... these normally energy-storing adipocytes become energy-releasing adipocytes. The calorie-burning capacity of brown and beige ... The adipocytes in this depot are derived from mesenchymal stem cells (MSC) which can give rise to fat cells, bone cells as well ... Apart from adipocytes, which comprise the highest percentage of cells within adipose tissue, other cell types are present, ...
Adipocytes secrete leptin in response to food intake. This hormone acts in the arcuate nucleus and inhibits the AgRP/NPY neuron ...
PLIN4 is a member of the perilipin family, a group of proteins that coat lipid droplets in adipocytes, the adipose tissue cells ... PLIN4 coats lipid droplets in adipocytes to protect them from lipases. The PLIN4 gene may be associated with insulin resistance ... Wolins NE, Skinner JR, Schoenfish MJ, Tzekov A, Bensch KG, Bickel PE (September 2003). "Adipocyte protein S3-12 coats nascent ... Wolins NE, Skinner JR, Schoenfish MJ, Tzekov A, Bensch KG, Bickel PE (September 2003). "Adipocyte protein S3-12 coats nascent ...
In fact, PLIN1 is greatly expressed in white adipocytes. It controls adipocyte lipid metabolism. It handles essential functions ... In humans, Perilipin A is the most abundant protein associated with the adipocyte LDs and lower PLIN1 expression is related ... Perilipin is a protein that coats lipid droplets (LDs) in adipocytes, the fat-storing cells in adipose tissue. ... March 2013). "FSP27 and PLIN1 interaction promotes the formation of large lipid droplets in human adipocytes". Biochemical and ...
Dawn L., Brasaemle (2007-09-18). "Thematic review series: adipocyte biology. The perilipin family of structural lipid droplet ...
The adipocyte, or fat cell, is designed for continuous synthesis and breakdown of triglycerides in animals, with breakdown ... Rosen ED, Spiegelman BM (December 2006). "Adipocytes as regulators of energy balance and glucose homeostasis". Nature. 444 ( ... Brasaemle DL (December 2007). "Thematic review series: adipocyte biology. The perilipin family of structural lipid droplet ...
C3 nephritic factor induces the lysis of adipocytes that secrete adipsin, a product identical to complement factor D. The ... Hegele RA, Joy TR, Al-Attar SA, Rutt BK (Jul 2007). "Thematic review series: Adipocyte Biology. Lipodystrophies: windows on ... which stimulates the transcription of genes responsible for growth and differentiation of adipocytes. A single report has ... distribution of the lipoatrophy is postulated to be dictated by the variable amounts of adipsin secreted by the adipocytes at ...
The silencing of MAP4K4 in adipocytes elevated the expression of peroxisome proliferator-activated receptor y (PPARy) - a ... Farmer SR (October 2006). "Transcriptional control of adipocyte formation". Cell Metabolism. 4 (4): 263-73. doi:10.1016/j.cmet. ... nuclear hormone receptor responsible for the regulation of genes associated with adipocyte differentiation, including GLUT4. ...
In adipocytes, lipid bodies tend to be larger and they may compose the majority of the cell, while in other cells they may only ... In non-adipocytes, lipid droplets are known to play a role in protection from lipotoxicity by storage of fatty acids in the ... In non-adipocytes, lipid storage, lipid droplet synthesis and lipid droplet growth can be induced by various stimuli including ... Lipid droplets are found in all eukaryotic organisms and store a large portion of lipids in mammalian adipocytes. Initially, ...
Brasaemle DL (December 2007). "Thematic review series: adipocyte biology. The perilipin family of structural lipid droplet ...
Pre-adipocytes are undifferentiated fibroblasts that can be stimulated to form adipocytes. Recent studies shed light into ... In biology, adipose tissue, body fat, or simply fat is a loose connective tissue composed mostly of adipocytes.[1] In addition ... these normally energy-storing adipocytes become energy-releasing adipocytes. The calorie-burning capacity of brown and beige ... The adipocytes in this depot are derived from mesenchymal stem cells (MSC) which can give rise to fat cells, bone cells as well ...
Adipocyte. 2017 Jul 3;6(3):193-204. doi: 10.1080/21623945.2017.1367881. Epub 2017 Aug 24. Review ... Recent research shows that marrow adipocytes are distinct from white, brown and beige adipocytes, indicating that the bone ... adipocyte progenitors; lineage tracing; marrow adipocyte differentiation; marrow adipose tissue; marrow fat ... Bone marrow adipocytes.. Horowitz MC1, Berry R1, Holtrup B2, Sebo Z2, Nelson T1, Fretz JA1, Lindskog D1, Kaplan JL3, Ables G4, ...
Adipocyte definition is - a specialized cell of adipose tissue that stores excess energy in the form of triglyceride droplets ... Learn More about adipocyte. Share adipocyte Post the Definition of adipocyte to Facebook Share the Definition of adipocyte on ... Rhyming Dictionary: Words that rhyme with adipocyte. Comments on adipocyte What made you want to look up adipocyte? Please tell ... First Known Use of adipocyte. 1906, in the meaning defined above. History and Etymology for adipocyte. probably borrowed from ...
... M. V. Dodson,1 P. S. Mir,2 G. J. Hausman,3 L. L. Guan,4 Min Du,1 Z. Jiang,1 M. E. ... M. V. Dodson, P. S. Mir, G. J. Hausman, et al., "Obesity, Metabolic Syndrome, and Adipocytes," Journal of Lipids, vol. 2011, ...
SBML L2V4 representation of Brännmark2013 - Insulin signalling in human adipocytes (normal condition). 69.86 KB. Preview , ... The paper describes insulin signalling in human adipocytes under normal and diabetic states using mathematical models based on ... With comment: Current version of Brännmark2013 - Insulin signalling in human adipocytes (normal condition) ... Brännmark2013 - Insulin signalling in human adipocytes (normal condition). ...
Over time, beige adipocytes gain a white adipocyte morphology and lose their thermogenic activity. Here we show that levels of ... Maintaining adipocyte-specific expression of Lsd1 in transgenic mice preserves the pool of beige adipocytes in old mice. Vice ... However, the mechanisms controlling the age-related transition of beige adipocytes to white adipocytes remain unclear. Lysine- ... In particular, with time, thermogenic-competent beige adipocytes progressively gain a white adipocyte morphology. ...
Adipocyte volume/tissue volume (AV/TV), mean adipocyte number (AD#), and mean adipocyte diameter (ADdiam) were quantified. ... Adipocytes Marrow fat Osteoporosis PPARγ Risedronate A summary of this work was presented at the 2nd Joint Meeting of the ... Naveiras O, Nardi V, Wenzel PL, Hauschka PV, Fahey F, Daley GQ (2009) Bone-marrow adipocytes as negative regulators of the ... Syed FA, Oursler MJ, Hefferanm TE, Peterson JM, Riggs BL, Khosla S (2008) Effects of estrogen therapy on bone marrow adipocytes ...
To understand this regulatory process, respiration was measured in primary rat adipocytes, mitochondria, and fat-fed mice. ... It is a desirable goal to stimulate fuel oxidation in adipocytes and shift the balance toward less fuel storage and more ... Respiration in adipocytes is inhibited by reactive oxygen species Obesity (Silver Spring). 2010 Aug;18(8):1493-502. doi: ... It is a desirable goal to stimulate fuel oxidation in adipocytes and shift the balance toward less fuel storage and more ...
No significant changes were observed in adiposity, adipocyte size, lean mass, or adipocyte proliferation as measured by Ki67 ... CDK4 is an essential insulin effector in adipocytes. Sylviane Lagarrigue,1,2 Isabel C. Lopez-Mejia,1 Pierre-Damien Denechaud,1 ... Briefly, extracts from Cdk4+/+and Cdk4nc mice or mature 3T3-L1 adipocytes were made using M-PER mammalian extraction buffer ( ... B) CDK4 protein level in the SVF and mature adipocytes isolated from VAT. (C) Subcellular localization of CCND1, CCND2, CCND3, ...
Pre-adipocytes are undifferentiated fibroblasts that can be stimulated to form adipocytes. Studies have shed light into ... Adipocytes are derived from mesenchymal stem cells which give rise to adipocytes through adipogenesis. In cell culture, ... to such animals precipitated a period of weight loss during which only mean adipocyte size returned to normal. Adipocyte number ... Adipocytes, also known as lipocytes and fat cells, are the cells that primarily compose adipose tissue, specialized in storing ...
... in lipid metabolism by use of 3T3-L1 adipocytes. Imidacloprid treatment potentiated lipid accumulation in 3T3-L1 adipocytes and ... Imidacloprid, a neonicotinoid insecticide, potentiates adipogenesis in 3T3-L1 adipocytes.. Park Y1, Kim Y, Kim J, Yoon KS, ... finding is the first report of a potential link between neonicotinoid insecticide exposure and lipid accumulation in adipocytes ... significantly increased expression of a key regulator of adipocyte differentiation and key regulators of lipogenesis. These ...
The aim of this study was to confirm BMP7-derived human adipocytes as a relevant in vitro model of human beige adipocyte by ... Rosenwald M, Wolfrum C (2014) The origin and definition of brite versus white and classical brown adipocytes. Adipocyte 3:4-9 ... UCP1-containing adipocytes molecularly distinct from classic brown adipocytes. J Biol Chem 285:7153-7164PubMedCentralPubMed ... By confirming the cellular identity and metabolic activity, this BMP7-induced human beige adipocytes from hASC should aid in ...
... at the heart of which is the adipocyte.Increasing evidence suggests the adipocyte not only stores excess energy, but initiates ... hormones secreted in large amounts by the adipocyte.Additionally, extracellular matrix (ECM) proteins secreted by adipocytes ... The adipocyte secretes over 50 cytokines and hormones that both enhance and suppress inflammation, secretes extracellular ... Moreover, ceramide, a known toxic lipid released by the adipocyte, was recently found to be exported out of the adipocyte ...
That same link to the Diabesity site is also on the image file at Image:Adipocyte.png and also does not work. ... article url =http://en.citizendium.org/wiki?title=Adipocyte&oldid=100730842 , subpage url = , cluster =. , now =. , ToA editor ... Retrieved from "http://en.citizendium.org/wiki?title=Talk:Adipocyte&oldid=100756740" ...
ac, white adipocyte. Scale bars: 80 μm. (. G. ) BeAT content of the iAT at P34. (. H. ) CIM showing relative UCP1 level in iAT ... Lack of breastfeeding and lack of neonatal AKG intake reduce beige adipocyte content in the iAT. ... which ultimately activates IL-6/STAT3 signaling in adipocytes and triggers BeAT development in the infant. Accordingly, lack of ...
adipocyte size, and (. G. ) plasma glycerol level in Leprdb/db. mice treated with vehicle or AKGs. Scale bars: 50 μm (H&E); 10 ... which ultimately activates IL-6/STAT3 signaling in adipocytes and triggers BeAT development in the infant. Accordingly, lack of ... μm (UCP1). Arrowheads show UCP1+ adipocyte. (. H. ) NGS analysis of vehicle- and AKG-treated ATMs, showing relative abundance ...
... an adipocyte potassium channel activator, an SUR 1 antagonist, and an adipocyte specific SUR 1 antagonist. The present ... invention recognizes the presence of the sulfonylurea receptor in adipocytes and its utility in identifying compounds and in ... The cultured adipocytes may be derived from any animal. Preferably the adipocytes are mammalian. More preferably the adipocytes ... Ca2+]i is measured in primary adipocytes. For primary adipocytes, 3 ml of cells are resuspended in 6 ml of HBSS and fura-2/AM ...
Adipocyte differentiation Is the Subject Area "Adipocyte differentiation" applicable to this article? Yes. No. ... Adipocytes Is the Subject Area "Adipocytes" applicable to this article? Yes. No. ... Adipose tissue is determined by the number and size of adipocytes. The increase in the number of adipocytes involves the ... Sirt1 inhibits adipogenesis by repressing PPARγ expression in cultured adipocytes [26] and decreases adipocyte formation during ...
... adipocyte differentiation, inflammation, cancer, lung diseases, neurodegenerative disorders, and obesity. ... Caffeic Acid Phenethyl Ester Regulates PPARs Levels in Stem Cells-Derived Adipocytes. Luca Vanella,1 Daniele Tibullo,2 Justyna ... "Caffeic Acid Phenethyl Ester Regulates PPARs Levels in Stem Cells-Derived Adipocytes," PPAR Research, vol. 2016, Article ID ...
Get free shipping at $35 and view promotions and reviews for Life Extension Advanced Anti-Adipocyte Formula, Veggie Caps ... Life Extension Advanced Anti-Adipocyte Formula, Veggie Caps at Walgreens. ...
Home / Newsroom / Releases / Fat Isnt All Bad: Skin Adipocytes Help Protect Against Infections ... It was not known that adipocytes could produce antimicrobials, let alone that they make almost as much as a neutrophil." ... Further tests confirmed that human adipocytes also produce cathelicidin, suggesting the immune response is similar in both ... "Defective AMP production by mature adipocytes can occur due to obesity or insulin resistance, resulting in greater ...
Saturated fatty Acid-Induced Insulin Resistance in Rat Adipocytes. John W Hunnicutt, Robert W Hardy, Jodie Williford, Jay M ... Saturated fatty Acid-Induced Insulin Resistance in Rat Adipocytes. John W Hunnicutt, Robert W Hardy, Jodie Williford, Jay M ... Saturated fatty Acid-Induced Insulin Resistance in Rat Adipocytes Message Subject (Your Name) has forwarded a page to you from ... Treatment of adipocytes for 15 min with 1 mM myristate (14:0), palmitate (16:0), or stearate (18:0) stimulates glucose ...
Murine fibroblasts and adipocytes were derived from 3T3-L1 cells (ATCC). 3T3-L1 cells were differentiated into adipocytes based ... Adipocytes protect leukemia cells against drug treatment. To further characterize the possible effects of adipocytes on ... Thus, adipocytes may actively contribute to leukemia cell survival in the face of multiagent chemotherapy. Adipocytes also ... Mechanisms of adipocyte-induced vincristine resistance. We considered the possibility that adipocytes might protect leukemia by ...
Conference Report: Renal Disease, Metformin, and the Adipocyte Message Subject (Your Name) has forwarded a page to you from ...
Adipocytes were extracted from diabetic C57BL6 male mice fed with either a vegetal or an animal High-Fat-Diet (HFD) for 20 ... A significant up-regulation of CD36 mRNA level was found in VSMC treated with adipocytes from HFD-fed mice. In conclusion, we ... The most extended effects on VSMC were triggered by adipocytes from mice fed with animal HFD. These effects were concurrent ... Aortic VSMC were extracted from 10 weeks old C57BL6 mice and incubated for 24 hr in adipocytes conditioned cell culture medium ...
The effects of adipocytes may be direct, local or remote. Direct effect refers to adipocyte or fatty infiltration of the ... The effects of adipocytes may be direct, local or remote. Direct effect refers to adipocyte or fatty infiltration of the ... Adipocytes can also have a remote effect on the myocardium arising from their systemic secretion of adipokines, cytokines and ... Obesity is defined by the expansion of adipose mass, making adipocytes a prime candidate to mediate the pro-arrhythmogenic ...
The month, day, and year a content piece was published electronically (as opposed to in print). Depending on the webpage, it may or may not be shown ...
... Obes Res. 2000 May;8(3):249-54. doi: 10.1038/oby.2000.29 ... We investigated whether rapamycin could inhibit human adipocyte differentiation. Research methods and procedures: The effect of ... Objective: The immunosuppressant drug rapamycin, has been reported to inhibit 3T3-L1 adipocyte differentiation by interfering ... Results: We have observed that rapamycin severely curtails human adipocyte differentiation of both omental and abdominal ...
Uptake of liposomes containing the photoprotein obelin by rat isolated adipocytes. Adhesion, endocytosis or fusion? Biochem J ( ... Lipogenesis in rat brown adipocytes. Effects of insulin and noradrenaline, contributions from glucose and lactate as precursors ... Comparison of triacylglycerol synthesis in rat brown and white adipocytes. Effects of hypothyroidism and streptozotocin- ... K. Stanton, H. Keen; Insulin Binding to Human Adipocytes. Clin Sci Mol Med 1 February 1976; 50 (2): 32P. doi: https://doi.org/ ...
Interestingly, incubation of APOE-deficient hMSC-Tert adipocytes with conditioned media from APOE3-overexpressing adipocytes or ... but were unable to induce adipocyte differentiation, asmore » judged by expression of adipocyte markers. Taken together, ... However, little is yet known if APOE functions in a similar manner in human adipocytes. This prompted us to compare lipid ... Differentiated hMSC-Tert were stably transduced with or without siRNA targeting APOE while murine adipocytes were isolated from ...
In adipocytes, aquaglyceroporins mediate glycerol uptake and release across the plasma membrane, which are two key steps for ... Nevertheless, our findings provide novel insights in understanding the LPS-induced adipocyte hypertrophy that accompanies ... treated differentiated 3T3-L1 adipocytes. Glycerol release, TAGs content and whole membrane glycerol permeability were ... In adipocytes, aquaglyceroporins mediate glycerol uptake and release across the plasma membrane, which are two key steps for ...
  • Recent research shows that marrow adipocytes are distinct from white, brown and beige adipocytes, indicating that the bone marrow is a distinct adipose depot. (nih.gov)
  • Adipocytes, also known as lipocytes and fat cells, are the cells that primarily compose adipose tissue, specialized in storing energy as fat. (wikipedia.org)
  • Exercise reduces both adipocyte size as well as marrow adipose tissue volume, as quantified by MRI or μCT imaging of bone stained with the lipid binder osmium. (wikipedia.org)
  • Analysis of their adipose tissue morphology revealed increases in both adipocyte size and number in most depots. (wikipedia.org)
  • This systemic inflammation is due to profound changes in the adipose tissue microenvironment, at the heart of which is the adipocyte. (frontiersin.org)
  • Increasing evidence suggests the adipocyte not only stores excess energy, but initiates an escalating pro-inflammatory cascade in adipose tissue during high-fat diet. (frontiersin.org)
  • Additionally, extracellular matrix (ECM) proteins secreted by adipocytes not only determine the architecture of the adipose tissue but also have the capacity to promote inflammation and regulate systemic metabolism. (frontiersin.org)
  • Breast milk AKGs are metabolized by adipose tissue macrophages (ATMs) to platelet-activating factor (PAF), which ultimately activates IL-6/STAT3 signaling in adipocytes and triggers BeAT development in the infant. (jci.org)
  • Obesity is defined by the expansion of adipose mass, making adipocytes a prime candidate to mediate the pro-arrhythmogenic effects of obesity. (frontiersin.org)
  • This study aims to investigate the role of mitogen-activated protein kinase phosphatase 2 (MKP-2) in inflammation during macrophage-adipocyte interaction.White adipose tissues (WAT) from mice either on a high-fat diet (HFD) or normal chow (NC) were isolated to examine the expression of MKP-2. (doaj.org)
  • The Adipocyte Differentiation Toolkit for Adipose-derived MSCs and Preadipocytes contains medium and reagents designed to induce adipogenesis in actively proliferating Adipose-Derived Mesenchymal Stem Cells and Preadipocytes with high efficiency, and to support maturation of derived adipocytes during lipid accumulation. (atcc.org)
  • The Adipocyte Differentiation Toolkit for Adipose-derived MSCs and Preadipocytes provides enough medium and reagents for differentiation of ~6.8 x 10 5 cells when plated at a recommended density of 18,000 viable cells/cm 2 in 4 wells of a 6 well tissue culture format. (atcc.org)
  • Lipolysis in adipocytes, the hydrolysis of triacylglycerol (TAG) to release fatty acids (FAs) and glycerol for use by other organs as energy substrates, is a unique function of white adipose tissue. (genome.jp)
  • Because adipocytes have been shown to promote breast and prostate cancer proliferation, and because the bone marrow adipose tissue accounts for up to 70% of bone marrow volume in adult humans, we examined the adipocyte-leukemia cell interactions to determine if they are essential for the growth and survival of AML. (bloodjournal.org)
  • Furthermore, we validated the regulation and release of selected adipokines in primary human adipocytes and in serum and adipose tissue biopsies from morbidly obese patients and normal-weight controls. (mcponline.org)
  • Because of the relevance of adipose tissue in the progression of these common diseases, multiple unbiased, proteomic approaches have characterized the secretome from both rodent and human adipocytes and adipose tissue ( 10 ⇓ ⇓ ⇓ ⇓ ⇓ ⇓ - 17 ). (mcponline.org)
  • ADIPOCYTE deals with the recognition that the adipose tissue is the largest endocrine organ in the body, and the realization that a growing number of chronic diseases including diabetes, hypertension, cardiovascular disease and cancer are linked to dysfunctional adipose tissue. (periodicals.com)
  • These computational models provided the first evidence that sustained deformations in weight-bearing adipose tissues, as in a sedentary lifestyle, can indeed activate a vicious cycle that takes the form of a positive feedback loop promoting "en mass" adipogenesis. (newton.ac.uk)
  • Adipocytes and adipose tissue are not inert and make substantial contributions to systemic metabolism by influencing energy homeostasis, insulin sensitivity, and lipid storage. (portlandpress.com)
  • STAT6, in contrast, is highly expressed in both preadipocytes and mature adipocytes, but is not considered to play a major role in regulating adipose tissue function. (portlandpress.com)
  • This review will summarize the latest research that pertains to the functions of STATs in adipocytes and adipose tissue. (portlandpress.com)
  • 3 - 6 In obesity, adipocyte inflammation promotes macrophage infiltration into adipose tissue, amplifying inflammatory responses and leading to insulin resistance. (ahajournals.org)
  • 11 Food intake was not affected, and adipocyte Abca1 deficiency only slightly increased energy expenditure, presumably because of a modest increase in thermogenesis, whereas brown adipose tissue function was unchanged. (ahajournals.org)
  • 2 These atypical receptors, now called β3-adrenoceptors, are found on the cell surface of both white and brown adipocytes where their stimulation promotes both lipolysis and energy expenditure in brown adipose tissue (BAT) and lipolysis in white adipose tissue (WAT). (dovepress.com)
  • The expression of the ghrelin receptor (growth hormone secretagogue receptor, GHS-R) was analyzed in omental adipose tissue using western blot and immunohistochemistry, and the effect of acylated ghrelin and desacyl ghrelin (0.1-1000 pmol l -1 ) on adipogenesis was determined in vitro in omental adipocytes. (cun.es)
  • Adipocytes together form adipose fat tissue. (sciencephoto.com)
  • Obesity is characterized by the rapid expansion of visceral adipose tissue, resulting in a hypoxic environment in adipose tissue which leads to a profound change of gene expression in adipocytes. (wellnessresources.com)
  • For example, the unidentified adipocyte-derived relaxing factor (ADRF) released from adipose tissue has been shown to relax arteries. (ugent.be)
  • Development of brown-like/beige adipocytes in white adipose tissue (WAT) helps to reduce obesity. (nature.com)
  • GABA(B) receptor 1 (GABA(B)R1) subunit was constitutively expressed by mouse embryonic fibroblasts differentiated into adipocytes and adipocytic 3T3-L1 cells in culture, as well as mouse white adipose tissue, with no responsiveness to GABA(B)R ligands. (sigmaaldrich.com)
  • Conclusions- We postulate that a paracrine loop involving FFAs and TNF-α between adipocytes and macrophages establishes a vicious cycle that aggravates inflammatory changes in the adipose tissue. (ahajournals.org)
  • The adipose tissue is composed of various cell types: lipid-laden mature adipocytes and the remaining stromal vascular fraction (SVF) that includes blood cells, endothelial cells, and macrophages. (ahajournals.org)
  • We examined the effects of eNOS knockdown on adiponectin synthesis in 3T3-L1 adipocytes and also examined plasma adiponectin levels and the mitochondria in adipose tissue of eNOS knockout (eNOS -/- ) mice with and without chronic administration of a NO donor. (scialert.net)
  • Adipocytes are not the only components of adipose tissue, which is also made of connective tissue and other cells such as preadipocytes, macrophages, fibroblasts, endothelial cells and stem cells. (promocell.com)
  • white, beige and brown adipocytes look different and mirror their different tasks in the highly plastic adipose tissue. (promocell.com)
  • Until the past decade, researchers thought brown adipose tissue was only active in infants and young children, and that it later transformed into white adipocyte tissue with aging. (promocell.com)
  • white adipose tissue and brown adipose tissue are made of adipocytes, connective tissue, immune cells and stem cells. (promocell.com)
  • In obesity, adipocyte hypertrophy and proinflammatory responses are closely associated with the development of insulin resistance in adipose tissue. (asm.org)
  • However, it is largely unknown whether adipocyte hypertrophy per se might be sufficient to provoke insulin resistance in obese adipose tissue. (asm.org)
  • In obesity, adipose tissue expands as a result of increases in adipocyte size (hypertrophy) and adipocyte number (hyperplasia) and actively modulates the population of immune cells ( 3 , 4 ). (asm.org)
  • High-fat diet induces emergence of brown-like adipocytes in white adipose tissue of spontaneously hypertensive rats. (biomedsearch.com)
  • In this study, we present evidence for high-fat diet (HFD)-induced emergence of brown-like adipocytes in white adipose tissue (WAT) of the spontaneously hypertensive rat (SHR). (biomedsearch.com)
  • Moreover, it has been recently shown that adipocytes play a role in the recruitment of cells involved in innate and adaptive immunity in adipose tissue. (clinicaltrials.gov)
  • It begins with a brief overview characterizing white adipose tissue and the adipocyte, and then proceeds to a discussion regarding the multifaceted dysfunction that accompanies obesity. (springer.com)
  • Cinti S. Transdifferentiation properties of adipocytes in the adipose organ. (springer.com)
  • Trayhurn P. Hypoxia and adipocyte physiology: implications for adipose tissue dysfunction in obesity. (springer.com)
  • False-colour scanning electron micrograph (SEM) of a fat-storing cell (brown), also known as adipocyte, which builds up the adipose connective tissue. (sciencephoto.com)
  • Cytokines secreted by adipose tissue macrophages (ATMs) significantly alter adipocyte function, inducing inflammatory responses and decreasing insulin sensitivity. (biomedcentral.com)
  • Lysine-specific demethylase 1 (Lsd1) is an epigenetic eraser enzyme positively regulating differentiation and function of adipocytes. (pnas.org)
  • Imidacloprid treatment potentiated lipid accumulation in 3T3-L1 adipocytes and significantly increased expression of a key regulator of adipocyte differentiation and key regulators of lipogenesis. (nih.gov)
  • This prompted us to compare lipid loading and expression of adipocyte differentiation markers in APOE-deficient and control adipocytes using the differentiated human mesenchymal stem cell line hMSC-Tert as well as primary human and mouse adipocytes as model systems. (osti.gov)
  • This correlated with strongly decreased gene expression levels of adipocyte markers such as adiponectin (ADIPOQ) and fatty acid binding protein 4 (FABP4) as well as the key transcription factor driving adipocyte differentiation, peroxisome proliferator activator receptor gamma (PPARG), in particular the PPARG2 isoform. (osti.gov)
  • Similarly, differentiation of murine Apoe-deficient adipocytes was characterized by reduced gene expression of Adipoq, Fabp4 and Pparg. (osti.gov)
  • Taken together, depletion of endogenous APOE in human adipocytes severely impairs lipid accumulation, which is associated with an inability to initiate differentiation. (osti.gov)
  • The rs1421085 T-to-C single-nucleotide variant disrupts a conserved motif for the ARID5B repressor, which leads to derepression of a potent preadipocyte enhancer and a doubling of IRX3 and IRX5 expression during early adipocyte differentiation. (mit.edu)
  • Differentiation of cells into adipocytes as demonstrated by Oil Red O staining. (atcc.org)
  • Validation experiments conducted for complement factor H, αB-crystallin, cartilage intermediate-layer protein, and heme oxygenase-1 show that the release and expression of these factors in adipocytes is regulated by differentiation and stimuli, which affect insulin sensitivity, as well as by obesity. (mcponline.org)
  • Here, we present a reliable and straightforward two-dimensional (2D) coculture system for studying the interaction between tumor cells and bone marrow adipocytes, which reveals a dual effect of melanoma cell-derived factors on the bone marrow adipocytes differentiation and also poses a classic method for the mechanistic study of bone metastasis. (jove.com)
  • This includes PPARγ (peroxisome proliferator-activator receptor γ) 11 that stimulates adipocyte differentiation. (ahajournals.org)
  • Adipocyte medium is used as a maintenance medium after differentiation. (bioscience.co.uk)
  • We show here that E2F1 induces PPAR gamma transcription during clonal expansion, whereas E2F4 represses PPARg amma expression during terminal adipocyte differentiation. (epfl.ch)
  • E2Fs hence represent the link between proliferative signaling pathways, triggering clonal expansion, and terminal adipocyte differentiation through regulation of PPAR gamma expression. (epfl.ch)
  • Isoform 2: May positively regulate MAP-kinase activity in adipocytes, leading to enhanced adipocyte proliferation and reduced adipocyte differentiation. (uniprot.org)
  • Therefore, our aim was to investigate the effect of serotonin on brown adipocyte metabolism and differentiation. (ovid.com)
  • Non-differentiated HIB1B cells and differentiated HIB1B brown adipocytes were treated with serotonin and their metabolism and differentiation examined. (ovid.com)
  • In parallel, serotonin led to 3-6-fold reduction in the gene expression of brown adipocyte differentiation markers, that is, Prdm16 (positive regulatory domain 16), Bmp7 (bone morphogenic protein 7) and Pparγ (peroxisome-proliferator-activated receptor γ). (ovid.com)
  • In addition, serotonin interferes with the differentiation process into brown adipocytes. (ovid.com)
  • Depletion of TAF7L reduced adipocyte-specific gene expression, compromised adipocyte differentiation, and WAT development as well. (elifesciences.org)
  • The formation of adipocytes, a process known as adipogenesis, has been extensively studied, but there remain major gaps in our knowledge: for example, the identities of many of the transcriptional regulators that are responsible for the differentiation of mesenchymal stem cells into adipocytes remain a mystery. (elifesciences.org)
  • now report that TAF7L-a gene that was previously thought to be involved only in the production of sperm cells-has two roles in the differentiation of stem cells to form adipocytes. (elifesciences.org)
  • In contrast, Stamp3 expression is modestly changed in adipocytes compared to preadipocytes, and has a biphasic expression pattern during the course of differentiation. (uio.no)
  • Furthermore, knockdown of Uqcrc1 and Letm1 expression shows that they are required not only for beige adipocyte differentiation but also for preadipocyte maturation. (sciencemag.org)
  • It is evident that not only hypertrophy of adipocytes and increase of fat deposit but also proliferation of preadipocytes and differentiation from pre-adipocytes to adipocytes have important roles for forming obesity. (omicsonline.org)
  • Obesity is characterized by the expansion of fat mass, through adipocyte size increase (hypertrophy) and, to a lesser extent, cell proliferation (hyperplasia). (wikipedia.org)
  • Among ECM proteins, Clusterin (apolipoprotein J), is secreted in increased amounts by the adipocyte in obesity, correlates with all components of the metabolic syndrome, and inhibits hepatic insulin action and expression of apolipoprotein A, a precursor of the high-density lipoprotein cholesterol particle. (frontiersin.org)
  • Adipocytes have also been shown to increase their capacity to present antigens and activate CD4+ Th1 cells leading to increase insulin resistance in obesity. (frontiersin.org)
  • Thus, in obesity, the adipocyte exerts immunomodulatory functions, using multiple novel mechanisms to regulate inflammation. (frontiersin.org)
  • A greater appreciation that the adipocyte assumes the role of an immune cell in obesity is critical to fighting this epidemic. (frontiersin.org)
  • In contrast, Sorl1 gene inactivation in mice accelerated breakdown of triacylglycerides in adipocytes and protected animals from diet-induced obesity. (jci.org)
  • Defective AMP production by mature adipocytes can occur due to obesity or insulin resistance, resulting in greater susceptibility to infection, but too much cathelicidin may provoke an unhealthy inflammatory response. (ucsd.edu)
  • The molecular mechanisms linking obesity and adipocytes to increased arrhythmogenicity in both the atria and ventricles remain poorly understood. (frontiersin.org)
  • By better understanding the molecular mechanisms connecting dysfunctional adipocytes and arrhythmias, novel therapies may be developed to sever the link between obesity and arrhythmias. (frontiersin.org)
  • Nevertheless, our findings provide novel insights in understanding the LPS-induced adipocyte hypertrophy that accompanies obesity. (mdpi.com)
  • Results Our data indicate that the FTO allele associated with obesity represses mitochondrial thermogenesis in adipocyte precursor cells in a tissue-autonomous manner. (mit.edu)
  • Conclusions Our results point to a pathway for adipocyte thermogenesis regulation involving ARID5B, rs1421085, IRX3, and IRX5, which, when manipulated, had pronounced pro-obesity and anti-obesity effects. (mit.edu)
  • Does adipocyte hypercellularity in obesity exist? (ebscohost.com)
  • CONCLUSIONS Adipocyte-derived clusterin is a novel ECM-related protein linking cardiometabolic disease and obesity through its actions in the liver. (diabetesjournals.org)
  • Our published studies overall provide the explanation regarding how maturing adipocytes deform each other in weight-bearing fat tissues, in a spiral that contributes to the adipogenesis at the cell-scale, and then to gain of fat mass, overweight and obesity at the tissue and body scales. (newton.ac.uk)
  • 2 During obesity, free cholesterol accumulation in adipocytes can increase ≤≈50% of the total body free cholesterol pool. (ahajournals.org)
  • 3 , 6 Deletion of Abca1 in adipocytes of aP2-CreAbca1 fl/fl mice enhances diet-induced obesity and insulin resistance. (ahajournals.org)
  • Using the adipocyte-specific adiponectin-Cre model, in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , Cuffe et al 11 elegantly show that adipocyte Abca1 impairs diet-induced obesity. (ahajournals.org)
  • Surprisingly, adipocyte Abca1 deficiency prevented weight gain in a diet-induced obesity model and decreased fat pad weight. (ahajournals.org)
  • Model of impaired diet-induced obesity in adipocyte Abca1 deficiency. (ahajournals.org)
  • Given the lipogenic effect of acylated ghrelin on visceral adipocytes, the herein-reported elevation of its circulating concentrations in obese individuals may play a role in excessive fat accumulation in obesity. (cun.es)
  • Quercetin Impacts Expression of Metabolism- and Obesity-Associated Genes in SGBS Adipocytes. (wellnessresources.com)
  • The sub-project examines the influence of adipocyte accumulation in the bone marrow: yellow bone marrow, rich in adipocytes, develops with age, but also with obesity and other metabolic diseases. (dife.de)
  • Thus we investigated the effects of resveratrol, a dietary polyphenol capable of preventing obesity and related complications in humans and animal models, on brown-like adipocyte formation in inguinal WAT (iWAT). (nature.com)
  • We hypothesize that adipocyte-derived angiotensin II mediates obesity-induced increases in systolic blood pressure in male high fat-fed C57BL/6 mice. (ahajournals.org)
  • Adipocyte angiotensinogen deficiency had no effect on diet-induced obesity. (ahajournals.org)
  • In order to elucidate the effect of genistein on obesity, we cultured adipocyte and observed of genisten to lipid accumulation in cells. (scirp.org)
  • In addition to being of fundamental interest, improving our knowledge of the properties and behavior of adipocytes is essential for tackling the increasing prevalence of obesity in the developed world. (elifesciences.org)
  • A promising research direction to identify novel therapies to prevent obesity has emerged from discoveries on development and function of brown/brite adipocytes in mammals. (uio.no)
  • Such thermogenic adipocytes have been considered as targets to develop a therapy for preventing obesity. (uio.no)
  • This short review seeks to highlight recent findings on the development and function of brown/brite adipocytes in humans and to discuss potential treatments based on these adipocytes to reduce obesity and its related disorders. (uio.no)
  • Together, our in vitro and in vivo data suggest that adipocyte hypertrophy alone may be crucial in causing insulin resistance in obesity. (asm.org)
  • This study presents a new model for research into the induction of beige adipocytes from aWAT in vivo, which, when combined with models where beige adipocytes are induced from sWAT, provides insight into therapeutic approaches for combating obesity-related diseases in humans. (sciencemag.org)
  • MVs derived from proinflammatory (M1) macrophages may, at least in part, contribute to the pathogenesis of obesity-induced insulin resistance, reducing insulin signal transduction and decreasing glucose uptake in human adipocytes, through NF-kappa B activation. (biomedcentral.com)
  • Stress imposed on adipocytes by LD formation and expansion is prominently reflected in the ER compartment and the activated UPR response could have an important role at visceral obesity in fish. (nofima.no)
  • Fig. 1 Obesity-related adipocyte degeneration and cfDNA release. (sciencemag.org)
  • Elbaz A, Wu X, Rivas D, Gimble JM, Duque G (2009) Inhibition of fatty acid biosynthesis prevents adipocyte lipotoxicity on human osteoblasts in vitro. (springer.com)
  • The aim of this study was to confirm BMP7-derived human adipocytes as a relevant in vitro model of human beige adipocyte by verifying the cellular lineage and metabolic activity. (springer.com)
  • Here, we report how adipocytes impair the leukemia response to vincristine in vivo and of several drugs in vitro . (aacrjournals.org)
  • Using in vivo and in vitro models of AML, we show that bone marrow adipocytes from the tumor microenvironment support the survival and proliferation of malignant cells from patients with AML. (bloodjournal.org)
  • We have further investigated the mechanical behavior of maturing adipocytes in vitro and in silico, to understand the biomechanical cell-cell interactions that potentially lead to increase in adipogenesis and eventually, gain of additional fat mass. (newton.ac.uk)
  • Resveratrol significantly increased mRNA and/or protein expression of brown adipocyte markers, including uncoupling protein 1 (UCP1), PR domain-containing 16, cell death-inducing DFFA-like effector A, elongation of very long-chain fatty acids protein 3, peroxisome proliferator-activated receptor-γ coactivator 1α, cytochrome c and pyruvate dehydrogenase, in differentiated iWAT stromal vascular cells (SVCs), suggesting that resveratrol induced brown-like adipocyte formation in vitro . (nature.com)
  • Here we developed an in vitro coculture system composed of adipocytes and macrophages and examined the molecular mechanism whereby these cells communicate. (ahajournals.org)
  • Using cocultures of mouse BM cells with OP9 stromal cells, we found that adipocyte-conditioned medium induces the generation of CD11b + Gr1 + myeloid cells, which inhibit B cell development in vitro. (jimmunol.org)
  • Researchers have developed a number of in vitro cell culture models to elucidate the details of differential gene regulation, and this approach has been used to characterize adipocytes-cells that store energy in the form of fat-for close to two decades. (elifesciences.org)
  • This present study was aimed at clarifying the detailed mechanism(s) with which CE increases the glucose uptake in vivo and in cell culture systems using 3T3-L1 adipocytes and C2C12 myotubes in vitro. (unboundmedicine.com)
  • The adipocyte secretes over 50 cytokines and hormones that both enhance and suppress inflammation, secretes extracellular matrix proteins that impact inflammation, produces and releases toxic lipids that aggravate inflammation, and, more recently, was shown to present antigen to activate CD4+ T cells. (frontiersin.org)
  • Moreover, ceramide, a known toxic lipid released by the adipocyte, was recently found to be exported out of the adipocyte through exosomes to promote inflammation in macrophages. (frontiersin.org)
  • Finally, recently described "batokines" secreted by brown adipocytes were found to regulate inflammation and systemic metabolism. (frontiersin.org)
  • The goal of this Research Topic is to define the immune functions of the adipocyte focusing on novel mechanisms by which the adipocyte promotes inflammation and damages target organs. (frontiersin.org)
  • Macrophage-adipocyte co-culture system was employed to investigate the role of MKP-2 in regulating inflammation during adipocyte-macrophage interaction. (doaj.org)
  • In addition, overexpression of MKP-2 in macrophages suppressed inflammation during macrophage-adipocyte interaction.MKP-2 is a negative regulator of macrophage M1 activation through JNK and p38 and inhibits inflammation during macrophage-adipocyte interaction. (doaj.org)
  • Romacho T, Glosse P, Richter I, Elsen M, Schoemaker MH, Van Tol EA, Eckel J. Nutritional Ingredients Modulate Adipokine Secretion and Inflammation in Human Primary Adipocytes. (mdpi.com)
  • 7 Increased plasma HDL cholesterol levels suppress inflammation and macrophage recruitment in a diet-induced obese mouse model, which was attributed to enhanced cholesterol efflux from adipocytes 5 and macrophages. (ahajournals.org)
  • At the same time, with increasing age and overweight, there is a mild systemic inflammation, which is also caused by the cytokine release from adipocytes. (dife.de)
  • A neutralizing antibody to TNF-α, which occurs mostly in macrophages, inhibits the inflammatory changes in 3T3-L1, suggesting that TNF-α is a major macrophage-derived mediator of inflammation in adipocytes. (ahajournals.org)
  • Conversely, free fatty acids (FFAs) may be important adipocyte-derived mediators of inflammation in macrophages, because the production of TNF-α in RAW264 is markedly increased by palmitate, a major FFA released from 3T3-L1. (ahajournals.org)
  • White adipocyte tissue also has endocrine functions and releases hormones such as leptin, adiponectin, fatty acids, and TNF-α that regulate nutrient homeostasis, food intake, inflammation, cardiovascular activity, and tissue regeneration ( Medina-Gómez, 2016 ). (promocell.com)
  • β-aminoisobutyric acid attenuates LPS-induced inflammation and insulin resistance in adipocytes through AMPK-mediated pathway. (unboundmedicine.com)
  • We used BAIBA treated fully differentiated 3T3T-L1 mouse adipocytes to investigate the effects of exogenous BAIBA on inflammation and insulin signaling in adipocytes. (unboundmedicine.com)
  • TY - JOUR T1 - β-aminoisobutyric acid attenuates LPS-induced inflammation and insulin resistance in adipocytes through AMPK-mediated pathway. (unboundmedicine.com)
  • Here, we demonstrate that lipid-overloaded hypertrophic adipocytes are insulin resistant independent of adipocyte inflammation. (asm.org)
  • Regardless of adipocyte inflammation, hypertrophic adipocytes with large and unilocular lipid droplets exhibited impaired insulin-dependent glucose uptake, associated with defects in GLUT4 trafficking to the plasma membrane. (asm.org)
  • 15 The analysis of gene expression profiles of adipocytes and SVF obtained from obese mice and humans revealed that macrophages produces almost all of the TNF-α, whereas mature adipocytes secrete the majority of leptin, and interleukin 6 (IL-6) is expressed roughly equally among adipocytes, macrophages, and nonmacrophage SVF. (ahajournals.org)
  • MVs were generated by stimulation of M1 or M2 phenotype THP-1 macrophages and incubated with human primary mature adipocytes and differentiated adipocytes. (biomedcentral.com)
  • M1 macrophage-derived MVs (M1 MVs) significantly reduced protein abundance of insulin-induced Akt phosphorylation in human primary mature adipocytes and differentiated adipocytes, when compared with the same concentration of M2 macrophage-derived MVs (M2 MVs). (biomedcentral.com)
  • Vice versa, using GFP reporter mice, we traced the fate of beige adipocytes and showed that adipocyte-specific loss of Lsd1 results in a premature beige-to-white adipocyte transition in vivo. (pnas.org)
  • Accordingly, adipocyte-specific increase of Lsd1 expression is sufficient to rescue the age-related transition of beige adipocytes to white adipocytes in vivo, whereas loss of Lsd1 precipitates it. (pnas.org)
  • Generally, adipocyte morphology may indicate pathological function in vivo . (haematologica.org)
  • Resveratrol also induced beige adipogenesis in vivo along with the appearance of multiocular adipocytes, increased UCP1 expression and enhanced fatty acid oxidation. (nature.com)
  • aP2 (adipocyte Protein 2) is a carrier protein for fatty acids that is primarily expressed in adipocytes and macrophages. (wikipedia.org)
  • Our results indicate that soluble and MV-associated HMGB1 that is released from macrophages exposed to tobacco smoke mediates harmful macrophage-adipocyte crosstalk through two pathways: via adipocyte RAGE to impair insulin signaling, and via adipocyte TLR2 to induce MCP1 secretion and monocyte recruitment. (ahajournals.org)
  • In this study, we hypothesized that pre-exposure of the stromal vascular (SV) fraction of primary human adipogenic precursor cells ( h ASC) to BMP7 would convert metabolically active brown adipocytes. (springer.com)
  • With increasing age, the body's ability to form metabolically active brown adipocytes decreases, which causes white adipocytes to accumulate. (dife.de)
  • However, PET scans have identified biologically active brown adipocytes in various locations under the skin in the supraclavicular region and around blood vessels and solid organs in adults ( Sacks and Symonds, 2013 ). (promocell.com)
  • Maintaining adipocyte-specific expression of Lsd1 in transgenic mice preserves the pool of beige adipocytes in old mice. (pnas.org)
  • Maintenance of beige adipocytes is mediated by the Lsd1 target gene peroxisome proliferator-activated receptor α (Ppara) and pharmacological activation of Ppara rescues the loss of beige adipocytes in Lsd1-KO mice. (pnas.org)
  • To understand this regulatory process, respiration was measured in primary rat adipocytes, mitochondria, and fat-fed mice. (nih.gov)
  • E ) Histology, ( F ) adipocyte size, and ( G ) plasma glycerol level in Lepr db/db mice treated with vehicle or AKGs. (jci.org)
  • The scientists confirmed their findings by analyzing S. aureus infections in mice unable to either effectively produce adipocytes or whose fat cells did not express sufficient antimicrobial peptides in general and CAMP in particular. (ucsd.edu)
  • Mice fed a high-iron diet and cultured adipocytes treated with iron exhibited decreased adiponectin mRNA and protein. (nih.gov)
  • Aortic VSMC were extracted from 10 weeks old C57BL6 mice and incubated for 24 hr in adipocytes conditioned cell culture medium. (scirp.org)
  • Adipocytes were extracted from diabetic C57BL6 male mice fed with either a vegetal or an animal High-Fat-Diet (HFD) for 20 weeks. (scirp.org)
  • The most extended effects on VSMC were triggered by adipocytes from mice fed with animal HFD. (scirp.org)
  • A significant up-regulation of CD36 mRNA level was found in VSMC treated with adipocytes from HFD-fed mice. (scirp.org)
  • Differentiated hMSC-Tert were stably transduced with or without siRNA targeting APOE while murine adipocytes were isolated from wild type and Apoe knockout mice. (osti.gov)
  • In response to Western diet feeding, an increase in adipocyte clusterin expression was associated with a progressive increase in liver fat, steatohepatitis, and fibrosis in aged LDLR −/− mice. (diabetesjournals.org)
  • Limited mitochondrial capacity of visceral versus subcutaneous white adipocytes in male C57BL/6N mice. (sigmaaldrich.com)
  • We assessed bioenergetic parameters of subcutaneous inguinal and visceral epididymal white adipocytes from male C57BL/6N mice employing a comprehensive respirometry setup of intact and permeabilized adipocytes as well as isolated mitochondria. (sigmaaldrich.com)
  • Systolic blood pressure was measured by radiotelemetry during week 16 of low-fat or high-fat feeding in Agt fl/fl and adipocyte angiotensinogen-deficient mice ( Agt aP2 ). (ahajournals.org)
  • Adipocytes could alter chemotherapy pharmacokinetics and/or induce drug resistance by secretion of adipokines. (aacrjournals.org)
  • We show that AML blasts alter metabolic processes in adipocytes to induce phosphorylation of hormone-sensitive lipase and consequently activate lipolysis, which then enables the transfer of fatty acids from adipocytes to AML blasts. (bloodjournal.org)
  • There are many transcriptional regulators, including PR domain-containing 16 (PRDM16), peroxisome proliferator-activated receptor-γ (PPARγ) coactivator 1α (PGC1α), CCAAT/enhancer-binding protein α and PPARγ, as well as various secreted mediators, such as bone morphogenetic protein 7, Irisin, fibroblast growth factor 21, atrial and brain natriuretic peptides, that can induce the formation of brown-like adipocytes. (nature.com)
  • Adipocytes induce epithelial mesenchymal transition of breast cancer cells through paracrine IL-6/Stat3 signalling. (nature.com)
  • Here we further characterize the ability of short-term treatment with free fatty acids to stimulate glucose transport in isolated rat adipocytes and demonstrate that prolonged treatment induces insulin resistance. (diabetesjournals.org)
  • Prolonged treatment (4 h) of rat adipocytes with 1 mM palmitate induces insulin resistance. (diabetesjournals.org)
  • AML induces adipocyte lipolysis of triglyceride to free fatty acids and subsequent transport by FABP4. (bloodjournal.org)
  • Resveratrol induces brown-like adipocyte formation in iWAT via AMPKα1 activation and suggest that its beneficial antiobesity effects may be partly due to the browning of WAT and, as a consequence, increased oxygen consumption. (nature.com)
  • Treatment with saturated or monounsaturated fatty acids resulted in adipocyte hypertrophy, but proinflammatory responses were observed only in adipocytes treated with saturated fatty acids. (asm.org)
  • We then identified the underlying molecular mechanism whereby SORLA promotes insulin-induced suppression of lipolysis in adipocytes. (jci.org)
  • 11 Although triglyceride lipolysis in adipocytes was unaffected, triglyceride synthesis was decreased, and this was accompanied by decreased expression of the active (cleaved) form of SREBP-1c (sterol regulatory element binding protein-1c). (ahajournals.org)
  • Bone marrow adipocytes have recently been shown to influence other cell populations within the marrow and can affect whole body metabolism by the secretion of a defined set of adipokines. (nih.gov)
  • Adipocytes can also have a remote effect on the myocardium arising from their systemic secretion of adipokines, cytokines and metabolites. (frontiersin.org)
  • The eCH concentration dependently increased adiponectin secretion in human primary adipocytes through its intrinsic peptide bioactivity, since the non-peptidic mixture, AA, could not mimic eCH's effects on adiponectin secretion. (mdpi.com)
  • However, only DHA and DHA/ARA exerted a potentanti-inflammatory effect reflected by prevention of tumor necrosis factor-α (TNF-α) induced NF-κB activation and MCP-1 secretion in human adipocytes. (mdpi.com)
  • In human adipocytes, palmitate enhanced clusterin secretion, and in human hepatocytes clusterin attenuated insulin signaling and APOA1 expression and stimulated hepatic gluconeogenesis. (diabetesjournals.org)
  • Adipocytes drive cancer progression through the secretion adipocytokines. (nature.com)
  • In cultured 3T3-L1 adipocytes, eNOS siRNA decreased rosiglitazone-induced adiponectin secretion, which was associated with decreases in mitochondrial proteins and biogenesis factors. (scialert.net)
  • These changes were also elicited by a rise in extracellular temperature from 25°C to over 42°C. Treatment with capsaicin, GSK1016790A and probenecid for 24 h increased IL-6 expression, and secretion in differentiated adipocytes. (omicsonline.org)
  • Exposure of adipocytes to rHMGB1 or TSE-MVs impaired insulin-induced phosphorylations of IRS1 (Tyr612) and AKT (Ser473) and induced MCP1 secretion and hence monocyte transmigration and adherence to the cultured adipocytes. (ahajournals.org)
  • In contrast, neutralizing antibodies against TLR2, but not RAGE, attenuated the induction of MCP1 secretion, and hence inhibited monocyte transmigration and adherence to cultured adipocytes exposed to rHMGB1 or TSE-MV. (ahajournals.org)
  • Thus, the purpose of this investigation was to determine the role of imidacloprid, a neonicotinoid insecticide, in lipid metabolism by use of 3T3-L1 adipocytes. (nih.gov)
  • These findings demonstrate a causal role for iron as a risk factor for metabolic syndrome and a role for adipocytes in modulating metabolism through adiponectin in response to iron stores. (nih.gov)
  • The aim of this study was to assess both glycerol permeability and metabolism in undifferentiated 3T3-L1 cells (UDCs) as well as in untreated (CTL-DCs) versus lipopolysaccharide (LPS-DCs)-treated differentiated 3T3-L1 adipocytes. (mdpi.com)
  • Serotonin leads to whitening of brown adipocytes, shifting their metabolism to fat accumulation rather than oxidation. (ovid.com)
  • WAT mainly stores energy in the form of lipids (triglycerides) in unilocular white adipocytes and secretes a number of adipokines and other factors, such as leptin, adiponectin, tumor necrosis factor α and interleukin-6, to regulate energy metabolism and immune function. (nature.com)
  • Rational: In reason of its ability to store fatty acids and to secrete numerous pro-inflammatory cytokines, the adipocyte appears as a key cell in the regulation of energy metabolism and immune response. (clinicaltrials.gov)
  • PFKFB3-dependent glucose metabolism regulates 3T3-L1 adipocyte development. (stembook.org)
  • Our objective was to determine 1 ) whether subcutaneous AT adipocyte (SAd) clusterin and serum clusterin are associated with insulin resistance (IR) and known markers of cardiometabolic risk and 2 ) how clusterin may contribute to increased risk. (diabetesjournals.org)
  • Cambridge Bioscience offers a range of ready to use subcutaneous adipocyte media with no need for growth factor or antibiotic supplementation. (bioscience.co.uk)
  • Adipocytes collected from subcutaneous fat biopsy samples after normal and restricted sleep conditions were exposed to incremental insulin concentrations. (annals.org)
  • Adipocytes are derived from mesenchymal stem cells which give rise to adipocytes through adipogenesis. (wikipedia.org)
  • Marrow adipocytes, are unilocular like white fat cells, however both brown and white fat cells are derived from mesenchymal stem cells. (wikipedia.org)
  • Mesenchymal stem cells can differentiate into adipocytes, connective tissue, muscle or bone. (wikipedia.org)
  • Immortalized human mesenchymal stem cells were used to study adipocyte development. (osti.gov)
  • Thus stimulating the development of beige adipocytes in WAT, so called 'browning', might reduce adverse effects of WAT and could help to improve metabolic health. (nature.com)
  • To better understand the development of beige adipocytes from mammalian WATs, especially aWAT, we induced beige adipocytes from bat aWAT and mouse sWAT by exposure to cold temperatures and analyzed their molecular signatures. (sciencemag.org)
  • Although discovered several decades ago, studies continue to identify pro-inflammatory roles for leptin and anti-inflammatory activities for adiponectin, hormones secreted in large amounts by the adipocyte. (frontiersin.org)
  • Conversely, organismal iron overload and increased adipocyte ferroportin expression because of hemochromatosis are associated with decreased adipocyte iron, increased adiponectin, improved glucose tolerance, and increased insulin sensitivity. (nih.gov)
  • Methods and Results- Coculture of differentiated 3T3-L1 adipocytes and macrophage cell line RAW264 results in the marked upregulation of proinflammatory cytokines, such as tumor necrosis factor α (TNF-α), and the downregulation of the antiinflammatory cytokine adiponectin. (ahajournals.org)
  • We recently reported that adiponectin synthesis is regulated by mitochondrial function in adipocytes. (scialert.net)
  • This study was undertaken to test the hypothesis that endothelial NO synthase (eNOS) plays an important role in adiponectin synthesis by producing NO and enhancing mitochondrial function in adipocytes. (scialert.net)
  • eNOS plays an important role in adiponectin synthesis in adipocytes by increasing mitochondrial biogenesis and enhancing mitochondrial function. (scialert.net)
  • Strikingly, non-differentiated HIB1B preadipocytes incubated with serotonin failed to differentiate into brown adipocytes. (ovid.com)
  • We investigated the expression of thermo-sensitive TRPVs and their roles on IL-6 production in mouse 3T3-L1 preadipocytes and differentiated adipocytes. (omicsonline.org)
  • Western blotting and immunocytochemical staining also showed the existence of TRPV1, TRPV2 and TRPV4 transcript in 3T3-L1 preadipocytes and differentiated adipocytes. (omicsonline.org)
  • Model simulations with inhibition of mTORC1 are comparable with experimental data on inhibition of mTORC1 using rapamycin in human adipocytes. (ebi.ac.uk)
  • ROS inhibition of O(2) consumption may explain the difficulty to identify effective strategies to increase fat burning in adipocytes. (nih.gov)
  • FABP4 inhibition using FABP4 short hairpin RNA knockdown or a small molecule inhibitor prevents AML proliferation on adipocytes. (bloodjournal.org)
  • Inhibition of human adipocyte fatty-acid binding protein (FABP4) has been proposed as a treatment for type 2 diabetes, fatty liver disease and atherosclerosis. (rcsb.org)
  • Additionally, niclosamide reversed adipocyte-induced EMT with a correlated inhibition of IL-6/Stat3 activation and downregulation of EMT-TFs TWIST and SNAIL. (nature.com)
  • Over time, beige adipocytes gain a white adipocyte morphology and lose their thermogenic activity. (pnas.org)
  • Together, we identified Lsd1 as a regulator of beige adipocyte maintenance. (pnas.org)
  • In particular, with time, thermogenic-competent beige adipocytes progressively gain a white adipocyte morphology. (pnas.org)
  • However, the mechanisms controlling the age-related transition of beige adipocytes to white adipocytes remain unclear. (pnas.org)
  • Lsd1 maintains beige adipocytes by controlling the expression of peroxisome proliferator-activated receptor α (Ppara), and treatment with a Ppara agonist is sufficient to rescue the loss of beige adipocytes caused by Lsd1 ablation. (pnas.org)
  • In summary, our data provide insights into the mechanism controlling the age-related beige-to-white adipocyte transition and identify Lsd1 as a regulator of beige fat cell maintenance. (pnas.org)
  • Our results showed that exposure of h ASC to human BMP7 was associated with significant escalation of (1) UCP1 gene expression, a signature gene of brown adipocytes, (2) beige specific marker gene expression (i.e. (springer.com)
  • Taken together, we demonstrated that BMP7 mediates conversion of h ASC into metabolically active beige adipocytes. (springer.com)
  • By confirming the cellular identity and metabolic activity, this BMP7-induced human beige adipocytes from h ASC should aid in the discovery and assessment of bioactive molecules to promote adaptive thermogenesis. (springer.com)
  • Lack of breastfeeding and lack of neonatal AKG intake reduce beige adipocyte content in the iAT. (jci.org)
  • This results in a cell-autonomous developmental shift from energy-dissipating beige (brite) adipocytes to energy-storing white adipocytes, with a reduction in mitochondrial thermogenesis by a factor of 5, as well as an increase in lipid storage. (mit.edu)
  • Scientists are investigating how beige/brite adipocytes develop and how they interact with other fat cells. (promocell.com)
  • Beige adipocytes can be induced from white adipocytes and precursors upon stimulation by cold temperatures and act like brown adipocytes to increase energy expenditure. (sciencemag.org)
  • malignant fat) develops into beige adipocytes remains obscure, largely because there is a lack of a good animal model for the induction of beige adipocytes from aWAT. (sciencemag.org)
  • RNA sequencing followed by whole genome-wide expression analysis shows that beige adipocytes induced from bat aWAT, rather than sWAT, have molecular signatures resembling those of mouse sWAT-induced beige adipocytes and exhibit dynamic profiles similar to those of classical brown adipocytes. (sciencemag.org)
  • In addition, we identified molecular markers that were highly enriched in beige adipocytes and conserved between bat aWAT and mouse sWAT, a set that included the genes Uqcrc1 and Letm1 . (sciencemag.org)
  • Recent studies reported that brown-like (beige) adipocytes could be a distinct type of thermogenic fat cell and are induced from WAT by exposure to cold and other stimuli ( 2 ). (sciencemag.org)
  • Differentiated HIB1B brown adipocytes treated with serotonin had reduced levels of the thermogenic markers uncoupling protein 1 (UCP1) and fibroblast growth factor 21 (FGF21) and increased levels of UCP2. (ovid.com)
  • In the resting phase, they resemble white adipocytes, but upon cold stimulation, they acquire a phenotype similar to that of brown adipocytes along with the thermogenic capacities of such cells ( Sidossis and Kajimura, 2015 ). (promocell.com)
  • Human thermogenic adipocytes: a reflection on types of adipocyte, develpmental origin, and potential Application. (uio.no)
  • Importantly, there is evidence for the presence and function of active thermogenic brown adipocytes in both infants and adult humans. (uio.no)
  • Several new investigations have shown that thermogenic adipocytes are beneficial to maintain glucose homeostasis, insulin sensitivity, and a healthy body fat content. (uio.no)
  • These findings highlight the role of the adipocyte in fostering leukemia chemotherapy resistance, and may help explain the increased leukemia relapse rate in obese children and adults. (aacrjournals.org)
  • The Sick Adipocyte Theory: The Forces of Clustering at Glance, Role of the Adipocyte in Development of Type 2 Diabetes Coleen Croniger, IntechOpen, DOI: 10.5772/20963. (intechopen.com)
  • Adipocytes were identified in human bone marrow more than a century ago, yet until recently little has been known about their origin, development, function or interactions with other cells in the bone marrow. (nih.gov)
  • Approximately 10% of fat cells are renewed annually at all adult ages and levels of body mass index without a significant increase in the overall number of adipocytes in adulthood. (wikipedia.org)
  • Caffeic Acid Phenethyl Ester Regulates PPAR's Levels in Stem Cells-Derived Adipocytes," PPAR Research , vol. 2016, Article ID 7359521, 13 pages, 2016. (hindawi.com)
  • Richard Gallo, MD, PhD, professor and chief of dermatology at UC San Diego School of Medicine, and colleagues have uncovered a previously unknown role for dermal fat cells, known as adipocytes: They produce antimicrobial peptides that help fend off invading bacteria and other pathogens. (ucsd.edu)
  • Akoum, S. , Cloutier, I. and Tanguay, J. (2013) Adipocytes modulate vascular smooth muscle cells migration potential through their secretions. (scirp.org)
  • Human APOE knockdown hMSC-Tert adipocytes accumulated markedly less triglycerides compared to control cells. (osti.gov)
  • c-Jun N-terminal kinase (JNK)- and p38-specific inhibitors were used to examine the mechanisms by which MKP-2 regulates macrophage activation and macrophage-adipocytes interaction.HFD changed the expression of MKP-2 in WAT, and MKP-2 was highly expressed in the stromal vascular cells (SVCs). (doaj.org)
  • We recently discovered that fat cells (adipocytes) are mechanosensitive and responsive to sustained mechanical loading. (newton.ac.uk)
  • Stained semi-thin sections (0.5 µm) also demonstrated abundant nuclei in multilocular adipocytes, in endothelial cells associated with the vasculature, and in interstitial cells. (dovepress.com)
  • In CL-treated obese rats, a clustering of several multilocular cells around the periphery of a white adipocyte was seen. (dovepress.com)
  • False-colour scanning electron micrograph of human fat cells, or adipocytes, in human skin. (sciencephoto.com)
  • There are limited reports regarding the regulation of the residual adipocytes by leukemic cells and their role in disease progression. (haematologica.org)
  • Online Supplementary Figure S1D,E ), indicating that adipocyte size change in the AML patients was not caused by a lack of space due to extensive invasion of leukemic cells. (haematologica.org)
  • These cells work together to maintain adipocyte integrity and hormonal balance. (promocell.com)
  • White adipocytes are quite large spherical cells with few mitochondria and a single lipid droplet. (promocell.com)
  • Adipocyte-conditioned medium-induced CD11b + Gr1 + cells express Arg1 (arginase) and Nos2 (inducible NO synthase) and suppress CD4 + T cell proliferation, indicating that these cells are myeloid-derived suppressor cells (MDSCs). (jimmunol.org)
  • The Department of Adipocyte Development and Nutrition, supported by the German Research Foundation and the European Research Council , investigates the developmental mechanisms that direct the formation of brown and white adipocytes (fat cells). (dife.de)
  • Consistent with the molecular changes, in HFD but not in ND rats, histological and immunohistochemistry-based analyses of WAT demonstrated the presence of small multilocular cells staining positively for uncoupling protein 1, indicating the emergence of brown-like adipocytes in WAT. (biomedsearch.com)
  • Fat not used in metabolic processes is channeled towards these cells through small capillaries and a few of them are visible behind the adipocyte as pink tubules. (sciencephoto.com)
  • We also used biochemical and morphological methods to show that the glucose transporter GLUT4 was translocated to caveolae in response to insulin in rat adipocytes, indicating fhat the caveola is the locale for glucose uptake in adipocytes. (diva-portal.org)
  • In contrast to M2 MVs, which enhanced the insulin-induced glucose uptake measured by 2-NBDG, M1 MVs decreased this effect in treated adipocytes. (biomedcentral.com)
  • Naveiras O, Nardi V, Wenzel PL, Hauschka PV, Fahey F, Daley GQ (2009) Bone-marrow adipocytes as negative regulators of the haematopoietic microenvironment. (springer.com)
  • It has been demonstrated that adipocytes in the bone marrow provide a pro-tumoral microenvironment during the initial stage of leukemia. (haematologica.org)
  • The microenvironment of breast cancer comprises predominantly of adipocytes. (nature.com)
  • Treatment approaches that can target adipocytes in the microenvironment and abrogate paracrine signals that drive breast cancer growth and metastasis are urgently needed. (nature.com)
  • The breast cancer microenvironment is unique since the breast tissue within which the tumour originates comprises predominantly of adipocyte. (nature.com)
  • However, little relevant information is available regarding the role of microvesicles (MVs) derived from ATMs in macrophage-adipocyte crosstalk. (biomedcentral.com)
  • Matsushima, T. , Yoshimura, N. and Koseki, Y. (2015) Effect of Soy Bean Isoflavon on Lipid Accumulation in 3T3-L1 Adipocytes. (scirp.org)
  • 3 Center of Animal Biotechnology and Gene Therapy and Department of Biochemistry and Molecular Biology, School of Veterinary Medicine, Universitat Autònoma de Barcelona, Bellaterra, and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, Barcelona, Spain. (jci.org)
  • Nevertheless, its underlying molecular mechanism is still obscure and thus the focus of this study was to explore the influence of quercetin on human SGBS (Simpson Golabi Behmel Syndrome) adipocytes' gene expression. (wellnessresources.com)
  • Positive regulation by GABA(B)R1 subunit of leptin expression through gene transactivation in adipocytes. (sigmaaldrich.com)
  • These findings suggest that TAF7L plays an integral role in adipocyte gene expression by targeting enhancers as a cofactor for PPARγ and promoters as a component of the core transcriptional machinery. (elifesciences.org)
  • Adipocytes express angiotensinogen and secrete angiotensin peptides. (ahajournals.org)
  • At the same time, altered white adipocyte mitochondrial bioenergetics has been implicated in the pathogenesis of insulin resistance and type 2 diabetes. (sigmaaldrich.com)
  • We therefore investigated whether the metabolic risk of visceral vs peripheral fat coincides with a difference in mitochondrial capacity of white adipocytes. (sigmaaldrich.com)
  • Inguinal adipocytes clearly featured a higher respiratory capacity attributable to increased mitochondrial respiratory chain content compared with epididymal adipocytes. (sigmaaldrich.com)
  • Feeding a high-fat diet (HFD) for 1 week reduced white adipocyte mitochondrial capacity, with stronger effects in epididymal when compared with inguinal adipocytes. (sigmaaldrich.com)
  • Maenhaut N, Van de Voorde J. Regulation of vascular tone by adipocytes. (ugent.be)
  • Conclusions: Our data point to an intimate relationship between metabolic regulation and immune responses in white adipocytes of a cold-blooded vertebrate. (nofima.no)
  • Bone marrow adipocytes. (nih.gov)
  • Bone marrow adipocytes support AML survival. (bloodjournal.org)
  • Adipocyte-enriched bone marrow is a determining factor for impaired bone homeostasis and delayed bone healing. (dife.de)
  • Our hypothesis is that different physiological factors such as nutrition and specific immune cell populations cause the accumulation of advantageous or disadvantageous bone marrow adipocytes. (dife.de)
  • 3 However, these adipocytes are rapidly reduced with the extensive proliferation of leukemic blasts in the bone marrow. (haematologica.org)
  • For example, large adipocytes occupy the bone marrow cavity in aplastic anemia and negatively regulate hematopoiesis. (haematologica.org)
  • To explore the morphological characteristics of bone marrow adipocytes in patients with acute myeloid leukemia (AML), we retrospectively analyzed the size of marrow adipocytes in bone marrow sections from 70 patients with primary AML and 70 controls. (haematologica.org)
  • Adipocytes, confirmed by immmunhistochemistry to be positive for Perilipin 1 staining, were fewer and smaller in the bone marrow sections from AML patients than from the controls ( Online Supplementary Figure S1A ). (haematologica.org)
  • Adipocyte fatty acid binding protein 4 (FABP4) inhibitors. (wikipedia.org)
  • Adipocyte lipid-binding protein (ALBP) is the adipocyte member of an intracellular hydrophobic ligand-binding protein family. (rcsb.org)
  • In addition, we report that fatty acid binding protein-4 (FABP4) messenger RNA is upregulated in adipocytes and AML when in coculture. (bloodjournal.org)
  • Therefore, we conducted a complementary protein profiling on concentrated conditioned medium derived from primary human adipocytes. (mcponline.org)
  • In differentiating omental adipocytes, incubation with both acylated and desacyl ghrelin significantly increased PPAR (peroxisome proliferator-activated receptor ) and SREBP1 (sterol-regulatory element binding protein-1) mRNA levels, as well as several fat storage-related proteins, including acetyl-CoA carboxylase, fatty acid synthase, lipoprotein lipase and perilipin. (cun.es)
  • 1996), 34 kDa IGF binding Protein (Kiddy and Hamilton, 1999), 30 kDa Adipocyte complement-related protein (Tsao et al. (thefreedictionary.com)
  • We have calculated that an average adipocyte caveola contains 18000 molecules of cholesterol, 6000 of sphingomyelin, 18000 of phosphoacylglycerol, 350 protein molecules, and about I 00 glycolipid molecules. (diva-portal.org)
  • Frontini A, Rousset S, Cassard-Doulcier AM, Zingaretti C, Ricquier D, Cinti S. Thymus uncoupling protein 1 is exclusive to typical brown adipocytes and is not found in thymocytes. (springer.com)
  • Imidacloprid, a neonicotinoid insecticide, potentiates adipogenesis in 3T3-L1 adipocytes. (nih.gov)
  • He Y, Li Y, Zhao T, Wang Y, Sun C (2013) Ursolic Acid Inhibits Adipogenesis in 3T3-L1 Adipocytes through LKB1/AMPK Pathway. (plos.org)
  • The paper describes insulin signalling in human adipocytes under normal and diabetic states using mathematical models based on experimental data. (ebi.ac.uk)
  • We report a systems level mechanistic understanding of insulin resistance, using systems wide and internally consistent data from human adipocytes. (ebi.ac.uk)
  • Modeling reveals that at the core of insulin resistance in human adipocytes is attenuation of a positive feedback from mTORC1 to the insulin receptor substrate-1, which explains reduced sensitivity and signal strength throughout the signaling network. (ebi.ac.uk)
  • Further tests confirmed that human adipocytes also produce cathelicidin, suggesting the immune response is similar in both rodents and humans. (ucsd.edu)
  • However, little is yet known if APOE functions in a similar manner in human adipocytes. (osti.gov)
  • This thesis presents results on fhe role of caveolae in insulin signalling in human and rat adipocytes. (diva-portal.org)
  • After isolation of caveolae and using electron microscopy on cell membranes, the insulin receptor was demonstrated to be localised in caveolae of human adipocytes. (diva-portal.org)
  • The combined model provides a systems-level understanding of insulin signaling in rat adipocytes, which, when combined with corresponding models for human adipocytes, may contribute to model-based drug development for diabetes. (diva-portal.org)
  • ABCA1 represents a major cholesterol efflux pathway in adipocytes. (ahajournals.org)
  • We have isolated caveolae from purified plasma membrane of primary rat adipocytes using ultrasonication to disrupt the membrane followed by density gradient ultracentrifugation. (diva-portal.org)
  • This finding is the first report of a potential link between neonicotinoid insecticide exposure and lipid accumulation in adipocytes. (nih.gov)
  • Most is stored as fat in adipocytes , but when these eventually fill up, excess lipid spills over into other tissues … - Phyllida Brown Leptin is an adipocyte -derived circulating hormone that provides information to the brain about energy stores. (merriam-webster.com)
  • Our results indicate that GABA(B)R1 subunit is constitutively expressed by adipocytes to primarily regulate leptin expression at the transcriptional level through a mechanism not relevant to the function as a partner of heterodimeric assembly to the functional GABA(B)R. (sigmaaldrich.com)
  • 6 5 We hypothesize that the residual marrow adipocytes are regulated to acquire special pathological characteristics in response to leukemic development. (haematologica.org)
  • The marrow adipocytes were divided into three subpopulations based on the values of the 25 and 75 percentiles of their diameter or area in the controls. (haematologica.org)
  • In contrast to the upper body fat cell response, the number of lower-body adipocytes did significantly increase during the course of experiment. (wikipedia.org)
  • We revealed for the first time that quercetin significantly changed expression of adipokine (Angptl4, adipsin, irisin and PAI-1) and glycolysis-involved (ENO2, PFKP and PFKFB4) genes, and that this effect not only antagonized but in part even overcompensated the effect mediated by hypoxia in adipocytes. (wellnessresources.com)
  • In males the epididymal and retroperitoneal fat pads were significantly enlarged nd adipocytes in these pads were hypertrophied. (sciencemag.org)
  • The secretome of white and brown primary murine adipocytes, with and without stimulation with norepinephrine (NE), has been determined by using mass spectrometry combined with AHA labeling and pulsed SILAC. (mcponline.org)
  • However, controversy still surrounds the cellular identity in BMP7-mediated transition of white to brown adipocytes. (springer.com)
  • Lipogenesis in rat brown adipocytes. (portlandpress.com)
  • Comparison of triacylglycerol synthesis in rat brown and white adipocytes. (portlandpress.com)
  • Our department examines the formation and physiological function of brown and white adipocytes. (dife.de)
  • Moreover, although BMP6-treated myoblasts can readily differentiate into brown adipocytes, serotonin interfered with this process. (ovid.com)
  • The main role of brown adipocytes is building a natural defense against hypothermia by burning fatty acids to maintain body temperature. (promocell.com)
  • Brown adipocytes are smaller than white ones, contain many mitochondria and several small lipid droplets. (promocell.com)
  • Our results suggest that SHR may have the capacity to increase energy expenditure in response to a chronic HFD that may be linked to the emergence of brown-like adipocytes in WAT. (biomedsearch.com)
  • 13 Abca1 deficiency thus decreases adipocyte size and triglyceride accumulation by suppression of SREBP-1c and PPARγ expression and their target genes ( Figure ). (ahajournals.org)
  • Genome-wide mRNA-seq expression profiling and ChIP-seq binding studies confirmed that TAF7L is required for activating adipocyte-specific genes via a dual mechanism wherein it interacts with PPARγ at enhancers and TBP/Pol II at core promoters. (elifesciences.org)
  • Using a combination of cellular, biochemical, genetic and genomic techniques, they show that TAF7L interacts with PPARγ, an important adipocyte transcriptional regulator at enhancer sites on the genome to increase the transcription of genes that are involved in adipogenesis. (elifesciences.org)
  • Knockdown of IRX3 or IRX5 in primary adipocytes from participants with the risk allele restored thermogenesis, increasing it by a factor of 7, and overexpression of these genes had the opposite effect in adipocytes from nonrisk-allele carriers. (mit.edu)
  • Adipocyte volume/tissue volume (AV/TV), mean adipocyte number (AD # ), and mean adipocyte diameter (AD diam ) were quantified. (springer.com)
  • Reintroduction of an ordinary chow diet to such animals precipitated a period of weight loss during which only mean adipocyte size returned to normal. (wikipedia.org)
  • Pre-adipocytes are undifferentiated fibroblasts that can be stimulated to form adipocytes. (wikipedia.org)