Adipocytes: 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.Adipocytes, White: Fat cells with light coloration and few MITOCHONDRIA. They contain a scant ring of CYTOPLASM surrounding a single large lipid droplet or vacuole.3T3-L1 Cells: 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.Adipose Tissue: 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.Lipolysis: 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.Insulin: 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).Glucose Transporter Type 4: 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.Adipogenesis: The differentiation of pre-adipocytes into mature ADIPOCYTES.3T3 Cells: 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.Monosaccharide Transport Proteins: A large group of membrane transport proteins that shuttle MONOSACCHARIDES across CELL MEMBRANES.Adipose Tissue, Brown: 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.Glucose: 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.Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.Adipose Tissue, White: 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.PPAR gamma: 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.Deoxyglucose: 2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.Cells, Cultured: 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.Muscle Proteins: The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.Receptor, Insulin: 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.Leptin: 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.Adiponectin: 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.Obesity: 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).Sterol Esterase: An enzyme that catalyzes the hydrolysis of CHOLESTEROL ESTERS and some other sterol esters, to liberate cholesterol plus a fatty acid anion.Insulin Resistance: 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, Messenger: 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.Lipid Metabolism: Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.Receptors, Adrenergic, beta-3: 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.Biological Transport: 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.Mice, Obese: 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.Insulin Receptor Substrate Proteins: 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.3-O-Methylglucose: 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)Glucose Transporter Type 1: 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.Epididymis: 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.Gene Expression Regulation: 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.Thiazolidinediones: 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).Lipoprotein Lipase: 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.MethylglucosidesIsoproterenol: 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.Phenylisopropyladenosine: N-Isopropyl-N-phenyl-adenosine. Antilipemic agent. Synonym: TH 162.Hypoglycemic Agents: Substances which lower blood glucose levels.Signal Transduction: 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.Subcutaneous Fat: Fatty tissue under the SKIN through out the body.Adipokines: 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.Insulin Antagonists: Compounds which inhibit or antagonize the biosynthesis or action of insulin.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.CCAAT-Enhancer-Binding Protein-alpha: 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.Glycerol: 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.PhosphoproteinsFatty Acids: 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)Cystinyl Aminopeptidase: A zinc-containing sialoglycoprotein that is used to study aminopeptidase activity in the pathogenesis of hypertension. EC 3.4.11.3.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Lipid Mobilization: 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.Mitochondrial Proteins: Proteins encoded by the mitochondrial genome or proteins encoded by the nuclear genome that are imported to and resident in the MITOCHONDRIA.Rats, Inbred Strains: 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.Mice, Inbred C57BLFatty Acid-Binding Proteins: 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.Thermogenesis: 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.Adrenergic beta-Agonists: Drugs that selectively bind to and activate beta-adrenergic receptors.1-Methyl-3-isobutylxanthine: 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 KINASESTriglyceridesPhosphatidylinositol 3-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.Kinetics: The rate dynamics in chemical or physical systems.Adrenergic beta-3 Receptor Agonists: Compounds that bind to and activate ADRENERGIC BETA-3 RECEPTORS.Omentum: A double-layered fold of peritoneum that attaches the STOMACH to other organs in the ABDOMINAL CAVITY.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Resistin: 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.Cyclic Nucleotide Phosphodiesterases, Type 3: 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.Receptors, Adrenergic, beta: 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.Reverse Transcriptase Polymerase Chain Reaction: 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.Lipids: 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, Ectopic: Hormones released from neoplasms or from other cells that are not the usual sources of hormones.Lipase: 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, Nonesterified: FATTY ACIDS found in the plasma that are complexed with SERUM ALBUMIN for transport. These fatty acids are not in glycerol ester form.DioxolesFatty Acid Synthases: Enzymes that catalyze the synthesis of FATTY ACIDS from acetyl-CoA and malonyl-CoA derivatives.Glycerolphosphate DehydrogenaseRats, Zucker: 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.Proto-Oncogene Proteins c-akt: 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.Androstadienes: Derivatives of the steroid androstane having two double bonds at any site in any of the rings.Ion Channels: 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.Mesenchymal Stromal Cells: 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.Blotting, Western: 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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Enzyme Activation: 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.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Dexamethasone: An anti-inflammatory 9-fluoro-glucocorticoid.Membrane Proteins: 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.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Tumor Necrosis Factor-alpha: 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.Diet, High-Fat: Consumption of excessive DIETARY FATS.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Protein Transport: 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.Proteins: 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.Receptors, Cytoplasmic and Nuclear: 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.Cyclic AMP: 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.Rats, Sprague-Dawley: 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.Epinephrine: 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.CCAAT-Enhancer-Binding Proteins: 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.Intra-Abdominal Fat: 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.Mice, Knockout: 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.Lipogenesis: 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.Norepinephrine: 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.ThiazolesSubcellular Fractions: 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)Sterol Regulatory Element Binding Protein 1: 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.Nicotinamide Phosphoribosyltransferase: 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).Palmitic Acid: A common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids.3',5'-Cyclic-AMP Phosphodiesterases: 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.HexosesDietary Fats: 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.Chromans: Benzopyrans saturated in the 2 and 3 positions.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Inflammation: 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.Oleic Acid: 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)Energy Metabolism: The chemical reactions involved in the production and utilization of various forms of energy in cells.Complement Factor D: 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.Body Weight: The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.Azo CompoundsCell Size: The quantity of volume or surface area of CELLS.rab4 GTP-Binding Proteins: 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.Colforsin: 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.Adenosine Deaminase: An enzyme that catalyzes the hydrolysis of ADENOSINE to INOSINE with the elimination of AMMONIA.Immunoblotting: 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.1-Acylglycerol-3-Phosphate O-Acyltransferase: 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.Gene Expression Regulation, Enzymologic: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.Adiposity: The amount of fat or lipid deposit at a site or an organ in the body, an indicator of body fat status.Intercellular Signaling Peptides and Proteins: 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.Interleukin-6: 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.Stem Cells: Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.Caveolae: 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.Down-Regulation: 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.Molecular Sequence Data: 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.Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.Caveolin 1: 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.Deoxy SugarsCCAAT-Enhancer-Binding Protein-beta: A CCAAT-enhancer-binding protein found in LIVER; INTESTINES; LUNG and ADIPOSE TISSUE. It is an important mediator of INTERLEUKIN-6 signaling.Subcutaneous Fat, Abdominal: Fatty tissue under the SKIN in the region of the ABDOMEN.Protein-Serine-Threonine Kinases: A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.Complement C3a: 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.Receptors, Leptin: 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.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Fatty Acid Transport Proteins: 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.Bucladesine: 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)Stromal Cells: 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.Cell Compartmentation: A partitioning within cells due to the selectively permeable membranes which enclose each of the separate parts, e.g., mitochondria, lysosomes, etc.Base Sequence: 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)

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 ...
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 ...
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.. ...
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, ...
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 ...
Comments, concepts and statistics about Pancreatic Lipase Inhibitory Gallotannins from Galla Rhois with Inhibitory Effects on Adipocyte Differentiation in 3T3-L1 Cells.
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 ...
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 ...
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
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 ...
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 ...
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 ...
"Beige adipocytes are a distinct type of thermogenic fat cell in mouse and human". Cell. 150 (2): 366-76. doi:10.1016/j.cell. ... Adipocyte. 2 (4): 289-93. doi:10.4161/adip.26082. PMC 3774709 . PMID 24052909. Boström P, Wu J, Jedrychowski MP, Korde A, Ye L ... "Irisin stimulates browning of white adipocytes through mitogen-activated protein kinase p38 MAP kinase and ERK MAP kinase ... "Irisin exerts dual effects on browning and adipogenesis of human white adipocytes". American Journal of Physiology. ...
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. ... Duque, G.; Li, W.; Adams, M.; Xu, S.; Phipps, R. (2011-05-01). "Effects of risedronate on bone marrow adipocytes in ... Flow cytometric quantification can be used to purify adipocytes from the stromal vascular fraction of most fat depots. Early ...
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 ...
Adipocyte. 2013; 2:176-83. Wagner M, Dudley AC. A three-party alliance in solid tumors: Adipocytes, macrophages and vascular ... Within adipose tissue, presence of dead adipocytes is a hallmark of obesity. Macrophages surrounding dying or dead adipocytes ... Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans. J Lipid Res 2005; 46: ... Adipocyte. 2013; 2:67-73. Appari M, Channon KM, McNeill E. Metabolic Regulation of Adipose Tissue Macrophage Function in ...
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 ... Lipolysis is directly induced in adipocytes by glucagon, epinephrine, norepinephrine, growth hormone, atrial natriuretic ...
C20orf3: encoding protein Adipocyte plasma membrane-associated protein. *C20orf43: encoding protein UPF0549 protein C20orf43 ...
Adipocytes also have an external lamina. Wheater's Functional Histology, 5th ed. Young, Lowe, Stevens and Heath.. ...
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 ...
Adipocytes secrete leptin in response to food intake. This hormone acts in the arcuate nucleus and inhibits the AgRP/NPY neuron ...
Brasaemle DL (December 2007). "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 ... "Adipocytes as regulators of energy balance and glucose homeostasis". Nature. 444 (7121): 847-53. doi:10.1038/nature05483. PMC ...
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: ...
... is the process of cell differentiation by which pre-adipocytes become adipocytes. Adipogenesis has been one of the ... 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 ... This mouse uses an inducible, adipose specific LacZ transgene, where one can label all the currently existing adipocytes as ...
The latter strategy is exhibited by neurons and adipocytes; the former by every other type of cell.[26] As a result, different ...
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. ...
Pre-adipocytes are undifferentiated fibroblasts that can be stimulated to form adipocytes. Recent studies shed light into ... or simply fat is a loose connective tissue composed mostly of adipocytes. In addition to adipocytes, adipose tissue contains ... these normally energy-storing adipocytes become energy-releasing adipocytes. UCP1 is a protein predominantly found in BAT. It ... The adipocytes in this depot are derived from mesenchymal stem cells (MSC) which can give rise to fat cells, bone cells as well ...
Brown adipocytes consist of densely packed mitochondria that contain uncoupling protein 1 (UCP-1). UCP-1 plays a key role in ... The activity of PRDM16 in white adipose tissue leads to the production of brown fat-like adipocytes within white adipose tissue ... This expression takes place primarily within mature adipocytes. Transgenic aP2-PRDM16 mice were used in a study to observe the ... PRDM16 acts as a transcription coregulator that controls the development of brown adipocytes in brown adipose tissue. ...
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 ...
Perilipin is a protein that coats lipid droplets in adipocytes, the fat-storing cells in adipose tissue. Perilipin acts as a ... 2004). "Evidence for an important role of perilipin in the regulation of human adipocyte lipolysis". Diabetologia. 46 (6): 789- ... Brasaemle DL (December 2007). "Thematic review series: adipocyte biology. The perilipin family of structural lipid droplet ... and perilipin A is the most abundant protein associated with the adipocyte lipid droplets. Perilipin is hyperphosphorylated by ...
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. ...
postgraduate thesis: Adipocyte fatty acid-binding protein: a link between inflammation and vascular dysfunction. *Show simple ... Adipocyte fatty acid-binding protein: a link between inflammation and vascular dysfunction. - ... Li, H. [李慧颖]. (2010). Adipocyte fatty acid-binding protein : a link between inflammation and vascular dysfunction. (Thesis). ... Li, H. [李慧颖]. (2010). Adipocyte fatty acid-binding protein : a link between inflammation and vascular dysfunction. (Thesis). ...
Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans. J Lipid Res 2005;46: ... Effects of adipocyte-derived cytokines on endothelial functions: implication of vascular disease. J Surg Res 2005;126:121-9. ... Although central (visceral) adipocytes are the most important source of adiponectin,11 the serum adiponectin concentration does ... Novel modulator for endothelial adhesion molecules: adipocyte-derived plasma protein adiponectin. Circulation 1999;100:2473-6. ...
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, ...
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. ...
Comparative Secretome Analyses of Primary Murine White and Brown Adipocytes Reveal Novel Adipokines Asrar Ali Khan, Jenny ... The secretome of white and brown primary murine adipocytes, with and without stimulation with norepinephrine (NE), has been ... The results reported reveal a comprehensive catalogue of novel adipokines secreted from white and brown adipocytes and ...
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 ...
... 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" ...
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 ...
gene inactivation in mice accelerated breakdown of triacylglycerides in adipocytes and protected animals from diet-induced ... identified the underlying molecular mechanism whereby SORLA promotes insulin-induced suppression of lipolysis in adipocytes. ...
However, the specific contribution of Rab18 to adipocyte function remains to be elucidated. Herein, we have analyzed Rab18 ... A role for Rab18 in the regulation of adipocyte biology under both normal and pathological conditions is proposed. ... the adipocytes. Proteomic analyses of LDs have consistently identified the small GTPase Rab18 as a component of the LD coat. ... thereby suggesting that this GTPase promotes fat accumulation in adipocytes. On the other hand, studies of the β-adrenergic ...
... which ultimately activates IL-6/STAT3 signaling in adipocytes and triggers BeAT development in the infant. Accordingly, lack of ...
E) Relative NADH-DH activity of adipocytes. (F) Ucp1 transcription in adipocytes. (G) Oxygen consumption of adipocytes treated ... Furthermore, iAT mass and adipocyte size were reduced (Supplemental Figure 14, B and C) and UCP1+ adipocytes were abundant ... or 1 adipocyte (D). (B) MFI of MitoTracker Green in adipocytes after treatment. (C) MitoTracker Red staining and transmission ... adipocytes were detectable in the iAT of AKG-treated mice (Figure 6E) along with a reduced adipocyte size (Figure 6F) and ...
... 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 ...
Further, loss of the adipocyte iron export channel, ferroportin, in mice resulted in adipocyte iron loading, decreased ... Adipocyte iron regulates adiponectin and insulin sensitivity J Clin Invest. 2012 Oct;122(10):3529-40. doi: 10.1172/JCI44421. ... These findings demonstrate a causal role for iron as a risk factor for metabolic syndrome and a role for adipocytes in ... Mice fed a high-iron diet and cultured adipocytes treated with iron exhibited decreased adiponectin mRNA and protein. We found ...
  • 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)
  • Delivery of miR-200a in adipocyte-derived exosomes to cardiomyocytes resulted in decreased TSC1 and subsequent mTOR activation, leading to cardiomyocyte hypertrophy. (jci.org)
  • In vivo, specific ablation of PPARγ in adipocytes was sufficient to blunt hypertrophy induced by RSG treatment. (jci.org)
  • By delineating mechanisms by which RSG elicits cardiac hypertrophy, we have identified pathways that mediate the crosstalk between adipocytes and cardiomyocytes to regulate cardiac remodeling. (jci.org)
  • CD137 and TMEM26), (3) glucose and fatty acid uptake, and (4) basal and cAMP-stimulated oxygen consumption rate compared to white adipocyte control. (springer.com)
  • Palmitate has been shown to stimulate glucose transport, translocation of GLUT4 and insulin receptor autophosphorylation in isolated rat adipocytes ( Biochem Biophys Res Commun 177:343-49, 1991). (diabetesjournals.org)
  • 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)
  • Treatment of adipocytes for 15 min with 1 mM myristate (14:0), palmitate (16:0), or stearate (18:0) stimulates glucose transport by 119 ± 33, 89 ± 29, and 114 ± 30%, respectively. (diabetesjournals.org)
  • After a 4-h preincubation with palmitate (1 mM), insulin stimulates glucose transport in rat adipocytes by 4.4-fold ± 0.8, vs. 8.8-fold ± 0.8 in controls ( n = 3). (diabetesjournals.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)
  • 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)
  • Several new investigations have shown that thermogenic adipocytes are beneficial to maintain glucose homeostasis, insulin sensitivity, and a healthy body fat content. (uio.no)
  • Transgenic mice overexpressing an adipocyte-specific, dominant-negative form of RhoA (DN-RhoA TG mice) showed decreased Rho-kinase activity in adipocytes, decreased HFD-induced weight gain, and improved glucose metabolism compared to wild-type littermates. (sciencemag.org)
  • Glucose transporter 4 (GLUT4) translocation and nuclear translocation of nuclear factor (NF)-kappa B were also analyzed in treated adipocytes. (biomedcentral.com)
  • 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)
  • Then, we stimulated 3T3-L1 adipocytes with exogenous tmTNF-α and sTNF-α respectively, and found that sTNF-α inhibited insulin- induced tyrosine phosphorylation of IRS-1 and AKT phosphorylation, leading to suppression of the glucose uptake induced by insulin. (omicsonline.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)
  • Mice fed a high-iron diet and cultured adipocytes treated with iron exhibited decreased adiponectin mRNA and protein. (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)
  • Hypoxia-inducible factor 1α regulates a SOCS3-STAT3-adiponectin signal transduction pathway in adipocytes. (sigmaaldrich.com)
  • Here, acriflavine (ACF), an inhibitor of HIF1α, induced the expression of adiponectin and reduced the expression of SOCS3 in cultured 3T3-L1 adipocytes. (sigmaaldrich.com)
  • 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)
  • Compared to normal adipocytes, this kind of adipocyte exhibits a series of characteristics, such as fibroblast-like phenotypes, smaller size, small and dispersed lipid droplets, overexpression of collagen VI, and low expression of adiponectin (APN) and other adipokines. (springermedizin.de)
  • Furthermore, we found that tmTNF-α downregulated the expression of IL-6 and MCP-1 through inactivation of NF-κB and upregulated the expression of adiponectin through PPAR-γ in 3T3-L1 adipocytes. (omicsonline.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)
  • 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)
  • 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)
  • Additionally, adipocytes directly transfer lipids to melanoma cells, which alters tumor cell metabolism. (aacrjournals.org)
  • The Center for Adipocyte Signaling - ADIPOSIGN at the Functional Genomics & Metabolism Research Unit, Department of Biochemistry and Molecular Biology, University of Southern Denmark, invites applications from outstanding candidates who are interested in joining our team as PhD students. (sdu.dk)
  • 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)
  • Adipocytes collected from subcutaneous fat biopsy samples after normal and restricted sleep conditions were exposed to incremental insulin concentrations. (annals.org)
  • Though subcutaneous tissues are largely composed of adipocytes, the mechanisms by which adipocytes influence melanoma are poorly understood. (aacrjournals.org)
  • 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)
  • To more precisely define the specific role of IRS-1 in adipocyte biology, we established brown adipocyte cell lines from wild-type and IRS-1 knockout (KO) animals. (asm.org)
  • Thus, IRS-1 appears to be an important mediator of brown adipocyte maturation. (asm.org)
  • 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)
  • When the body requires additional energy, the droplets of triglycerides contained in adipocytes undergo enzymatic hydrolysis to produce free fatty acids and glycerol. (merriam-webster.com)
  • In conclusion, we have shown that the development of adipocyte-induced VSMC alterations is linked to diet fatty acid composition and the degree of metabolic alterations. (scirp.org)
  • Direct effect refers to adipocyte or fatty infiltration of the atrial and ventricular myocardium itself, possibly causing increased dispersion of normal myocardial electrical signals and fibrotic substrate of adipocytes that promote reentry or adipocytes serving as a direct source of aberrant signals. (frontiersin.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)
  • The main role of brown adipocytes is building a natural defense against hypothermia by burning fatty acids to maintain body temperature. (promocell.com)
  • Small molecule inhibitors of adipocyte fatty-acid binding protein (A-FABP) have gained renewed interest following the recent publication of pharmacologically beneficial effects of such inhibitors. (rcsb.org)
  • 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)
  • 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)
  • The view that γ-aminobutyric acid (GABA) plays a functional role in non-neuronal tissues, in addition to an inhibitory neurotransmitter role in the mammalian central nervous system, is prevailing, while little attention has been paid to GABAergic signaling machineries expressed by adipocytes to date. (sigmaaldrich.com)
  • In this study, we attempted to demonstrate the possible functional expression of GABAergic signaling machineries by adipocytes. (sigmaaldrich.com)
  • Here, we combined existing data and models for rat adipocytes with new data collected for the signaling network between IR and GLUT4 to create a model also for their interconnections. (diva-portal.org)
  • Here, we identify adipocyte signaling through the guanosine triphosphatase Rho and its effector Rho-kinase as one such mechanism. (sciencemag.org)
  • Cultured 3T3-L1 adipocytes were incubated for 24h with rHMGB1 or TSE-MVs, in the absence or presence of neutralizing antibodies against different receptors, followed by assays of signaling responses to insulin and chemoattraction of monocytes across a Boyden chamber. (ahajournals.org)
  • Neutralizing antibodies against RAGE, but not TLR2, improved insulin signaling in adipocytes exposed to rHMGB1 or TSE-MVs. (ahajournals.org)
  • Recent studies shed light into potential molecular mechanisms in the fate determination of pre-adipocytes although the exact lineage of adipocyte is still unclear. (wikipedia.org)
  • 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)
  • You will also implement other experimental methods for analysis of adipocytes. (sdu.dk)
  • 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)