The differentiation of pre-adipocytes into mature 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.
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.
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.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
A CCAAT-enhancer-binding protein found in LIVER; INTESTINES; LUNG and ADIPOSE TISSUE. It is an important mediator of INTERLEUKIN-6 signaling.
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.
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.
Fat cells with light coloration and few MITOCHONDRIA. They contain a scant ring of CYTOPLASM surrounding a single large lipid droplet or vacuole.
Fat cells with dark coloration due to the densely packed MITOCHONDRIA. They contain numerous small lipid droplets or vacuoles. Their stored lipids can be converted directly to energy as heat by the mitochondria.
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.
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.
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.
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).
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.
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).
The process of bone formation. Histogenesis of bone including ossification.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
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.
Agents that increase energy expenditure and weight loss by neural and chemical regulation. Beta-adrenergic agents and serotoninergic drugs have been experimentally used in patients with non-insulin dependent diabetes mellitus (NIDDM) to treat obesity.
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.
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
A member of the C-EBP protein family of transcription factors. It plays a key role in G0 PHASE mammary EPITHELIAL CELL growth arrest, and it is involved in transcriptional regulation of INTERLEUKIN 1; INTERLEUKIN 6; and TUMOR NECROSIS FACTOR-ALPHA.
Fatty tissue under the SKIN through out the body.
The artificial induction of GENE SILENCING by the use of RNA INTERFERENCE to reduce the expression of a specific gene. It includes the use of DOUBLE-STRANDED RNA, such as SMALL INTERFERING RNA and RNA containing HAIRPIN LOOP SEQUENCE, and ANTI-SENSE OLIGONUCLEOTIDES.
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.
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.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
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.
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).
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.
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.
An organochlorine compound that was formerly used as an insecticide. Its manufacture and use has been discontinued in the United States. (From Merck Index, 11th ed)
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A collection of heterogenous conditions resulting from defective LIPID METABOLISM and characterized by ADIPOSE TISSUE atrophy. Often there is redistribution of body fat resulting in peripheral fat wasting and central adiposity. They include generalized, localized, congenital, and acquired lipodystrophy.
A potent cyclic nucleotide phosphodiesterase inhibitor; due to this action, the compound increases cyclic AMP and cyclic GMP in tissue and thereby activates CYCLIC NUCLEOTIDE-REGULATED PROTEIN KINASES
Wnt proteins are a large family of secreted glycoproteins that play essential roles in EMBRYONIC AND FETAL DEVELOPMENT, and tissue maintenance. They bind to FRIZZLED RECEPTORS and act as PARACRINE PROTEIN FACTORS to initiate a variety of SIGNAL TRANSDUCTION PATHWAYS. The canonical Wnt signaling pathway stabilizes the transcriptional coactivator BETA CATENIN.
An anti-inflammatory 9-fluoro-glucocorticoid.
Bone-forming cells which secrete an EXTRACELLULAR MATRIX. HYDROXYAPATITE crystals are then deposited into the matrix to form bone.
The amount of fat or lipid deposit at a site or an organ in the body, an indicator of body fat status.
An autoimmune disorder of the EYE, occurring in patients with Graves disease. Subtypes include congestive (inflammation of the orbital connective tissue), myopathic (swelling and dysfunction of the extraocular muscles), and mixed congestive-myopathic ophthalmopathy.
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.
Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.
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.
A thermogenic form of adipose tissue composed of BROWN ADIPOCYTES. It is found in newborns of many species including humans, and in hibernating mammals. Brown fat is richly vascularized, innervated, and densely packed with MITOCHONDRIA which can generate heat directly from the stored lipids.
A gene silencing phenomenon whereby specific dsRNAs (RNA, DOUBLE-STRANDED) trigger the degradation of homologous mRNA (RNA, MESSENGER). The specific dsRNAs are processed into SMALL INTERFERING RNA (siRNA) which serves as a guide for cleavage of the homologous mRNA in the RNA-INDUCED SILENCING COMPLEX. DNA METHYLATION may also be triggered during this process.
Established cell cultures that have the potential to propagate indefinitely.
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.
Bony cavity that holds the eyeball and its associated tissues and appendages.
A DNA-binding orphan nuclear receptor that negatively regulates expression of ARNTL TRANSCRIPTION FACTORS and plays a role as a regulatory component of the circadian clock system. The Nr1d1 nuclear receptor expression is cyclically-regulated by a feedback loop involving its positive regulation by CLOCK PROTEIN; BMAL1 PROTEIN heterodimers and its negative regulation by CRYPTOCHROME and PERIOD PROTEINS.
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.
A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. Beta catenin binds CADHERINS and helps link their cytoplasmic tails to the ACTIN in the CYTOSKELETON via ALPHA CATENIN. It also serves as a transcriptional co-activator and downstream component of WNT PROTEIN-mediated SIGNAL TRANSDUCTION PATHWAYS.
A technique for identifying specific DNA sequences that are bound, in vivo, to proteins of interest. It involves formaldehyde fixation of CHROMATIN to crosslink the DNA-BINDING PROTEINS to the DNA. After shearing the DNA into small fragments, specific DNA-protein complexes are isolated by immunoprecipitation with protein-specific ANTIBODIES. Then, the DNA isolated from the complex can be identified by PCR amplification and sequencing.
Regulatory proteins and peptides that are signaling molecules involved in the process of PARACRINE COMMUNICATION. They are generally considered factors that are expressed by one cell and are responded to by receptors on another nearby cell. They are distinguished from HORMONES in that their actions are local rather than distal.
A continuous cell line of high contact-inhibition established from NIH Swiss mouse embryo cultures. The cells are useful for DNA transfection and transformation studies. (From ATCC [Internet]. Virginia: American Type Culture Collection; c2002 [cited 2002 Sept 26]. Available from
Organometallic compounds which contain tin and three alkyl groups.
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.

Induction of chondro-, osteo- and adipogenesis in embryonic stem cells by bone morphogenetic protein-2: effect of cofactors on differentiating lineages. (1/1177)

BACKGROUND: Recently, tissue engineering has merged with stem cell technology with interest to develop new sources of transplantable material for injury or disease treatment. Eminently interesting, are bone and joint injuries/disorders because of the low self-regenerating capacity of the matrix secreting cells, particularly chondrocytes. ES cells have the unlimited capacity to self-renew and maintain their pluripotency in culture. Upon induction of various signals they will then differentiate into distinctive cell types such as neurons, cardiomyocytes and osteoblasts. RESULTS: We present here that BMP-2 can drive ES cells to the cartilage, osteoblast or adipogenic fate depending on supplementary co-factors. TGFbeta1, insulin and ascorbic acid were identified as signals that together with BMP-2 induce a chondrocytic phenotype that is characterized by increased expression of cartilage marker genes in a timely co-ordinated fashion. Expression of collagen type IIB and aggrecan, indicative of a fully mature state, continuously ascend until reaching a peak at day 32 of culture to approximately 80-fold over control values. Sox9 and scleraxis, cartilage specific transcription factors, are highly expressed at very early stages and show decreased expression over the time course of EB differentiation. Some smaller proteoglycans, such as decorin and biglycan, are expressed at earlier stages. Overall, proteoglycan biosynthesis is up-regulated 7-fold in response to the supplements added. BMP-2 induced chondrocytes undergo hypertrophy and begin to alter their expression profile towards osteoblasts. Supplying mineralization factors such as beta-glycerophosphate and vitamin D3 with the culture medium can facilitate this process. Moreover, gene expression studies show that adipocytes can also differentiate from BMP-2 treated ES cells. CONCLUSIONS: Ultimately, we have found that ES cells can be successfully triggered to differentiate into chondrocyte-like cells, which can further alter their fate to become hypertrophic, and adipocytes. Compared with previous reports using a brief BMP-2 supplementation early in differentiation, prolonged exposure increased chondrogenic output, while supplementation with insulin and ascorbic acid prevented dedifferentiation. These results provide a foundation for the use of ES cells as a potential therapy in joint injury and disease.  (+info)

Role of Gas-6 in adipogenesis and nutritionally induced adipose tissue development in mice. (2/1177)

OBJECTIVE: A potential role of growth arrest-specific gene 6 (Gas-6) in energy storage in adipose tissue was investigated in murine models of obesity. Gas-6 is a ligand for the Axl, C-Mer, and Sky family of tyrosine kinase receptors. METHODS AND RESULTS: Whereas Gas-6, C-Mer, and Sky were expressed in mature murine adipocytes, the expression of Axl was restricted to the stromal-vascular fraction, which includes pre-adipocytes. During the in vitro conversion of adipogenic 3T3-F442A cells into mature adipocytes, the expression of Gas-6 increased in undifferentiated confluent pre-adipocytes during a transient phase of growth arrest. On treatment of these cells with an adipogenic medium, Gas-6 expression decreased sharply, coinciding with expression of early adipocytes markers. This modulation was not observed in the nonadipogenic 3T3-C2 cells. The Gas-6 mRNA level was transiently downregulated during nutritionally induced expansion of adipose tissues in vivo. When kept on a standard diet, no significant difference in either total body weight or weight of gonadal or subcutaneous fat pads was observed between Gas-6 deficient and wild-type mice. On exposure to a high-fat diet, however, Gas-6-deficient mice had significantly less fat mass than their wild-type counterparts. CONCLUSIONS: Gas-6 enhances the accumulation of adipose tissue in diet-induced obese mice.  (+info)

Mesenchymal stem cells from the outer ear: a novel adult stem cell model system for the study of adipogenesis. (3/1177)

Adipocytes arise from multipotent stem cells of mesodermal origin, which also give rise to the muscle, bone, and cartilage lineages. However, signals and early molecular events that commit multipotent stem cells into the adipocyte lineage are not well established mainly due to lack of an adequate model system. We have identified a novel source of adult stem cells from the external murine ears referred to here as an ear mesenchymal stem cells (EMSC). EMSC have been isolated from several standard and mutant strains of mice. They are self-renewing, clonogenic, and multipotent, since they give rise to osteocytes, chondrocytes, and adipocytes. The in vitro characterization of EMSC indicates very facile adipogenic differentiation. Morphological, histochemical, and molecular analysis after the induction of differentiation showed that EMSC maintain adipogenic potentials up to fifth passage. A comparison of EMSC to the stromal-vascular (S-V) fraction of fat depots, under identical culture conditions (isobutyl-methylxanthine, dexamethasone, and insulin), revealed much more robust and consistent adipogenesis in EMSC than in the S-V fraction. In summary, we show that EMSC can provide a novel, easily obtainable, primary culture model for the study of adipogenesis.  (+info)

Generation of a vascularized organoid using skeletal muscle as the inductive source. (4/1177)

The technology required for creating an in vivo microenvironment and a neovasculature that can grow with and service new tissue is lacking, precluding the possibility of engineering complex three-dimensional organs. We have shown that when an arterio-venous (AV) loop is constructed in vivo in the rat groin, and placed inside a semisealed chamber, an extensive functional vasculature is generated. To test whether this unusually angiogenic environment supports the survival and growth of implanted tissue or cells, we inserted various preparations of rat and human skeletal muscle. We show that after 6 weeks incubation of muscle tissue, the chamber filled with predominantly well-vascularized recipient-derived adipose tissue, but some new donor-derived skeletal muscle and connective tissue were also evident. When primary cultured myoblasts were inserted into the chamber with the AV loop, they converted to mature striated muscle fibers. Furthermore, we identify novel adipogenesis-inducing properties of skeletal muscle. This represents the first report of a specific three-dimensional tissue grown on its own vascular supply.  (+info)

The transcription factor GATA2 regulates differentiation of brown adipocytes. (5/1177)

Brown adipose tissue (BAT) is a specialized mammalian tissue and a site of adaptive thermogenesis. Although the metabolic functions of brown and white adipocytes are distinct, terminal differentiation of both adipocyte lineages is regulated by well-characterized common transcription factors. However, the early stages of adipocyte differentiation and regulation of precursor cells are not well understood. We report here that GATA2 is expressed in brown adipocyte precursors, and its expression is downregulated in a differentiation-dependent manner. Constitutive expression of GATA2 suppressed expression of BAT-specific genes in brown adipocytes, whereas disruption of a GATA2 allele in brown preadipocytes resulted in significantly elevated differentiation and expression of several markers of brown adipogenesis. Collectively, these results show that GATA2 functions to suppress brown adipocyte differentiation, whereas reduction of GATA2 promotes brown adipogenesis.  (+info)

The G0/G1 switch gene 2 is a novel PPAR target gene. (6/1177)

PPARs (peroxisome-proliferator-activated receptors) alpha, beta/delta and gamma are a group of transcription factors that are involved in numerous processes, including lipid metabolism and adipogenesis. By comparing liver mRNAs of wild-type and PPARalpha-null mice using microarrays, a novel putative target gene of PPARalpha, G0S2 (G0/G1 switch gene 2), was identified. Hepatic expression of G0S2 was up-regulated by fasting and by the PPARalpha agonist Wy14643 in a PPARalpha-dependent manner. Surprisingly, the G0S2 mRNA level was highest in brown and white adipose tissue and was greatly up-regulated during mouse 3T3-L1 and human SGBS (Simpson-Golabi-Behmel syndrome) adipogenesis. Transactivation, gel shift and chromatin immunoprecipitation assays indicated that G0S2 is a direct PPARgamma and probable PPARalpha target gene with a functional PPRE (PPAR-responsive element) in its promoter. Up-regulation of G0S2 mRNA seemed to be specific for adipogenesis, and was not observed during osteogenesis or myogenesis. In 3T3-L1 fibroblasts, expression of G0S2 was associated with growth arrest, which is required for 3T3-L1 adipogenesis. Together, these data indicate that G0S2 is a novel target gene of PPARs that may be involved in adipocyte differentiation.  (+info)

Brain and muscle Arnt-like protein-1 (BMAL1), a component of the molecular clock, regulates adipogenesis. (7/1177)

Brain and muscle Arnt-like protein-1 (BMAL1; also known as MOP3 or Arnt3) is a transcription factor known to regulate circadian rhythm. Here, we established its involvement in the control of adipogenesis and lipid metabolism activity in mature adipocytes. During adipose differentiation in 3T3-L1 cells, the level of BMAL1 mRNA began to increase 4 days after induction and was highly expressed in differentiated cells. In white adipose tissues isolated from C57BL/6J mice, BMAL1 was predominantly expressed in a fraction containing adipocytes, as compared with the stromal-vascular fraction. BMAL1 knockout mice embryonic fibroblast cells failed to be differentiated into adipocytes. Importantly, adding BMAL1 back by adenovirus gene transfer restored the ability of BMAL1 knockout mice embryonic fibroblast cells to differentiate. Knock-down of BMAL1 expression in 3T3-L1 cells by an RNA interference technique allowed the cells to accumulate only minimum amounts of lipid droplets in the cells. Adenovirus-mediated expression of BMAL1 in 3T3-L1 adipocytes resulted in induction of several factors involved in lipogenesis. The promoter activity of these genes was stimulated in a BMAL1-dependent manner. Interestingly, expression of these factors showed clear circadian rhythm in mice adipose tissue. Furthermore, overexpression of BMAL1 in adipocytes increased lipid synthesis activity. These results indicate that BMAL1, a master regulator of circadian rhythm, also plays important roles in the regulation of adipose differentiation and lipogenesis in mature adipocytes.  (+info)

Gene expression analysis suggests that EBF-1 and PPARgamma2 induce adipogenesis of NIH-3T3 cells with similar efficiency and kinetics. (8/1177)

Differentiation of multipotent mesenchymal stem cells into lipid-accumulating adipocytes is a physiological process induced by transcription factors in combination with hormonal stimulation. We have used Affymetrix microarrays to compare the adipogenic differentiation pathways of NIH-3T3 fibroblasts induced to undergo in vitro differentiation by ectopic expression of early B cell factor (EBF)-1 or peroxisome proliferator-activated receptor (PPAR)gamma2. These experiments revealed that commitment to the adipogenic pathway in the NIH-3T3 cells was not reflected in gene expression until 4 days after induction of differentiation. Furthermore, gene expression patterns at the earlier time points after stimulation indicated that EBF-1 and PPARgamma2 induced different sets of genes, while the similarities increased upon differentiation, and that several genes linked to adipocyte differentiation were also transiently induced in the vector-transduced cells. These data suggest that the initial activation of genes associated with adipocyte development is independent of commitment to the adipogenic pathway and that EBF-1 and PPARgamma2 induce adipocyte differentiation with comparable kinetics and efficiency.  (+info)

The current epidemic of obesity has caused a surge of interest in the study of adipose tissue formation. While major progress has been made in defining the molecular networks that control adipocyte terminal differentiation, the early steps of adipocyte development and the embryonic origin of this lineage remain largely unknown. Here we performed genome-wide analysis of gene expression during adipogenesis of mouse embryonic stem cells (ESCs). We then pursued comprehensive bioinformatic analyses, including de novo functional annotation and curation of the generated data within the context of biological pathways, to uncover novel biological functions associated with the early steps of adipocyte development. By combining in-depth gene regulation studies and in silico analysis of transcription factor binding site enrichment, we also provide insights into the transcriptional networks that might govern these early steps. This study supports several biological findings: firstly, adipocyte development in mouse
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
ERRERA, Flavia I.V. et al. COL18A1 is highly expressed during human adipocyte differentiation and the SNP c.1136C , T in its frizzled motif is associated with obesity in diabetes type 2 patients. An. Acad. Bras. Ciênc. [online]. 2008, vol.80, n.1, pp.167-177. ISSN 1678-2690. Collagen XVIII can generate two fragments, NC11-728 containing a frizzled motif which possibly acts in Wnt signaling and Endostatin, which is cleaved from the NC1 and is a potent inhibitor of angiogenesis. Collagen XVIII and Wnt signaling have recently been associated with adipogenic differentiation and obesity in some animal models, but not in humans. In the present report, we have shown that COL18A1 expression increases during human adipogenic differentiation. We also tested if polymorphisms in the Frizzled (c.1136C,T; Thr379Met) and Endostatin (c.4349G,A; Asp1437Asn) regions contribute towards susceptibility to obesity in patients with type 2 diabetes (113 obese, BMI ...
Despite detailed knowledge about the molecular mechanisms that control adipocyte differentiation in vitro, little is known about how adipogenesis progresses in vivo, particularly in obesity. Our live-cell imaging has revealed that adipogenesis takes place within adipogenic/angiogenic cell clusters that also contain various stromal cells and blood vessels and that angiogenesis is an essential part of adipogenesis in obesity.. Macrophages reportedly accumulate within obese adipose tissue (11,28) so that the presence of macrophage markers is significantly and positively correlated with both adipocyte size and body mass (34). However, little is known about the roles such macrophages play in adipogenesis and obesity. Although infiltration by macrophages of the area surrounding small adipocytes has been previously described in older obese animals (11,28), their functions have been related to adipocyte cell death (22). The present report is the first, to our knowledge, to describe adipocyte-associated ...
Adipogenesis is a complex process, in which immature pre-adipocytes change morphology, micro-anatomy and physiology to become mature adipocytes. These store and accumulate fat and release diverse hormones. Massive changes in protein content and protein composition of the transforming cell take place within a short time-frame. In a previous study we analyzed changes in the abundance of free and polysomal, i.e. ribosome bound, RNAs in the first hours of adipogenesis in the murine cell line 3T3-L1. Here we analyze changes of mRNA levels and their potential contribution to the changing protein pool by determination of mRNA levels and ribosome binding to mRNAs in 3T3-L1 cells stimulated for adipogenesis. We grouped mRNA species into categories with respect to up- or down-regulated transcription and translation and analyzed the groups regarding specific functionalities based on Gene Ontology (GO). A shift towards up-regulation of gene expression in early adipogenesis was detected. Genes up-regulated at the
The ubiquity of obesity has increased exponentially, and the health burden of obesity-related diseases including type 2 diabetes, metabolic disorders, heart diseases, and some types of cancers is growing. Obesity is characterized by the excess accumulation of fat and adipose tissue and driven by adipogenesis, which is the process in which stem cells differentiate into adipocytes. We utilize human adipose derived stem cells (hASCs) isolated from adult fat tissue to study adipogenesis (the formation of fat tissue). This physiological potential, combined with non-invasive collection methods, make hASCs favorable in the search for new clinical stem cell treatments and for the study of cellular processes and differentiation. We are interested in understanding the function of MED12 in adipogenesis and determining its role in initiating cell type specific gene expression in hopes that this research can be used in treatments for obesity and related metabolic disorders. MED12 is a subunit of the Mediator complex
Background Ursolic acid (UA) is a triterpenoid compound with multiple biological functions. This compound has recently been reported to possess an anti-obesity effect; however, the mechanisms are less understood. Objective As adipogenesis plays a critical role in obesity, the present study was conducted to investigate the effect of UA on adipogenesis and mechanisms of action in 3T3-L1 preadipocytes. Methods and Results The 3T3-L1 preadipocytes were induced to differentiate in the presence or absence of UA for 6 days. The cells were determined for proliferation, differentiation, fat accumulation as well as the protein expressions of molecular targets that regulate or are involved in fatty acid synthesis and oxidation. The results demonstrated that ursolic acid at concentrations ranging from 2.5 µM to 10 µM dose-dependently attenuated adipogenesis, accompanied by reduced protein expression of CCAAT element binding protein β (C/EBPβ), peroxisome proliferator-activated receptor γ (PPARγ), CCAAT
TY - JOUR. T1 - Regulation of brown fat adipogenesis by protein tyrosine phosphatase 1B. AU - Matsuo, Kosuke. AU - Bettaieb, Ahmed. AU - Nagata, Naoto. AU - Matsuo, Izumi. AU - Keilhack, Heike. AU - Haj, Fawaz. PY - 2011. Y1 - 2011. N2 - Background: Protein-tyrosine phosphatase 1B (PTP1B) is a physiological regulator of insulin signaling and energy balance, but its role in brown fat adipogenesis requires additional investigation. Methodology/Principal Findings: To precisely determine the role of PTP1B in adipogenesis, we established preadipocyte cell lines from wild type and PTP1B knockout (KO) mice. In addition, we reconstituted KO cells with wild type, substratetrapping (D/A) and sumoylation-resistant (K/R) PTP1B mutants, then characterized differentiation and signaling in these cells. KO, D/A- and WT-reconstituted cells fully differentiated into mature adipocytes with KO and D/A cells exhibiting a trend for enhanced differentiation. In contrast, K/R cells exhibited marked attenuation in ...
Human Platelets were purchased from HEMOCARE for the production of PRP. Human adipose-derived stem cells were isolated as per laboratory protocol. The ASCs were cultured under four conditions: 1. Regular DMEM medium, 2. Regular DMEM medium with PRP 3. Adipogenic medium 4. Adipogenic medium with PRP. The cell proliferation was assessed by CYQUANT and the adipogenesis were evaluated by AdipoRed stain and the qPCR of PPAR-gamma and FABP4 gene expression. The mRNA of stemness gene expression of ASCs was compared by qPCR of SOX-2, Nanog and Oct-4 .The angiogenesis of ASCs was evaluated by qPCR of VEGF gene expression and endothelium tube formation assay. The nude mice were implant with fat graft with PRP as experiment and fat graft only as control group. The survival rate was analyzed by volume retention, the histomophometry of mature adipocyte area and vessel density assay by CD31 immunohistochemical stain ...
We have previously identified a WD‐repeat propeller‐FYVE protein, ProF, as an interaction partner for the kinases PKCζ and Akt in 3T3‐L1 cells (Fritzius et al, 2006). Furthermore, we have shown that ProF forms a trimeric complex with PKCζ and its substrate VAMP2. In this complex, ProF was found to act as an adaptor‐like protein for facilitated substrate phosphorylation of VAMP2 by the active kinase PKCζ (Fritzius et al, 2007).. In this study, we identified a role for ProF during adipogenesis and showed complex formation of ProF with the kinase Akt and the kinase substrate Foxo1. The protein kinase Akt was found to affect adipogenesis after the expression of C/EBPβ and C/EBPδ, but before the expression of PPARγ and C/EBPα (Peng et al, 2003; Baudry et al, 2006), which resembled the effects of ProF on adipogenesis. Akt phosphorylation of Foxo1 at Ser253, in the Foxo1 DNA binding domain, has been demonstrated to decrease its transcriptional activity (Zhang et al, 2002). We have shown ...
TY - JOUR. T1 - CXCL3 positively regulates adipogenic differentiation. AU - Kusuyama, Joji. AU - Komorizono, Anna. AU - Bandow, Kenjiro. AU - Ohnishi, Tomokazu. AU - Matsuguchi, Tetsuya. PY - 2016/10. Y1 - 2016/10. N2 - Chemokines are a family of cytokines inducing cell migration and inflammation. Recent reports have implicated the roles of chemokines in cell differentiation. However, little is known about the functional roles of chemokines in adipocytes. Here, we explored gene expression levels of chemokines and chemokine receptors during adipogenic differentiation. We have found that two chemokines, chemokine (C-X-C motif) ligand 3 (CXCL3) and CXCL13, as well as CXC chemokine receptor 2(CXCR2), a CXCL3 receptor, are highly expressed in mature adipocytes. When 3T3-L1 cells and ST2 cells were induced to differentiate, both the number of lipid droplets and the expression levels of adipogenic markers were significantly promoted by the addition of CXCL3, but not CXCL13. Conversely, gene knockdown ...
University of Pittsburgh Introduction: Human adipose derived stem cells (ASC) may have broad applications to plastic and reconstructive surgery. For soft tissue reconstruction, the ability to induce adipogenesis and angiogenesis is vital for long term graft survival. However the gene expression and cellular fate of these cells is governed by molecular signaling. Wnt signaling is well evidenced in inhibiting adipogenesis and influence cell differentiation. We hypothesized that regulation of this signaling cascade in adipose stem cells could enhance adipogenesis.. Purpose: This study aims to antagonize Wnt signaling by lentiviral overexpression of secreted frizzled-related protein1 (sFRP1) in ASCs to assess adipogenesis and angiogenic growth factor secretion.. Methods: Wnt antagonistic studies were carried out in lentiviral sFRP1 transfected and flow cytometry selected GFP reporter positive ASCs. mRNA gene expression of signaling cascade were analyzed for adipogenic marker genes (PPARy, FABP4, ...
Compared to standard 2D culture systems, new methods for 3D cell culture of adipocytes could provide more physiologically accurate data and a deeper understanding of metabolic diseases such as diabetes. By resuspending living cells in a bioink of nanocellulose and hyaluronic acid, we were able to print 3D scaffolds with uniform cell distribution. After one week in culture, cell viability was 95%, and after two weeks the cells displayed a more mature phenotype with larger lipid droplets than standard 2D cultured cells. Unlike cells in 2D culture, the 3D bioprinted cells did not detach upon lipid accumulation. After two weeks, the gene expression of the adipogenic marker genes PPAR. and FABP4 was increased 2.0- and 2.2-fold, respectively, for cells in 3D bioprinted constructs compared with 2D cultured cells. Our 3D bioprinted culture system produces better adipogenic differentiation of mesenchymal stem cells and a more mature cell phenotype than conventional
In this study, we have continued to investigate the roles of the E2F and pocket proteins in the regulation of adipocyte differentiation. It was previously shown that hormone-induced adipogenesis is promoted by the loss of either E2F4 or p107 and p130 (25, 26). It seemed highly likely that the shared activity of E2F4 and p107/p130 simply reflects their participation in transcriptionally repressive complexes. However, our current analyses of compound mutant MEFs do not support this hypothesis. Instead, they suggest that the E2F and pocket proteins contribute to the regulation of adipocyte differentiation through three distinct mechanisms. Moreover, each one of these can be separated from effects on cell cycle control.. The first mechanism involves the E2F4 transcription factor. We have found that E2F4 loss predisposes MEFs to undergo adipogenesis. This phenotype includes increasing the proportion of cells that differentiate in response to the standard hormone treatment as well as enabling ...
To our knowledge, these are the first results that demonstrate the effects of maternal isocaloric pair-fed high-carbohydrate (LF-HCD) versus high-fat diet (HF-LCD) during gestation and lactation on gene expression and serum levels of formation and resorption markers in bone, as well as adipogenic and lipogenic markers in retroperitoneal fat mass of mice offspring at adolescence. The results of the present study showed that maternal LF-HCD during gestation and lactation lead to up-regulation of Runx2 and Ctnnb1, as well as Runx2, OPG, OPG/RANK-L ratio and Ctnnb1 mRNA expression in bone of female and male offspring, respectively. Also, serum levels of OPG/RNK-L ratio which is the marker of osteogenesis [22] were increased in the LF-HCD-fed group, compared with the HF-LCD. PPARγ2 mRNA expression, as well as other adipogenic genes measured in the current study and serum levels of proteins were increased in the offspring of HF-LCD-fed mothers. Our results showed that mRNA expression of OPG and ...
Rising obesity epidemic makes the better understanding of transcription factor networks regulating adipogenesis very challenging. Adipogenesis begins with the commitment of pluripotent mesenchymal stem cells to the adipocyte lineage, followed by terminal differentiation of preadipocytes to mature ad …
Abstract: There is great concern with an increase in the number of Americans who are overweight and obese. Fat cells or adipocytes play a central role in obesity. These cells are metabolically active and play a fundamental role in energy allocation and storage. The adipocyte functions as the energy storage cell by storing excess energy in the forms of triglycerides in lipid vesicles within the cell. The morphology of mitochondria is a dynamic process that varies from cell type to cell type and in response to a variety of signals and conditions (Wilson-Fritch, 2002; Wilson-Fritch, 2004). The morphology of mitochondria in the cell often reflects the functions of that type of cell. In my thesis I characterize the changes in mitochondrial morphology and actin during adipogenesis. In this thesis I found that mitochondria undergo a radical change in morphology during the first two days of adipogenesis. In the pre-adipocyte cell mitochondria assume a reticular morphology that is distributed uniformly ...
CUL4B participates in the regulation of a broad spectrum of biological processes. In the current study, we provided several lines of evidence that CUL4B functions as a negative regulator of adipogenesis. First, CUL4B expression was downregulated during adipocyte differentiation in obese mice and was inversely correlated with BMI. Second, knockdown of CUL4B in 3T1-L1 cells led to increased adipocyte differentiation, whereas the overexpression of CUL4B had the opposite effect. Third, most importantly, the deletion of CUL4B in adipose tissues greatly facilitated adipogenesis. When challenged with HFD, AKO mice exhibited increased body weight gain and fat mass. Mechanistically, we demonstrated that the negative regulation of adipogenesis by CUL4B is mediated by the polyubiquitination of PPARγ, a master regulator of adipogenesis and insulin sensitivity. In particular, the treatment with PPARγ inhibitor GW9662 in HFD-fed AKO mice could efficiently block the increased adipogenesis and decreased ...
Title:. A Novel pro-adipogenesis factor abundant in adipose tissues and over-expressed in obesity acts upstream of PPARg and C/EBPa. Authors:. Yuhui Ni, Chenbo Ji, Bin Wang, Jie Qiu, Jiwu Wang, Xirong Guo Abstract:. An important question about adipogenesis is how master adipogenesis factors (defined as being able to initiate adipogenesis when expressed alone) peroxisome proliferator-activated receptor (PPAR) initiate adipogenesis only in differentiating preadipocytes. The objective of our research was to find previously unidentified factors that are unique or highly enriched in cells of the adipocyte lineage during adipogenesis that may provide functional tissue specificity to preadipocytes. We reasoned that such factors may alter expression profile specifically in obese individuals. Omental adipose tissues were obtained from obese and non-obese male patients undergoing emergency abdominal surgery. mRNAs extracted from either group were used for suppression subtraction hybridization (SSH). Genes ...
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TY - JOUR. T1 - The combination of DHEA, histamine, and insulin increases adipogenic differentiation and enhances tissue transplantation outcome in mice. AU - Park, Yoorim. AU - Jung, Min Kyung. AU - Yoon, Sun Young. AU - Lee, Ha Reum. AU - Hur, Dae Young. AU - Kim, Daejin. AU - Yang, Yoolhee. AU - Kim, Tae Sung. AU - Kim, Seonghan. AU - Yoon, Suk Ran. AU - Park, Hyun Jeong. AU - Bang, Sa Ik. AU - Cho, Dae Ho. PY - 2013/5/1. Y1 - 2013/5/1. N2 - Adipose stem cells (ASCs) are pluripotent cells that can generate pure fat tissue for regeneration. Differentiated adipose cells have been generated by a common inducer cocktail composed of dexamethasone, insulin, and isobutylmethylxanthine (DIM). The major drawbacks of adipose cells are their tendency to float on the culture media and their cost. To overcome some of these disadvantages, a new inducer cocktail that includes insulin, dehydroepiandrosterone, and histamine (DHIH) was tested. As a result, lipid accumulation was elevated more than twofold with ...
Adipocytes arise from mesodermal stem cells, which have the capacity to differentiate into a variety of other cell types, including myocytes (1). Once committed to the adipocyte lineage, preadipocytes can remain quiescent, multiply, or undergo differentiation and become adipocytes. 3T3-L1 and 3T3-F442A cells are established mouse preadipocyte models. Both cell lines can be induced to differentiate in cell culture, but 3T3-F442A cells are thought to be arrested at a later point in development (2). Studies of these cellular models have revealed some of the molecular events that orchestrate adipogenesis, including the role of C/EBPs and PPARγ in mediating the expression of adipocyte-specific genes (3, 4).. Wnts are a family of paracrine and autocrine factors that regulate cell growth and cell fate (5). Signaling is initiated when Wnt ligands bind to transmembrane receptors of the Frizzled family. In the canonical Wnt signaling pathway, Frizzleds signal through Dishevelled to inhibit the kinase ...
The present results provide direct evidence for a regulatory role of mechanical stress in adipocyte differentiation, mediated through the activation of the ERK/MAPK system. Controversial observations concerning the role of ERK/MAPK in adipocyte differentiation have been reported by several laboratories - the activation of the ERK/MAPK pathway has been shown to be involved in both the inhibition (Font de Mora et al., 1997; Hu et al., 1996; Kim et al., 2001; Shimba et al., 2001) and the promotion (Bost et al., 2002; Klemm et al., 2001; Machinal-Quelin et al., 2002; Prusty et al., 2002; Zhang et al., 1996) of adipocyte differentiation. Along these lines, Prusty et al. recently suggested that stimulation of the ERK/MAPK pathway might have opposing effects in the process of adipogenesis, depending on the time of activation during the differentiation process (Prusty et al., 2002). In the present study, the activated state of ERK1/2 was more prolonged during the induction period in response to the ...
People who have Type 2 diabetes mellitus (T2DM) have reduced bone LY2784544 tissue nutrient density and an elevated threat of fractures because of altered mesenchymal stem cell (MSC) differentiation in the bone tissue marrow. of metformin had been seen in multipotent C3H10T1/2 MSCs where metformin exerted reciprocal control over the actions of Runx2 as well as the adipogenic transcription aspect PPARγ resulting in suppression of adipogenesis. These effects were unbiased of AMPK activation but through the suppression from the mTOR/p70S6K signalling pathway rather. Basal AMPK and mTOR/p70S6K activity do seem to be necessary for adipogenesis as showed through the AMPK inhibitor substance C. This observation was additional supported through the use of AMPK knockout mouse embryo fibroblasts (MEFs) where adipogenesis as evaluated by decreased lipid deposition and expression from the adipogeneic transcription aspect C/EBPβ was discovered to display a total requirement of AMPK. Further activation of ...
Adipose tissue is a highly specialized compartment of cells actively involved in maintaining global metabolic homeostasis through lipid synthesis and storage, adipokine secretion, and insulin responsiveness (1). Adipocytes compose the majority of cells in adipose tissue and play a critical role in normal physiology, but their dysfunction is also at the center of a diverse range of diseases, including obesity, diabetes, and lipodystrophies (2). Furthermore, primary preadipocytes and adipose-derived stem cells have shown promise in treating multiple conditions (3-5). Therefore, it is critical to understand the process by which spindly fibroblastic precursor cells undergo conversion into round lipid-laden fat cells.. In vitro models of adipogenesis, such as the extensively studied committed preadipocyte cell line 3T3-L1 cells, have elucidated two major phases of adipogenesis: commitment and terminal differentiation (6, 7). Terminal differentiation is characterized by the induction of metabolic ...
The effect of n-6 polyunsaturated fatty acids (n-6 PUFAs) on adipogenesis and obesity is controversial. Using in vitro cell culture models, we show that n-6 PUFAs was pro-adipogenic under conditions with base-line levels of cAMP, but anti-adipogenic when the levels of cAMP were elevated. The anti-adipogenic action of n-6 PUFAs was dependent on a ...
Cripps, R. L. and Ozanne, S. E. (2010) Early-Life Programming of Adipogenesis and Adiposity, in Adipose Tissue in Health and Disease (eds T. Leff and J. G. Granneman), Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim, Germany. doi: 10.1002/9783527629527.ch24 ...
LXR α 0h 4h 8h 18h 1D 2D 3D 4D 5D 6D 7D 8D h 2d d Induction MediumDifferentiation Medium NR Expression during Adipogenesis of 3T3-L1 Cells (2) Fu et al., Mol. Endo. 19: 2437 (2005) Nur77 PPAR γ NUR77 LXR  PPAR 
Fibroblast growth factor (FGF) has been shown to inhibit the differentiation of myogenic and adipogenic cell lines without inducing a proliferative response. We have previously shown that agents capable of activating protein kinase C (PKC), such as FGF and the phorbol ester tetradecanoyl phorbol-13-acetate (TPA), inhibit the differentiation of the adipogenic cell line TA1, as measured by the rapid loss of adipocyte-specific RNAs. We report here that the treatment of fully differentiated TA1 adipocytes with FGF at 10 ng/ml induces the reversal of adipocyte differentiation, even in cells where PKC activity has been down-regulated by TPA pretreatment. In contrast, TPA or lower concentrations of FGF (1 ng/ml), both effective inducers of c-fos RNA in adipocytes, fail to reverse adipocyte differentiation. The adipocytes, however, will extinguish differentiation-specific functions in response to TPA by the addition of a calcium ionophore. Therefore, we propose that there are two FGF-sensitive pathways ...
Adipose tissue progenitors (or precursors), often located in the vicinity of the vascular network, constitute a heterogeneous population. They can be discriminated through their capacity to differentiate into mature adipocytes and also by their level of commitment into the adipocyte differentiation program. The application of flow cytometry using various markers as well as single-cell RNA sequencing has enabled the identification of multiple cell populations. The CD9hi progenitors exhibited very limited adipogenic capacity with a high propensity for the production of extracellular matrix components. CD9hi progenitors include mesothelial cells, whose contribution in adipose tissue remodeling is currently unresolved. Further investigations are still needed to establish the relationship between these various populations of progenitors. In addition, a better understanding of the critical functional determinants and whether acquired phenotypes are reversible is needed ...
Dr. Rayalam has worked in the areas of obesity, body weight regulation, phytochemicals and adipocyte biochemistry for over 8 years. Her research interests include: 1) to study the adipocyte life cycle and to understand the interaction of adipocytes with other cell types as an approach to address several problems associated with obesity; 2) to develop novel treatment strategies for obesity by inducing transdifferentiation of white to beige adipocytes and to inhibit lipid accumulation in white adipocytes; and 3) to identify combinations of phytochemicals and vitamins that have synergistic anti-adipogenic effects with an ultimate goal of developing pharmaceuticals or nutraceuticals for prevention and treatment of obesity and associated disorders. Aging is accompanied by an accumulation of adipocytes in bone marrow and Dr. Rayalams other interest is to understand the fat-bone interaction and to identify molecular targets for the prevention of weight gain and bone loss associated with aging. Dr. ...
I think this is part of the puzzle as to why refined carbs in particular can be so fattening. It is well documented that the digestibility of carbohydrates determines the corresponding postprandial blood sugar spike ( glycemic index ). In addition, I suppose you could say that, being insulin resistant in muscle leads to exaggerated and prolonged elevated postprandial glucose levels, and these high glucose concentrations ( could potentially ) activate adipogenic pathways, in both muscle and fat tissue ...
PPARγ plays a central role in regulating the expression of a wide range of genes involved in adipogenesis, lipid metabolism, insulin sensitivity, energy storage, inflammation and differentiation (Kroker and Bruning, 2015; Lefterova and Lazar, 2009). In particular, the crucial role of PPARγ in adipogenesis has been extensively studied by many researchers (Lefterova and Lazar, 2009). Although PPARγ functions as the master transcriptional regulator of adipocyte differentiation, few genes have been validated as direct PPARγ regulators or targets (Lefterova and Lazar, 2009). Thus, the identification of novel regulators of PPARγ is important for understanding the transcriptional regulatory mechanism of PPARγ in various cell types or tissues. PPARγ contains AF-1 and DBD in the N-terminal region, the flexible hinge domain in the middle, and LBD and AF-2 in the C-terminal region (Kroker and Bruning, 2015). Upon the binding of the PPARγ ligand, PPARγ forms a heterodimer with RXRα through their ...
Dr. Marlatt is interested in the role of dietary and exercise interventions to facilitate healthy aging and metabolic health as it relates to women, particularly in the transition through menopause. She currently is focusing her research efforts on the impact of a drug intervention in post-menopausal women; the impact of hormones and race on adipogenesis and adipocyte morphology; as well as intermittent hypoxia in individuals with diabetes ...
Pharmacological dosing of all-trans-retinoic acid (atRA) controls adiposity in rodents by inhibiting adipogenesis and inducing fatty acid oxidation. Retinol dehydrogenases (Rdh) catalyze the first reaction that activate retinol into atRA. This study examined post-natal contributions of Rdh10 to atRA biosynthesis and physiological functions of endogenous atRA. Embryonic fibroblasts from Rdh10 heterozygote hypomorphs or with a total Rdh10 knockout exhibit decreased atRA biosynthesis and escalated adipogenesis. atRA or a RAR pan-agonist reversed the phenotype. Eliminating one Rdh10 copy in vivo (Rdh10+/-) yielded a modest decrease (≤25%) in the atRA concentration of liver and adipose, but increased adiposity in male and female mice fed a high-fat diet, increased liver steatosis, glucose intolerance and insulin resistance in males fed a high-fat diet, and activated bone marrow adipocyte formation in females, regardless of dietary fat. Chronic dosing with low dose atRA corrected the metabolic ...
carbon skeleton use as energy source or converted to glycogen or fat Formation of Urea urea Growth and repair O H synthesis NH3 (ammonia) HO C C NH2 R excess O H HO C C NH2 amino acid R carbon skeleton use as energy source or converted to glycogen or fat
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Background Exhibits a cytosolic function in lipogenesis, adipogenic differentiation, and lipid homeostasis by increasing the activity of ACLY, possibly preventing its dephosphorylation. May act as a transcriptional repressor....
PMID 22527884] Genetic variation in the carbonyl reductase 3 gene confers risk of type 2 diabetes and insulin resistance: a potential regulator of adipogenesis ...
The development of mature adipocytes from pre-adipocytes is a highly regulated process. CD24 is a glycophosphatidylinositol-linked cell surface receptor that has been identified as a critical cell surface marker for identifying pre-adipocytes that are able to reconstitute white adipose tissue (WAT) in vivo. Here, we examined the role and regulation of CD24 during adipogenesis in vitro. We found that CD24 mRNA and protein expression is upregulated early during adipogenesis in the 3T3-L1 pre-adipocytes and in murine primary pre-adipocytes isolated from subcutaneous and visceral WAT, followed by downregulation in mature adipocytes. CD24 mRNA expression was found to be dependent on increased transcription due to increased promoter activity in response to activation of a preexisting transcriptional regulator. Furthermore, either intracellular cAMP or dexamethasone were sufficient to increase expression in pre-adipocytes, while both additively increased CD24 expression. Preventing the increase in CD24 ...
Obesity involves inflammation. MCP-1, an inflammatory chemokine, and MCP-1-induced protein (MCPIP) are known to induce adipogenesis that causes increase in the number of adipocytes. Here we elucidate the intermediate processes through which MCPIP induces adipogenesis. Forced expression of MCPIP in 3T3-L1 preadipocytes caused increased reactive oxygen/nitrogen species (ROS/RNS) production and inducible-nitric oxide synthase (iNOS) expression, endoplasnnic reticulum stress (ER), as indicated by expression of ER chaperones and protein disulfide isomerase, and autophagy as indicated by expression of beclin-1 and cleavage of LC3. Treatment of ROS inhibitor, apocynin attenuated MCPIP induction of adipogenesis as measured by the induction of transcription factors involved in adipogenesis, adipocyte markers and lipid droplet accumulation. Inhibition of ER stress with taurursodeoxycholate or knockdown of inositol requiring enzyme 1 (IRE1) inhibited MCPIP induced autophagy and adipogenesis. Preadipocytes in
Satellite cells are skeletal muscle progenitor/stem cells that reside between the basal lamina and plasma membranes of skeletal fibers in vivo. These cells can give rise to both myogenic and adipogenic cells. Given the possible role for differentiation of satellite cells into adipocytes in marbling and in some pathological disorders like sarcopenia, knowledge of the proteins involved in such process remains obscure. Using two-dimensional polyacrylamide gel electrophoresis coupled with mass spectrometry, we investigated the proteins that are differentially expressed during adipogenic differentiation of satellite cells from bovine longissimus muscle. Our proteome mapping strategy to identify the differentially expressed intracellular proteins during adipogenic differentiation revealed a total of 25 different proteins. The proteins up-regulated during adipogenic differentiation of satellite cells like Cathepsin H precursor, Retinal dehydrogenase 1, Enoyl-CoA hydratase, Ubiquinol-cytochrome-c ...
eng] Retinoblastoma (Rb1) has been described as an essential player in white adipocyte differentiation in mice. No studies have been reported thus far in human adipose tissue or human adipocytes. We aimed to investigate the possible role and regulation of RB1 in adipose tissue in obesity using human samples and animal and cell models. Adipose RB1 (mRNA, protein, and activity) was negatively associated with BMI and insulin resistance (HOMA-IR) while positively associated with the expression of adipogenic genes (PPARγ and IRS1) in both visceral and subcutaneous human adipose tissue. BMI increase was the main contributor to adipose RB1 downregulation. In rats, adipose Rb1 gene expression and activity decreased in parallel to dietary-induced weight gain and returned to baseline with weight loss. RB1 gene and protein expression and activity increased significantly during human adipocyte differentiation. In fully differentiated adipocytes, transient knockdown of Rb1 led to loss of the adipogenic ...
TY - JOUR. T1 - Effect of germinated brown rice extracts on pancreatic lipase, adipogenesis and lipolysis in 3T3-L1 adipocytes. AU - See Meng, Lim. AU - Goh, Yong Meng. AU - Kuan, Wen Bin. AU - Loh, Su Peng. PY - 2014/11/3. Y1 - 2014/11/3. N2 - Background: This study investigated anti-obesity effects of seven different solvent (n-hexane, toluene, dicholoromethane, ethyl acetate, absolute methanol, 80% methanol and deionized water) extracts of germinated brown rice (GBR) on pancreatic lipase activity, adipogenesis and lipolysis in 3T3-L1 adipocytes. Methods: GBR were extracted separately by employing different solvents with ultrasound-assisted. Pancreatic lipase activity was determined spectrophotometrically by measuring the hydrolysis of p-nitrophenyl butyrate (p-NPB) to p-nitrophenol at 405 nm. Adipogenesis and lipolysis were assayed in fully differentiated 3T3-L1 adipocytes by using Oil Red O staining and glycerol release measurement. Results: GBR extract using hexane showed the highest ...
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. ...
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 ...
White adipose tissue includes subcutaneous and visceral adipose tissue (SAT and VAT) with different metabolic features. SAT protects from metabolic disorders, while VAT promotes them. The proliferative and adipogenic potentials of adipose-derived stem cells (ADSCs) are critical for maintaining adipose tissue homeostasis through driving adipocyte hyperplasia and inhibiting pathological hypertrophy. However, it remains to be elucidated the critical molecules that regulate different potentials of subcutaneous and visceral ADSCs (S-ADSCs, V-ADSCs) and mediate distinct metabolic properties of SAT and VAT. CD90 is a glycosylphosphatidylinositol-anchored protein on various cells, which is also expressed on ADSCs. However, its expression patterns and differential regulation on S-ADSCs and V-ADSCs remain unclear. S-ADSCs and V-ADSCs were detected for CD90 expression. Proliferation, colony formation, cell cycle, mitotic clonal expansion, and adipogenic differentiation were assayed in S-ADSCs, V-ADSCs, or CD90
In todays study we investigated the consequences of genistein on adipogenic differentiation of mouse bone tissue marrow-derived mesenchymal stem cell (BMSC) cultures and its own potential signaling pathway. differentiation. Genistein decreased the phosphorylation of ERK1/2 in mouse BMSC ethnicities dose-dependently. Genistein incubation for the whole tradition period in adition to that applied through the early stage of the tradition period considerably inhibited Rabbit Polyclonal to Cox1. Vorinostat the adipogenic Vorinostat differentiation of mouse BMSC ethnicities. While genistein was incubated in the past due stage (after day time 9) no inhibitory influence on adipogenic differentiation was noticed. BMSC ethnicities treated with genistein in the current presence of fibroblast growth element-2 (FGF-2) an activator from the ERK1/2 signaling pathway indicated normal degrees of ERK1/2 activity and by doing this can handle going through adipogenesis. Our outcomes claim Vorinostat that activation ...
Marian Blanca Ramírez from the CSIC in Spain has been studying the effects of LRRK2, a protein associated with Parkinsons disease, on cell motility. A Travelling Fellowship from Journal of Cell Science allowed her to spend time in Prof Maddy Parsons lab at Kings College London, learning new cell migration assays and analysing fibroblasts cultured from individuals with Parkinsons. Read more on her story here. Where could your research take you? The deadline to apply for the current round of Travelling Fellowships is 30 Nov 2017. Apply now!. ...
Artificial adipose tissue (AT) constructs are urgently needed to treat severe wounds, to replace removed tissue, or for the use as in vitro model to screen for potential drugs or study metabolic pathways. The clinical translation of products is mostly prevented by the absence of a vascular component that would allow a sustainable maintenance and an extension of the construct to a relevant size. With this study, we aimed to evaluate the suitability of a novel material based on bacterial cellulose (CBM) on the defined adipogenic differentiation of human adipose-derived stem cells (ASCs) and the maintenance of the received adipocytes (diffASCs) and human microvascular endothelial cells (mvECs) in mono- and coculture. A slight acceleration of adipogenic differentiation over regular tissue culture polystyrene (TCPS) was seen on CBM under defined conditions, whereas on the maintenance of the generated adipocytes, comparable effects were detected for both materials. CBM facilitated the formation of ...
הבידול של adipocytes לבן ובייז של רקמת שומן אבות כלי הדם נושא פוטנציאל שיפור חילוף החומרים ההשמנה. נתאר פרוטוקולים של CD34 + CD31 +...
Yağ dokusu vasküler ataları gelen beyaz ve bej adiposit farklılaşma obezite metabolik iyileştirme için potansiyel taşımaktadır. CD34 +...
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 ...
The differentiation of bone mesenchymal stem cells (BMSCs) into adipogenesis (AD) rather than osteogenesis (OS) is an important pathological feature of osteoporosis. Illuminating the detailed mechanisms of the differentiation of BMSCs into OS and AD would contribute to the interpretation of osteoporosis pathology. To identify the regulated mechanism in lineage commitment of the BMSCs into OS and AD in the early stages, the gene expression profiles with temporal series were downloaded to reveal the distinct fates when BMSCs adopt a committed lineage. For both OS and AD lineages, the profiles of days 2-4 were compared with day 0 to screen the differentially expressed genes (DEGs), respectively. Next, the functional enrichment analysis was utilized to find out the biological function, and protein-protein interaction network to predict the central genes. Finally, experiments were performed to verify our finding. FoxO signaling pathway with central genes like FoxO3, IL6, and CAT is the crucial mechanism of
PLSCR3 (phospholipid scramblase 3 Scr3) is one of the superfamily of membrane-associated transcription regulators named Tubby-like protein (TULPs). medium LAQ824 by means of extracellular microvesicles (exosomes). Alternatively Scr3 expression didnt decrease as well as the secretion of Scr3 significantly?in 3T3 Swiss-albino fibroblasts (a parental cell-line of 3T3-L1) had not been increased by differentiation treatment. Overexpression of human being Scr3 during 3T3-L1 differentiation suppressed triacylglycerol build up and inhibited induction from the mRNAs lately stage pro-adipogenic transcription elements [CCAAT/enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ)] and X-box-binding proteins 1 (XBP1). Manifestation of early stage pro-adipogenic transcription elements (C/EBPβ and C/EBPδ) had not been considerably affected. These outcomes claim that Scr3 features as a poor regulator of adipogenesis in 3T3-L1 cells at a particular differentiation ...
Adipocytes and fat cells play critical roles in the regulation of energy homeostasis. Adipogenesis (adipocyte differentiation) is regulated via a complex process including coordinated changes in hormone sensitivity and gene expression. According to the study by the Osaka University of Pharmaceutical Sciences, Prostaglandins (PGs), which are lipid mediators, are associated with the regulation of PPARγ function in adipocytes. Prostacyclin promotes the differentiation of adipocyte-precursor cells to adipose cells via activation of the expression of C/EBPβ and δ. These proteins are important transcription factors in the activation of the early phase of adipogenesis, and they activate the expression of PPARγ, which event precedes the maturation of adipocytes. PGE(2) and PGF(2α) strongly suppress the early phase of adipocyte differentiation by enhancing their own production via receptor-mediated elevation of the expression of cycloxygenase-2, and they also suppress the function of PPARγ(24). ...
Coordinating terminal differentiation and cell cycle arrest involves coupling the activity of the transcriptional regulators that activate lineage‐specific gene expression programs to the cell cycle machinery. The importance of such coordination is illustrated by the observation that ectopic expression of cell cycle promoting factors is able to interfere with differentiation of numerous cell types. Well‐characterized examples include the ability of the c‐Myc oncoprotein to block the differentiation of adipocytes by repressing the transcription of C/EBPα, a key inducer of adipogenesis (Freytag and Geddes, 1992), and the ability of Cyclin D1/Cdk4 to inhibit myogenesis through binding to MyoD (Zhang et al, 1999). However, in other cases, the molecular mechanisms are not clear. E2F‐1 can block granulopoiesis (Strom et al, 1998), adipogenesis (Porse et al, 2001) and myogenesis (Wang et al, 1995), but the relevant molecular targets are not defined. Cdk6 inhibits osteogenic differentiation by ...
Bone chips were obtained by minimally irrigated implant drilling technique from 10 human donors. Isolated cells were studied with respect to their colony-forming efficiency, surface marker expression by immunofluorescence staining, fluorescence-activated cell sorting analysis and self-renewal potency. To verify the differentiation activity, in vitro osteogenic and adipogenic gene expressions were evaluated by reverse transcription-polymerase chain reaction, and in vitro formation of mineralized nodule and adipocytes was also evaluated. In vivo bone-forming activity was assessed by ectopic transplantation in immunocompromised mice (n = 5 ...
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 ...
To elucidate the roles of adipose tissue and skeletal muscle in the early development of insulin resistance, we characterized gene expression profiles of isolated adipose cells and skeletal muscle of non-diabetic insulin-resistant first-degree relatives of type 2 diabetic patients using oligonucleot …
A research team has managed to decode the process of adipogenesis by identifying the precise proteins that play the leading roles in fat absorption. There are many actors involved in the process of adipogenesis, used by the body to store the fat that it absorbs from food. Up to now there had been some uncertainty as to how it was regulated. Yet, understanding this mechanism is of crucial importance to prevent the diseases related to fat accumulation in adipose tissue ...
Obesity is a growing epidemic around the world and dramatically increases the risk of developing a number of chronic diseases (Gambero and Ribeiro, 2015).
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Oil Red O Lipid Stain kit is used to demonstrate adipocites and neutral triglicerides. This is also useful to demonstrate adipogenesis. Fat cells and neutral fat will be coloured in red and the nuclei in blue.
Creb3l4-KO mice showed adipocyte hyperplasia, lead to improved metabolic parameters. (a) Adipogenic potential of mouse embryonic fibroblasts (MEFs) derived from
Characteristics of human MSCs. (A) Cells in culture on day 3 (left) and day 8 (right) from subculture from passage 4. (B) Adipogenic differentiation of human MS
Cryptic fragment α4 LG4-5 derived from laminin α4 chain inhibits de novo adipogenesis by modulating the effect of fibroblast growth factor-2 ...
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.
The failure to commit to adipogenesis is primarily due to active FOXO1 arresting the cell in G0/G1 through activation of yet ... FOXO1 negatively regulates adipogenesis. Presently, the exact mechanism by which this is accomplished is not entirely ... Rising levels of PPARG are required to initiate adipogenesis; by preventing its transcription, FOXO1 is preventing the onset of ... In the currently accepted model, FOXO1 negatively regulates adipogenesis by binding to the promoter sites of PPARG and ...
It plays a role in pluripotency and adipogenesis. Long non-coding RNA GRCh38: Ensembl release 89: ENSG00000213468 - Ensembl, ... "Long noncoding RNAs regulate adipogenesis". Proceedings of the National Academy of Sciences of the United States of America. ...
Studies to determine what role pluripotent stem cells play in adipogenesis, were examined in the immortalized human bone marrow ... Romao JM, Jin W, Dodson MV, Hausman GJ, Moore SS, Guan LL (September 2011). "MicroRNA regulation in mammalian adipogenesis". ... Conversely, ectopic expression of the miRNAs 155,221, and 222 significantly inhibited adipogenesis and repressed induction of ... alpha expression by C/EBP beta during adipogenesis requires a peroxisome proliferator-activated receptor-gamma-associated ...
Cao, Yihai (2007-09-01). "Angiogenesis modulates adipogenesis and obesity". The Journal of Clinical Investigation. 117 (9): ...
... cell-autonomously regulates adipogenesis. In the muscle, Baf60c promotes a switch from oxidative to glycolytic myofiber ... "DEPTOR cell-autonomously promotes adipogenesis, and its expression is associated with obesity". Cell Metabolism. 16 (2): 202-12 ...
The phrase "goose bumps" derives from the phenomenon's association with goose skin. Goose feathers grow from stores in the epidermis which resemble human hair follicles. When a goose's feathers are plucked, its skin has protrusions where the feathers were, and these bumps are what the human phenomenon resembles. It is not clear why the particular fowl, goose, was chosen in English, as most other birds share this same anatomical feature. Some authors have applied "goosebumps" to the symptoms of sexually-transmitted diseases.[3] "Bitten by a Winchester goose" was a common euphemism for having contracted syphilis[4] in the 16th century.[5] "Winchester geese" was the nickname for the prostitutes of Southern London,[6] licensed by the Bishop of Winchester in the area around his London palace. This etymology does not explain why many other languages use the same bird as in English. "Goose skin" is used in German (Gänsehaut), Swedish (gåshud), Danish and Norwegian (gåsehud), Icelandic (gæsahúð), ...
... is the soft outer tissue covering vertebrates.. Other animal coverings, such as the arthropod exoskeleton, have different developmental origin, structure and chemical composition. The adjective cutaneous means "of the skin" (from Latin cutis, skin). In mammals, the skin is an organ of the integumentary system made up of multiple layers of ectodermal tissue, and guards the underlying muscles, bones, ligaments and internal organs. Skin of a different nature exists in amphibians, reptiles, and birds.[1] All mammals have some hair on their skin, even marine mammals like whales, dolphins, and porpoises which appear to be hairless. The skin interfaces with the environment and is the first line of defense from external factors. For example, the skin plays a key role in protecting the body against pathogens[2] and excessive water loss.[3] Its other functions are insulation, temperature regulation, sensation, and the production of vitamin D folates. Severely damaged skin may heal by forming scar ...
2000). "Inhibition of adipogenesis by Wnt signaling". Science. 289 (5481): 950-3. doi:10.1126/science.289.5481.950. PMID ... a molecular switch that governs adipogenesis. Gain-of-function of Wnt10b in mouse hearts has shown to improve cardiac tissue ...
... is also a key regulator of adipogenesis, including adipocyte development and differentiation. Oh, Da Young; Talukdar, ... 2007). "The regulation of adipogenesis through GPR120". Biochemical and Biophysical Research Communications. 354 (2): 591-7. ...
Serlachius M, Andersson LC (Jun 2004). "Upregulated expression of stanniocalcin-1 during adipogenesis". Experimental Cell ...
... fat cell recruitment and development adipogenesis; (3) dissolving and reforming the structures around fat tissue (extracellular ...
PPARγ has a crucial role in adipogenesis and lipid accumulation within adipocytes (fat cells). Activated NEDD8 stabilizes PPARγ ... allowing increased adipogenesis. In experiments with mice, Pevonedistat, a drug inhibiting activation of NEDD8, prevented high- ... "PPARγ neddylation essential for adipogenesis is a potential target for treating obesity". Cell Death and Differentiation. 23 (8 ...
"ADAM 12 protease induces adipogenesis in transgenic mice". Am. J. Pathol. 160 (5): 1895-903. doi:10.1016/S0002-9440(10)61136-4 ...
"FTO influences adipogenesis by regulating mitotic clonal expansion". Nature Communications. 6: 6792. Bibcode:2015NatCo...6.6792 ... "FTO-dependent demethylation of N6-methyladenosine regulates mRNA splicing and is required for adipogenesis". Cell Research. 24 ...
"Adipogenesis and obesity: rounding out the big picture". Cell. 87 (3): 377-89. doi:10.1016/S0092-8674(00)81359-8. PMID 8898192 ...
Barquissau V, Ghandour RA, Ailhaud G, Klingenspor M, Langin D, Amri EZ, Pisani DF (2017). "Control of adipogenesis by oxylipins ...
Mouse cathepsin L is homologous to human cathepsin V. Mouse cathepsin L has been shown to play a role in adipogenesis and ... "Cathepsin L activity controls adipogenesis and glucose tolerance". Nat. Cell Biol. 9 (8): 970-7. doi:10.1038/ncb1623. PMC ...
KMT2C and KMT2D are essential for adipogenesis and myogenesis. Similar functions are seen in neuronal and osteoblast ... "MLL3/MLL4 are required for CBP/p300 binding on enhancers and super-enhancer formation in brown adipogenesis". Nucleic Acids ... recruits and requires KMT2D to establish a subset of adipogenic enhancers during adipogenesis. Depletion of KMT2D prior to ...
Synonyms are: AGIF Adipogenesis inhibitory factor Interleukin-11 precursor. Oprelvekin is produced in Escherichia coli (E. coli ... the inhibition of adipogenesis, the induction of acute phase protein synthesis (e.g., fibrinogen), and inhibition of ...
2009). "Role of follistatin in promoting adipogenesis in women". J. Clin. Endocrinol. Metab. 94 (8): 3003-9. doi:10.1210/jc. ...
"Exogenous Sodium Pyruvate Stimulates Adipogenesis of 3T3-L1 Cells". Journal of Cellular Biochemistry. 117 (1): 39-48. doi: ...
"Molecular architecture of transcription factor hotspots in early adipogenesis". Cell Reports. 7 (5): 1434-42. doi:10.1016/j. ...
"A biotin analog inhibits acetyl-CoA carboxylase activity and adipogenesis". The Journal of Biological Chemistry. 277 (19): ...
BMPs are also involved in adipogenesis and functional regulation of adipose tissue. BMP4 favors white adipogenesis, whereas ...
Lin Q, Gao Z, Alarcon RM, Ye J, Yun Z (2009). "A role of miR-27 in the regulation of adipogenesis". FEBS J. 276 (8): 2348-58. ... acting by blocking the expression of two main regulators of adipogenesis. MicroRNAs miR-27a and -27b have been found to ...
... a new adipokine that modulates adipogenesis via its own receptor". Biochem. Biophys. Res. Commun. 362 (4): 1013-8. doi:10.1016/ ... a novel adipokine that regulates adipogenesis and adipocyte metabolism". J. Biol. Chem. 282 (38): 28175-88. doi:10.1074/jbc. ...
As an adipokine receptor it has a role in adipogenesis and adipocyte maturation. It seems also to have a role in peripheral ... a novel adipokine that regulates adipogenesis and adipocyte metabolism". The Journal of Biological Chemistry. 282 (38): 28175- ...
"Targeting senescent cells enhances adipogenesis and metabolic function in old age". eLife. 4: e12997. doi:10.7554/eLife.12997. ...
These proteins have been implicated in oncogenesis, adipogenesis etc and in several other developmental processes, including ... "Wnt Signaling Inhibits Adipogenesis through β-Catenin-dependent and -independent Mechanisms". Journal of Biological Chemistry. ...
Janesick A, Blumberg B (March 2011). "Endocrine disrupting chemicals and the developmental programming of adipogenesis and ... "Endocrine-disrupting organotin compounds are potent inducers of adipogenesis in vertebrates" (PDF). Mol. Endocrinol. 20 (9): ... Monoethyl-hexyl-phthalate Is a Selective Peroxisome Proliferator-activated Receptor γ Modulator That Promotes Adipogenesis". J ...
Adipogenesis and Cilia. Fat differentiation is a highly dynamic process. In fact, 10% of our adipocytes turn over every year ... We want to further understand what signals and pathways initiate adipogenesis, and what the epigenetic and proteo-genomic ... Since pre-adipocyte are uniformly ciliated and the primary cilium is required for adipogenesis, we are particularly interested ...
... and triiodothyronine effectively induce adipogenesis in preadipocytes. Insulin regulates adipogenesis through insulin-like ... Reduced adipogenesis in obese persons is due to increased senescent cells in adipose tissue rather than reduced numbers of stem ... Adipogenesis is the formation of adipocytes (fat cells) from stem cells. It involves 2 phases, determination, and terminal ... cAMP, an inducer of adipogenesis, can promote expression of C/EBPβ and C/EBPδ. At the early stage of differentiation, the ...
... Chuanhai Zhang,1,2 Yibing Weng,3 Fangxiong Shi,1 and Wanzhu Jin2 ... P. Tontonoz, E. Hu, and B. M. Spiegelman, "Stimulation of adipogenesis in fibroblasts by PPARγ2, a lipid-activated ... E. D. Rosen, "C/EBPalpha induces adipogenesis through PPARgamma: a unified pathway," Genes & Development, vol. 16, no. 1, pp. ... S. Carobbio, B. Rosen, and A. Vidal-Puig, "Adipogenesis: new insights into brown adipose tissue differentiation," Journal of ...
... and brown adipogenesis (BMP7) (34,47,48). We here focus on white adipogenesis and the effect of BMP4, although BMP2 can have ... New role of bone morphogenetic protein 7 in brown adipogenesis and energy expenditure. Nature 2008;454:1000-1004pmid:18719589. ... Adipogenesis: tightly regulated by cell commitment and differentiation. Figure 2 shows a schematic figure of the overarching ... Reduced adipogenesis in hypertrophic obesity. It is well established that subcutaneous adipose cell size can differ markedly ...
Inducible brown adipogenesis of supraclavicular fat in adult humans.. Lee P1, Swarbrick MM, Zhao JT, Ho KK. ... This study provides the first evidence of inducible brown adipogenesis in the supraclavicular region in adult humans. ...
c. Functional studies of the role of O/E proteins in adipogenesis.. The bHLH protein O/E-1 has been shown to promote ... function experiments designed to place O/E-1 and other O/E isoforms in the transcriptional cascade leading to adipogenesis. In ... adipogenesis in NIH-3T3 fibroblasts. We are performing both gain-of-function and loss-of- ...
... adipogenesis) are of basic and biomedical interest. Cellular models of adipogenesis have proven extremely valuable in defining ... biomolecules-primarily genes and proteins-that regulate adipogenesis. Here, the analysis of different … ... Monoalkylglycerol ether lipids promote adipogenesis J Am Chem Soc. 2011 Apr 13;133(14):5178-81. doi: 10.1021/ja111173c. Epub ... Cellular models of adipogenesis have proven extremely valuable in defining biomolecules-primarily genes and proteins-that ...
Neovascularization and adipogenesis are temporally and spatially coupled processes during prenatal life and they continue to ... Angiogenesis modulates adipogenesis and obesity J Clin Invest. 2007 Sep;117(9):2362-8. doi: 10.1172/JCI32239. ... Neovascularization and adipogenesis are temporally and spatially coupled processes during prenatal life and they continue to ...
... 12589. Toggle Between Dark and Light Modes Filter: * ... The Adipogenesis Marker Antibody Sampler Kit provides an economical means to evaluate proteins involved in the regulation of ... Adipogenesis is the cellular process where preadipocytes differentiate into adipocytes.. Fatty acid binding proteins (FABPs) ... and Ser230 by GSK-3 may be required for adipogenesis (12). ... Adipogenesis Marker Antibody Sampler Kit Adipogenesis Marker ...
Imidacloprid, a neonicotinoid insecticide, potentiates adipogenesis in 3T3-L1 adipocytes.. Park Y1, Kim Y, Kim J, Yoon KS, ... These results imply the involvement of imidacloprid in altered adipogenesis, resulting in increased fat accumulation. This ...
Quantification of Human Adipogenesis. The safety and scientific validity of this study is the responsibility of the study ...
Adipogenesis supports healthy adipose tissue remodeling in obesity. Impaired adipogenesis in obesity: cause or consequence? ... Adipogenesis and metabolic health. Nat Rev Mol Cell Biol. 2019;20(4):242-258.. View this article via: PubMed CrossRef Google ... Driving adipogenesis from PDGFRβ+ precursors through Pparg overexpression (Mural-PpargTG mice) led to a doubling of the de novo ... molecular mechanisms controlling adipogenesis during development appear distinct from those controlling adipogenesis in ...
A better understanding of adipose stem cell biology and adipogenesis may lead to novel strategies to uncouple obesity from ... recent human and rodent studies that support the notion that the ability to recruit new fat cells through adipogenesis is a ...
Objective As adipogenesis plays a critical role in obesity, the present study was conducted to investigate the effect of UA on ... Conclusions Ursolic acid inhibited 3T3-L1 preadipocyte differentiation and adipogenesis through the LKB1/AMPK pathway. There is ... adipogenesis and mechanisms of action in 3T3-L1 preadipocytes. Methods and Results The 3T3-L1 preadipocytes were induced to ... results demonstrated that ursolic acid at concentrations ranging from 2.5 µM to 10 µM dose-dependently attenuated adipogenesis ...
Preadipocyte Preparation and Adipogenesis Assay. On day seven of diabetes inception, the rats were anesthetized with ether and ... To examine the effect of S. securidaca on adipogenesis, Oil Red O was used to stain accumulated intracellular triglycerides in ... Effects of Securigera securidaca Extract on Lipolysis and Adipogenesis in Diabetic Rats. Ahmad Ghorbani,1 Reyhaneh Moradi ... Effects of S. securidaca on Adipogenesis. Incubation of differentiating cells with S. securidaca extract decreased ...
A panel containing eight adipogenesis inducers useful for differentiation of preadipocyte to mature adipocyte. Shop ... A panel containing eight adipogenesis inducers useful for differentiation of preadipocyte to mature adipocyte. ...
E2F4s Role in Adipogenesis Can Be Separated from Its Role in Cell Cycle Regulation.. The induction of adipogenesis in vitro ... As reported (25, 26), the absence of either E2F4 or p107 and p130 led to a 2- to 5-fold increase in adipogenesis (Fig. 1B). ... The role of E2F4 in adipogenesis is independent of its cell cycle regulatory activity. Rebecca L. Landsberg, Julia E. Sero, ... pRB Is Required for Adipogenesis in the Absence of E2F4.. Previous studies have shown that Rb−/− cells fail to significantly ...
Cross-Talk Between Interferon-γ and Hedgehog Signaling Regulates Adipogenesis. Jelena Todoric, Birgit Strobl, Alexander Jais, ... Cross-Talk Between Interferon-γ and Hedgehog Signaling Regulates Adipogenesis. Jelena Todoric, Birgit Strobl, Alexander Jais, ... Cross-Talk Between Interferon-γ and Hedgehog Signaling Regulates Adipogenesis Message Subject (Your Name) has forwarded a page ...
Mesenchymal stem cells Chondrogenesis Adipogenesis Osteogenesis Ultrastructure The research was conducted in part for the ... Chondrogenesis, osteogenesis and adipogenesis of canine mesenchymal stem cells: a biochemical, morphological and ...
Lee H, Li H, Kweon M, Choi Y, Kim MJ, Ryu J-H. Isobavachalcone from Angelica keiskei Inhibits Adipogenesis and Prevents Lipid ... Lee, H.; Li, H.; Kweon, M.; Choi, Y.; Kim, M.J.; Ryu, J.-H. Isobavachalcone from Angelica keiskei Inhibits Adipogenesis and ... Keywords: Angelica keiskei; isobavachalcone; 3T3-L1 adipocyte; adipogenesis; clonal expansion; autophagy Angelica keiskei; ... "Isobavachalcone from Angelica keiskei Inhibits Adipogenesis and Prevents Lipid Accumulation." Int. J. Mol. Sci. 19, no. 6: 1693 ...
When it is on, adipogenesis is repressed; when it is off, adipogenesis is initiated. The crucial role of Wnt signaling in the ... Inhibition of Adipogenesis by Wnt Signaling. By Sarah E. Ross, Nahid Hemati, Kenneth A. Longo, Christina N. Bennett, Peter C. ... Inhibition of Adipogenesis by Wnt Signaling. By Sarah E. Ross, Nahid Hemati, Kenneth A. Longo, Christina N. Bennett, Peter C. ... 4E), which is consistent with the idea that a decrease in Wnt-10b is required for adipogenesis to occur. Wnt-10b may act ...
PPARgamma knockdown by engineered transcription factors: exogenous PPARgamma2 but not PPARgamma1 reactivates adipogenesis. ... adipogenesis, and insulin sensitivity. The PPAR family consists of three members, PPARα, γ, and δ.87 PPARγ is the receptor for ... expression of genes related to adipogenesis was decreased, and although total lipid mass was maintained in one of the models, ... TNFalpha and CCAAT/enhancer-binding protein homologous protein with aging predispose preadipocytes to resist adipogenesis. ...
Cripps, R. L. and Ozanne, S. E. (2010) Early-Life Programming of Adipogenesis and Adiposity, in Adipose Tissue in Health and ...
Angiotensin type 2 receptor activation promotes browning of white adipose tissue and brown adipogenesis. *Aung Than1. *, ... Apelin enhances brown adipogenesis and browning of white adipocytes. . J Biol Chem 2015; 290: 14679-14691. ... Apelin inhibits adipogenesis and lipolysis through distinct molecular pathways. . Mol Cell Endocrinol 2012; 362: 227-241. ... Restricted adipogenesis in hypertrophic obesity: the role of WISP2, WNT, and BMP4. . Diabetes 2013; 62: 2997-3004. ...
Et Zucc, inhibits adipogenesis and fat accumulation. This study was conducted to investigate the molecular mechanism of ... Et Zucc, inhibits adipogenesis and fat accumulation. This study was conducted to investigate the molecular mechanism of the ... SIGNIFICANCE: This study clearly shows that shikonin inhibits adipogenesis by the modulation of WNT/β-catenin pathway in vitro ... Shikonin-induced reductions of the major transcription factors of adipogenesis including peroxisome proliferator-activated ...
This conference will present recent research exploring adipogenesis focusing on brown adipose tissue, and will explore its ... The Good Fat: Understanding Adipogenesis and Function of Brown Fat. Tuesday, March 12, 2013. The New York Academy of Sciences ... Role of Bone Morphogenetic Proteins in Brown Adipogenesis, Thermoregulation, and Energy Homeostasis. Yu-Hua Tseng, PhD, Joslin ... This conference is aimed at presenting recent developments in the field of adipogenesis research. Animal studies suggest that ...
... can affect adipogenesis in fat cells. The effects of HA on adipogenesis were investigated in vitro in 3T3-L1 cells and in vivo ... In vitro adipogenesis in 3T3-L1 cells was inhibited by treating them with exogenous hyaluronidase (HYAL) and with 4- ... as accumulation of high molecular weight of HA by HAS and degradation of HA by endogenous HYAL were essential for adipogenesis ... Adipogenesis can be spatially and temporally regulated by extracellular matrix (ECM). We hypothesized that the regulation of ...
... by CP treatment because of up-regulation of specific lipolysis enzymes such as HSL and AMPK and down-regulation of adipogenesis ... "Citrus Peel Ethanol Extract Inhibits the Adipogenesis Caused from High Fat-Induced DIO Model" written by Mustafa Zafer ...
Adipogenesis inhibitory factor. A novel inhibitory regulator of adipose conversion in bone marrow. FEBS Lett. 288, 13-16 (1991 ... Tracking adipogenesis during white adipose tissue development, expansion and regeneration. Nat. Med. 19, 1338-1344 (2013).. ... Committing progenitors to adipogenesis. Promoting the "browning" of white fat has been proposed as a strategy to combat obesity ... JAK2/STAT3 pathway is involved in the early stage of adipogenesis through regulating C/EBPβ transcription. J. Cell. Biochem. ...
Phospholipidosis and steatosis are toxic side effects of lipid metabolism that can be triggered by drugs or other compounds. Phospholipidosis is a lysosomal storage disorder associated with cationic amphiphilic drugs and characterized by the accumulation of excess phospholipid complexes within the internal lysosomal membranes. Steatosis is the abnormal retention of lipids within a cell due to impairment of the normal processes of synthesis and elimination of triglyceride fats.
  • Adipogenesis is the formation of adipocytes (fat cells) from stem cells. (
  • Adipogenesis is a tightly regulated cellular differentiation process, in which mesenchymal stem cells committing to preadipocytes and preadipocytes differentiating into adipocytes. (
  • Imidacloprid, a neonicotinoid insecticide, potentiates adipogenesis in 3T3-L1 adipocytes. (
  • He Y, Li Y, Zhao T, Wang Y, Sun C (2013) Ursolic Acid Inhibits Adipogenesis in 3T3-L1 Adipocytes through LKB1/AMPK Pathway. (
  • Also, to evaluate adipogenesis, preadipocytes were isolated from adipose tissue and differentiated to adipocytes in the presence of the extract. (
  • During adipogenesis, regulation of the expression of various genes that are specifically involved in the formation of ECM and cytoskeletal elements is necessary for the transformation of pre-adipocytes into mature adipocytes. (
  • Adipocytes play a vital role in energy homeostasis and adipogenesis is a hierarchically regulated cellular differentiation process, in which the precursor mesenchymal stem cells are differentiated into mature adipocytes. (
  • The differentiation of mesoderm cells into adipocytes is called adipogenesis and is driven by the activation of specific transcription factors and proteins, including PPARγ, C/EBPα, GLUT4, and FABP4 [1]. (
  • Adipogenic RHAMM peptides were identified by screening for their ability to promote adipogenesis in culture assays using rat bone marrow mesenchymal stem cells, mouse pre-adipocyte cell lines and primary human subcutaneous pre-adipocytes. (
  • Although treatment of preadipocytes with S1P induced message expression of the early adipogenesis transcription factor CC AAT/ binding proteinalpha, continued treatment did not fully support the development of differentiated adipocytes. (
  • Study I showed that the transcription factor, MAFB, was associated with increased adiposity and involved in regulation of TNFα-mediated inflammatory response, yet did not seem to directly influence adipogenesis or metabolism in human adipocytes. (
  • Adipogenesis is the process of differentiation of different cell types into adipocytes, the primary fat storage cell type. (
  • These results suggest that the reorganization of mitochondrial morphology is established early during adipogenesis and may play a role in the functions of fully differentiated adipocytes. (
  • To investigate how PPARγ ligand troglitazone regulates adipogenesis in female mice, we examined the effects of the troglitazone on adipose tissue mass, morphological changes of adipocytes, and the expression of PPARγ target and adipocyte-specific genes in low fat diet-fed female C57BL/6 mice. (
  • Here, we examined the effects of baicalein in adipogenesis and investigated its molecular mechanism in adipocytes. (
  • These results indicate that baicalein decreased the intracellular lipid accumulation by down-regulation of glucose uptake via repression of Akt-C/EBPα-GLUT4 signaling in the very early stage of adipogenesis of 3T3-L1 adipocytes. (
  • Next, we measured changes in the expression levels of the adipogenic and lipogenic genes in cells which were differentiating into adipocytes in medium containing baicalein or not during days 0-2, days 0-6 during the 6-day-adipogenesis. (
  • Finally, similar positive regulation of DNA-PKcs expression and activity was observed during differentiation of primary culture of pre-adipocytes isolated from human sub-cutaneous adipose tissue.Our results show that DNA DSBs repair activity is up regulated during the early commitment into adipogenesis due to an up-regulation of DNA-PK expression and activity. (
  • Two TRPs were found to be developmentally expressed during human adipogenesis: TRPP3, for the first time implicated in brown adipogenesis and TRPM8, previously reported in adipocytes, but my findings are the first, to ascribe it a role in brown adipogenesis. (
  • The excessive accumulation of adipose tissue is caused by increased adipogenesis accompanied by adipocyte differentiation, which converts immature pre-adipocytes into adipocytes. (
  • Therefore, the aim of this study is to explore the inhibitory effect of betanin on adipogenesis in 3T3-L1 adipocytes and its mechanism action. (
  • Increased proliferation and differentiation of pre-adipocytes to mature adipocytes (adipogenesis) within the fat tissues are central to obesity. (
  • The significance of the proposed research is that once we establish the molecular mechanisms of adipogenesis which result in increased survival of adipocytes, we can manipulate targets of the apoptosis pathway to devise new and innovative approaches to prevent or reverse weight gain and obesity. (
  • By showing that alternative splicing of apoptotic genes modulate differentiation and maturation of pre-adipocytes, the proposed studies will establish a new paradigm for adipogenesis and reveal new targets for treatment of obesity. (
  • In cosmetology, there is an interest in identifying compounds with an adipogenesis inhibitory action (which corresponds to the differentiation of pre-adipocytes into mature fat storing adipocytes) or with a lipolysis stimulating action (which corresponds to the destruction of stored fat). (
  • To elucidate the role of PTP-BL and of its catalytic activity during adipogenesis we use siRNA techniques in 3T3-L1 pre-adipocytes, and mouse embryonic fibroblasts that lack wildtype PTP-BL and instead express a variant without the PTP domain (Delta P/Delta P MEFs). (
  • en] Obesity is an ever-growing epidemic where tissue homeostasis is influenced by the differentiation of adipocytes that function in lipid metabolism, endocrine and inflammatory processes. (
  • Lee H, Li H, Kweon M, Choi Y, Kim MJ, Ryu J-H. Isobavachalcone from Angelica keiskei Inhibits Adipogenesis and Prevents Lipid Accumulation. (
  • Shikonin inhibits adipogenesis by modulation of the WNT/β-catenin pathway. (
  • Et Zucc, inhibits adipogenesis and fat accumulation. (
  • SIGNIFICANCE: This study clearly shows that shikonin inhibits adipogenesis by the modulation of WNT/β-catenin pathway in vitro, and also suggests that WNT/β-catenin pathway can be used as a therapeutic target for obesity and related diseases using a natural compound like shikonin, even though the in vivo effects of shikonin and its clinical significance remain to be elucidated. (
  • Tumour necrosis factor-α inhibits adipogenesis via a β-catenin/TCF4(TCF7L2)-dependent pathway. (
  • Adrenomedullin inhibits adipogenesis under transcriptional control of insulin. (
  • Long non-coding RNA MEG3 inhibits adipogenesis and promotes osteogenesis of human adipose-derived. (
  • Our hypothesis is that resveratrol inhibits adipogenesis through modulation of mitotic clonal expansion (MCE) and cell signaling pathways in the early phase of differentiation. (
  • Foxo1 inhibits adipogenesis at least partially by repressing PPARγ gene transcription ( Armoni et al , 2006 ). (
  • Inhibition of differentiation was also observed when Wnt signaling was activated by lithium or β-catS33Y ( Fig. 1 A). Thus, Wnt signaling appears to inhibit adipogenesis in vitro. (
  • We investigated the effects of HA by degradation of pre-existing or synthesized HA and artificial inhibition of HA synthesis in adipogenesis. (
  • however, extracellular S1P does not rescue the effect of SPHK1 inhibition on adipogenesis. (
  • and BMP4 also partially rescued ISL1 inhibition of adipogenesis, an effect which is additive with rosiglitazone. (
  • The inhibition of Wnt and β-catenin in adipogenesis was reversed by CHIR 99021. (
  • Resveratrol is known as a potent antiobesity compound that acts partly through inhibition of adipogenesis. (
  • The antiadipogenic effect of resveratrol is through inhibition of the MCE and IR-dependent insulin signaling pathway in the early phase of adipogenesis. (
  • Inhibition during only the first 1.5 h after the initiation of adipogenesis by baicalein or an Akt inhibitor was enough to decrease the lipid contents in the cells undergoing adipocyte differentiation for 6 days. (
  • Conversely, this study demonstrates that NRF2 regulates expression of Ahr and subsequently modulates several downstream events of the AHR signaling cascade, including (i) transcriptional control of the xenobiotic metabolism genes Cyp1a1 and Cyp1b1 and (ii) inhibition of adipogenesis in mouse embryonic fibroblasts (MEFs). (
  • 28. The method of claim 17, wherein the scaffold, the cell homing composition, or the adipogenic composition comprises a secretase γ inhibitor, a Notch gamma secretase inhibitor, or a MAPk inhibitor in an amount effect to reduce, substantially reduce, or eliminate adipogenesis inhibition by an EGF receptor comprised of the progenitor cell. (
  • However, there is substantial evidence to suggest that there are other factors that mediate the interaction between FOXO1 and the PPARG promoter, and that inhibition of adipogenesis is not entirely dependent on FOXO1 preventing transcription of PPARG. (
  • Transcription factors, peroxis proliferator-activated receptor γ (PPARγ) and CCAAT enhancer-binding proteins (C/EBPs) are main regulators of adipogenesis. (
  • PPARγ is a member of the nuclear-receptor superfamily and is the master regulator of adipogenesis. (
  • The results demonstrated that ursolic acid at concentrations ranging from 2.5 µM to 10 µM dose-dependently attenuated adipogenesis, accompanied by reduced protein expression of CCAAT element binding protein β (C/EBP β ), peroxisome proliferator-activated receptor γ (PPAR γ ), CCAAT element binding protein α (C/EBP α ) and sterol regulatory element binding protein 1c (SREBP-1c), respectively. (
  • Studies of these cellular models have revealed some of the molecular events that orchestrate adipogenesis, including the role of C/EBPs and PPARγ in mediating the expression of adipocyte-specific genes ( 3 , 4 ). (
  • The LIM protein Ajuba promotes adipogenesis by enhancing PPARγ and p300/CBP interaction. (
  • Prusty, D., Park, B.H., Davis, K.E. and Farmer, S.R. (2002) Activation of MEK/ERK signaling promotes adipogenesis by enhancing peroxisome proliferator-activated receptor γ(PPARγ) and C/EBPα gene expression during the differentiation of 3T3-L1 preadipocytes. (
  • Both BPA and BPS can enhance 3T3-L1 adipocyte differentiation in a dose-dependent manner and require PPARγ to induce adipogenesis. (
  • Expansion of the orbital fat seemed to be the underlying cause and we have investigated the effects of a PPARγ agonist and an antagonist on the adipogenesis of preadipocytes from several fat depots, including TED orbits. (
  • The percentage of differentiating cells, assessed by oil red O staining, morphological changes and PPARγ transcript expression levels, was determined for preadipocytes in a hormone induced model of adipogenesis supplemented or not with PPARγ agonist or antagonist. (
  • The PPARγ agonist resulted in a 2 to 10 fold increase and a PPARγ antagonist produced a 2 to 7 fold reduction in adipogenesis in the hormone induced model and are illustrated in the bar chart. (
  • While PPARγ agonists may in other contexts have anti-inflammatory properties, in TED the reactivation of orbital adipogenesis in this patient leads us to recommend close supervision of any patient with a history of Graves' disease or TED that is treated with a PPARγ agonist. (
  • The peroxisome proliferator-activated receptor γ (PPARγ) plays a central role in adipogenesis and lipid storage. (
  • The PPARγ ligands, thiazolidinediones (TZDs), enhance in vitro adipogenesis in several cell types, but the role of the TZDs on in vivo adipogenesis is still poorly understood. (
  • Our results demonstrate an inhibitory effect of RCB on adipogenesis through the reduction of the adipogenic factors PPARγ, C/EBPα, and phospho-Akt. (
  • PPARγ and C/EBPα also play important roles as major transcription factors in adipogenesis [ 5 ]. (
  • Western blotting results of adipogenesis-specific markers.Representative image of 3 repeats and quantification of (A) PPARγ, (B) C/EBPα, and (C) Acetyl CoA carboxylase adipogenic marker proteins. (
  • To study the effect of the Wnt regulators on adipogenesis in ADSCs at the protein level, immunoblotting was performed using antibodies against the key adipogenic marker proteins PPARγ, CCAAT enhancer binding protein (C/EBPα), and acetyl CoA carboxylase. (
  • Cells at this time point possess a greater proportion of PS (required for EV generation) whilst corresponding EVs are enriched in signalling fatty acids, such as arachidonic acid, and markers of adipogenesis, such as PREF-1 and PPARγ. (
  • As adipogenesis plays a critical role in obesity, the present study was conducted to investigate the effect of UA on adipogenesis and mechanisms of action in 3T3-L1 preadipocytes. (
  • To examine the role of Wnt signaling in adipogenesis, we tested whether Wnt expression in 3T3-L1 preadipocytes affected their ability to differentiate. (
  • KEY FINDINGS: Shikonin prevented the down-regulation of β-catenin and increased the level of its transcriptional product, cyclin D1, during adipogenesis of 3T3-L1 cells, preadipocytes originally derived from mouse embryo. (
  • The proliferation and adipogenesis of preadipocytes played important roles in the development of adipose tissue and contributed much to the processes of obesity. (
  • Attenuation JAK2/STAT or AMPK-dependent cPLA2 expression reduced LPS-mediated adipogenesis of preadipocytes. (
  • Collectively, these results indicated that LPS increased preadipocytes proliferation and adipogenesis via JAK/STAT and AMPK-dependent cPLA2 expression. (
  • In accordance with in vivo results, Oil red O staining results showed that CAPE significantly suppressed MDI-induced adipogenesis of 3T3-L1 preadipocytes. (
  • To test this, we examined the effects of resveratrol on MCE and insulin signaling pathway in the early phase of adipogenesis in murine preadipocytes. (
  • During the first 24 hours of adipogenesis, resveratrol impaired the progression of MCE by suppressing the cell cycle entry of preadipocytes to G2/M phase, and expression of cell cycle regulators cyclin A and cyclin-dependent kinase 2. (
  • Adipogenesis can be restored by overexpressing adipogenic transcription factors in preadipocytes from old animals. (
  • Alternatively, for analysis of adipogenesis in live cells over time, 3T3-L1 mouse fi broblasts can be stained with HCS LipidTOX neutral lipid stains and placed in StemPro Adipocyte Differentiation Medium for ongoing culture and differentiation. (
  • Expanding MSCs in growth medium for 2-4 days before refeeding with complete StemPro Adipocyte Differentiation Medium can enhance adipogenesis. (
  • Paracrine regulation of angiogenesis and adipocyte differentiation during in vivo adipogenesis. (
  • ProF was found to be strongly expressed in 3T3‐L1 cells, a well‐established cell line for the study of adipocyte differentiation or adipogenesis ( Green and Kehinde, 1975 ). (
  • Conclusions: These data indicate that PTP1B is a modulator of brown fat adipogenesis and suggest that adipocyte differentiation requires regulated expression of PTP1B. (
  • Since AHR negatively controls adipocyte differentiation, we postulated that NRF2 would inhibit adipogenesis through the interaction with the AHR pathway. (
  • These results suggest that type XII collagen may be associated with adipocyte differentiation and adipose formation in cattle and is a potentially useful marker for adipogenesis. (
  • To investigate the role of claudin-6 in adipogenesis, claudin-6 mRNA was examined in adipose tissues and adipocyte differentiation. (
  • This review aimed to discuss the molecular mechanisms underlying adipogenesis and the inhibitory effects of various phytochemicals, including those from natural sources, on the early stage of adipogenesis. (
  • These results suggest that CAPE exerts an antiobesity effect in vivo, presumably through inhibiting adipogenesis at an early stage of adipogenesis. (
  • These reductions were also observed even when baicalein was added in only early stage of adipogenesis (0-2 days) of 6-day-adipogenesis. (
  • Decreased expression of adipogenesis-related genes by baicalein in early stage of adipogenesis.A, Expression levels of the adipogenic and lipogenic genes. (
  • PREF-1 was increased at day 0 whilst adiponectin was higher at day 15 indicating EV protein content reflects the stage of adipogenesis of the cell. (
  • In vitro adipogenesis in 3T3-L1 cells was inhibited by treating them with exogenous hyaluronidase (HYAL) and with 4-methylumbelliferone, which inhibited the synthesis of HA in a concentration-dependent manner. (
  • Moreover, Fyn expression increases progressively in 3T3-L1 cells during in vitro adipogenesis, which correlates with its kinase activity. (
  • Regulation of in vitro adipogenesis by estradiol. (
  • TNFα and IL-1β) inhibit adipogenesis through various pathways. (
  • During stimulation by insulin, FOXO1 is excluded from the nucleus and is subsequently unable to prevent transcription of PPARG and inhibit adipogenesis. (
  • Despite the fact that the balance has been comprehensively scrutinized between adipogenesis and osteogenesis and between chondrogenesis and osteogenesis, few reviews discuss the relationship between chondrogenesis and adipogenesis. (
  • A study was conducted to understand the effects of 25-hydroxyvitamin D 3 (25OHD) and 1,25-dihydroxyvitamin D 3 (1,25OHD) administration on the expression of key genes related to osteogenesis, adipogenesis, myogenesis, and vitamin D 3 metabolism in the chicken embryo. (
  • At 3h, the early osteogenesis differentiation marker, ALP , was increased by 1,25D-H and 25D-H, and 25D-H also stimulated the expression of adipogenesis markers ( FAPB4 and FASN ). (
  • In conclusion, the results suggested both 1,25OHD and 25OHD induced chicken embryo osteogenesis and adipogenesis, but inhibited myogenesis during early chicken embryo development. (
  • The current study demonstrated that MEG3 was downregulated during adipogenesis and upregulated during osteogenesis of hASCs. (
  • Moreover, miR-140-5p was upregulated during adipogenesis and downregulated during osteogenesis in hASCs, which was negatively correlated with MEG3. (
  • Caffeic acid phenethyl ester, a major component of propolis, suppresses high fat diet-induced obesity through inhibiting adipogenesis at the mitotic clonal expansion stage. (
  • FACS analysis results showed that CAPE delayed MDI-stimulated cell cycle progression, thereby contributing to inhibit mitotic clonal expansion (MCE), which is a prerequisite step for adipogenesis. (
  • An inhibitory effect of resveratrol in the mitotic clonal expansion and insulin signaling pathway in the early phase of adipogenesis. (
  • Fyn regulates adipogenesis by promoting PIKE-A/STAT5a interaction. (
  • Stromelysin-1 regulates adipogenesis during mammary gland involution. (
  • FOXO1 negatively regulates adipogenesis. (
  • In the currently accepted model, FOXO1 negatively regulates adipogenesis by binding to the promoter sites of PPARG and preventing its transcription. (
  • The bHLH protein O/E-1 has been shown to promote adipogenesis in NIH-3T3 fibroblasts. (
  • In this study, we have used compound E2F and pocket protein mutant mouse embryonic fibroblasts to dissect the role of these proteins in adipogenesis. (
  • Here we demonstrate the measurement of adipogenesis over the course of differentiation from mouse fibroblasts, using the HCS LipidTOX Green Neutral Lipid Stain in both live and fixed cells. (
  • Additionally, embryonic fibroblasts derived from Akt1/Akt2 double knockout mice show impaired adipogenesis and also decreased Foxo1 phosphorylation and inactivation ( Peng et al , 2003 ). (
  • The inhibitory effect of CD8+ T cells on beige adipogenesis was reversed by blockade of IFN-γ. (
  • Here, we demonstrate enhanced energy dissipation in Rag1-/- mice, increased catecholaminergic input to subcutaneous WAT, and significant beige adipogenesis. (
  • Adoptive transfer experiments demonstrated that CD8+ T cell deficiency accounts for the enhanced beige adipogenesis in Rag1-/- mice. (
  • Consistently, we identified that CD8-/- mice also presented with enhanced beige adipogenesis. (
  • Compositions and methods for white to beige adipogenesis" by Denise Ratzlaff Cooper, Ryan Adam Kirchoffer et al. (
  • Methods: We performed reduced representation bisulfite sequencing (RRBS) and RNA-seq to depict a genome-wide integrative view of the DNA methylome and transcriptome during brown and white adipogenesis. (
  • We hypothesized that the regulation of hyaluronic acid (HA), a component of the ECM, can affect adipogenesis in fat cells. (
  • Evidence suggests that adipogenesis is one of the biological events involved in the regulation of cytokines, and pro-inflammatory cytokines (e.g. (
  • These results suggest that ISL1 is intimately involved in early regulation of adipogenesis, modulating PPARgamma expression and activity via BMP4-dependent and -independent mechanisms. (
  • Positive regulation of DNA double strand break repair activity during differentiation of long life span cells: the example of adipogenesis. (
  • Adipogenesis, the process of adipose cell development, is associated with multiple steps in the regulation of several transcription factors. (
  • In this review, we will discuss adipose tissue and adipogenesis, signaling pathways involved in the regulation of adipogenesis, role of energy sensor protein of the body AMPK, and recently reported plant products in the management of obesity. (
  • FOXO1 is a transcription factor that plays important roles in regulation of gluconeogenesis and glycogenolysis by insulin signaling, and is also central to the decision for a preadipocyte to commit to adipogenesis. (
  • Therefore, transcription factors are crucial for adipogenesis. (
  • Shikonin-induced reductions of the major transcription factors of adipogenesis including peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α, and lipid metabolizing enzymes including fatty acid binding protein 4 and lipoprotein lipase, as well as intracellular fat accumulation, were all significantly recovered by siRNA-mediated knockdown of β-catenin. (
  • The transcription factors involved in adipogenesis are shown in the current pathway. (
  • While adipogenesis is controlled by a cascade of transcription factors, the global gene expression profiles in the early phase of adipogenesis are not well defined. (
  • This thesis aimed to study inflammation and adipogenesis capacity in human subcutaneous white adipose tissue with respect to the development of obesity and associated comorbidities, including insulin resistance. (
  • Obesity-associated insulin resistance is marked by impaired SC adipogenesis, mediated, at least in a subset of individuals, by elevated local levels of IL-6. (
  • Concomitantly, resveratrol inhibited insulin signaling pathway in the early phase of adipogenesis. (
  • ProF binds to the transcription factor Foxo1 (Forkhead box O1), a negative regulator of insulin action and adipogenesis, and facilitates the phosphorylation and thus inactivation of Foxo1 by Akt. (
  • Background: Protein-tyrosine phosphatase 1B (PTP1B) is a physiological regulator of insulin signaling and energy balance, but its role in brown fat adipogenesis requires additional investigation. (
  • We are performing both gain-of-function and loss-of-function experiments designed to place O/E-1 and other O/E isoforms in the transcriptional cascade leading to adipogenesis. (
  • Transcriptional networks and chromatin remodeling controlling adipogenesis. (
  • This leads to reduced transcriptional activity of Foxo1 and thus to increased adipogenesis and glucose uptake in differentiated cells. (
  • The present study was carried out to further investigate the effects of this plant on lipid metabolism, lipolysis, and adipogenesis, in diabetic rats. (
  • These data suggested FALP might be involved in fatty acid metabolism during adipogenesis. (
  • We here review basic pathways regulating adipogenesis, focusing on the limited expandability of the subcutaneous adipose tissue and the development of hypertrophic obesity with a dysregulated adipose tissue and ectopic fat accumulation. (
  • These results imply the involvement of imidacloprid in altered adipogenesis, resulting in increased fat accumulation. (
  • Changes in the ECM such as accumulation of high molecular weight of HA by HAS and degradation of HA by endogenous HYAL were essential for adipogenesis both in vitro and in vivo . (
  • Adipogenesis Assay Kit is used for quantifying triglyceride accumulation in cells and tissues. (
  • The Adipogenesis Assay Kit quantifies triglyceride accumulation in cells and tissues. (
  • We observed that the antiadipogenic action of resveratrol is largely limited to the early phase of adipogenesis. (
  • The aim of the current study was to investigate whether MFGM could prevent obesity through inhibiting adipogenesis and promoting brown remodeling of white adipose tissue (WAT) in mice fed with high-fat diet. (
  • While these studies pointed out a number of key factors involved in adipogenesis, the list of molecular components is far from complete. (
  • Understanding mechanisms that limit subcutaneous adipogenesis in humans should provide novel targets for the treatment of obesity-related metabolic complications. (
  • Here, we show that CD44 expression is required for subcutaneous adipogenesis, whereas RHAMM expression suppresses this process. (
  • We designed RHAMM function blocking peptides to promote subcutaneous adipogenesis as a clinical and tissue engineering tool. (
  • Blocking RHAMM function by peptide injection or topical application is a novel and minimally invasive method for potentially promoting subcutaneous adipogenesis in lipodystrophic diseases and a complementary tool to subcutaneous fat augmentation techniques. (
  • The hypothesis that maintenance of normal subcutaneous (SC) adipogenesis accounts, at least partially, for this protective phenotype and whether it can be abrogated by chronic exposure to IL-6 was investigated. (
  • Middle: Pathologic obesity is often characterized by a relative adipocyte deficiency: limited expandability of the subcutaneous fat tissue, preferential expansion of visceral adipose tissue depots, and unhealthy adipose tissue remodeling (inflammation, fibrosis, limited adipogenesis). (
  • Functional studies of the role of O/E proteins in adipogenesis. (
  • Here, we highlight recent human and rodent studies that support the notion that the ability to recruit new fat cells through adipogenesis is a critical determinant of healthy adipose tissue distribution and remodeling in obesity. (
  • The effects of HA on adipogenesis were investigated in vitro in 3T3-L1 cells and in vivo in high-fat diet-feeding C57BL/6J mice. (
  • 3T3-L1 cells were treated with S1P and expression of early adipogenesis transcription markers was measured by real time PCR. (
  • Adipose stromal cells repair pressure ulcers in both young and elderly mice: potential role of adipogenesis in skin repair. (
  • In addition, early and late adipogenesis markers correlated negatively with fat cell size, suggesting impaired production of new fat cells in WAT hypertrophy. (
  • Adipose-derived stromal cell supplementation resulted in a quantitative difference in angiogenesis and adipogenesis during adipose remodeling according to the concentration of adipose-derived stromal cells. (
  • STAT5A expression in Swiss 3T3 cells promotes adipogenesis in vivo in an athymic mice model system. (
  • Additionally, dominant‐negative Foxo1 restores adipogenesis in ProF knockdown cells. (
  • Activation of the Wnt signalling pathway has inhibited adipogenesis from precursor cells. (
  • Ursolic acid inhibited 3T3-L1 preadipocyte differentiation and adipogenesis through the LKB1/AMPK pathway. (
  • A panel containing eight adipogenesis inducers useful for differentiation of preadipocyte to mature adipocyte. (
  • Conclusion: These results demonstrate that the contribution of SPHK and S1P to adipogenesis is mediated primarily through biphasic activation of SPHK1 and 2 with extracellular S1P and S1PRs playing little role during preadipocyte differentiation. (
  • Methodology/Principal Findings: To precisely determine the role of PTP1B in adipogenesis, we established preadipocyte cell lines from wild type and PTP1B knockout (KO) mice. (
  • In conclusion, S. securidaca decreases lipolysis and adipogenesis without cytotoxicity, which makes it a good candidate for management of dyslipidemia and reduction of cardiovascular risks in diabetes. (
  • We examined the effects of 4- and 8-week β-GPA feeding on serum myostatin levels and expression of genes and proteins related to adipogenesis, lipolysis, and liposynthesis in epididymal WAT (eWAT) and brown adipose tissue (BAT) in 3-week-old, juvenile male mice. (
  • cAMP, an inducer of adipogenesis, can promote expression of C/EBPβ and C/EBPδ. (
  • MAFB expression was upregulated during adipogenesis, and knocking down MAFB mRNA led to reduced TNFα-mediated inflammation. (
  • Knockdown of Suv39h markedly increased C/EBPα expression and promoted adipogenesis. (
  • During the first 24 h following the commitment into adipogenesis, we show an increase in the expression and activity of the catalytic sub-unit of the DNA-PK complex, DNA-PKcs. (
  • I provided evidence for the differential expression of TRP channels during in vitro white or brown adipogenesis. (
  • The profile of gene expression during bovine adipogenesis: Clo. (
  • Nrf2 -/- MEFs showed markedly accelerated adipogenesis upon stimulation, while Keap1 -/- MEFs (which exhibit higher NRF2 signaling) differentiated slowly compared to their congenic wild-type MEFs. (
  • Cellular models of adipogenesis have proven extremely valuable in defining biomolecules-primarily genes and proteins-that regulate adipogenesis. (
  • This review focuses on the cytokines currently known to regulate adipogenesis under physiological and pathophysiological circumstances. (
  • We want to further understand what signals and pathways initiate adipogenesis, and what the epigenetic and proteo-genomic changes are that allow the pre-adipocyte to become a mature, lipid-laden fat cell. (
  • Downregulation of protein tyrosine phosphatase PTP-BL represses adipogenesis. (
  • The molecular mechanisms that lead to the generation of adipose tissue (adipogenesis) are of basic and biomedical interest. (
  • Here we show that Wnt signaling, likely mediated by Wnt-10b, is a molecular switch that governs adipogenesis. (
  • The advance of high-throughput technologies has sparked many experimental studies aimed at the identification of novel molecular components regulating adipogenesis. (
  • Our long-term goal is to elucidate the cellular and molecular mechanisms underlying adipogenesis. (
  • We sought to define the characteristics of adipocyte-derived EVs before and after adipogenesis, hypothesising that adipogenesis would affect EV structure, molecular composition and function. (
  • We have isolated a set of subtracted cDNA fragments whose respective mRNA levels are up regulated during adipogenesis. (
  • Here we demonstrate that ProF is a positive regulator of adipogenesis. (
  • These results suggest that claudin-6 is another important regulator in adipogenesis and fat deposition. (
  • However, the mechanisms regulating the Akt‐dependent phosphorylation of Foxo1 and thus adipogenesis remain largely unknown to date. (
  • We identified 31 genes whose promoters were significantly differentially methylated between white and brown adipogenesis at all three time points of differentiation. (
  • Using overexpression and knockdown experiments, we will elucidate the link between these genes, adipogenesis and apoptosis. (
  • MacroH2A1.2 overexpression markedly inhibited adipogenesis, while overexpression of macroH2A1.1 had opposite effects. (