Adipogenic Transcription Factors (adipogenic + transcription_factor)

Distribution by Scientific Domains


Selected Abstracts


Anti-adipogenic effects of Garcinia extract on the lipid droplet accumulation and the expression of transcription factor

BIOFACTORS, Issue 1-4 2004
Myung-Sunny Kim
Abstract Garcinia extract was used as a potential anti-obesity agent. In this study, we found that Garcinia extract inhibits the cytoplasmic lipid accumulation as well as adipogenic differentiation of preadipocytes. The mechanisms that regulate the inhibition of insulin-induced differentiation by Garcinia extracts include the inhibition of expression of the early adipogenic transcription factor, CCAAT element binding protein (C/EBP), that regulate adipogenesis. These results suggest that the specific targets of Garcinia extract on differentiation process of 3T3-L1 cells could be, at least, early adipogenic differentiation factor. [source]


Adipogenic Phenotype of Hepatic Stellate Cells

ALCOHOLISM, Issue 2005
Hide Tsukamoto
Abstract: Transdifferentiation of hepatic stellate cells (HSC) constitutes a major cellular event in the genesis of alcoholic liver fibrosis and cirrhosis and molecular mechanisms underlying this process is incompletely understood. Our laboratory proposed several years ago that HSC quiescence requires the transcriptional program known to be integral to preadipocyte to adipocyte differentiation. In support of the hypothesis, our research demonstrates the expression of adipogenic transcription factors (C/EBPs, PPAR,, SREBP-1c, LXR,) and adipocyte-specific genes (adipsin, resistin) are high in quiescent HSC and depleted in activated HSC. Three gain-of-function approaches have been taken to test this notion: the treatment of activated HSC with the adipocyte differentiation cocktail; ectopic expression of PPAR, or SREBP-1c. All three treatments coordinately upregulate a panel of putative adipogenic transcrition factors and cause morphologic and biochemical reversal of activated HSC to quiescent cells. These findings establish a new conceptual framework for the treatment of liver fibrosis and propose an intriguing notion concerning the plasticity of HSC. [source]


Citri Reticulatae Pericarpium extract suppresses adipogenesis in 3T3-L1 preadipocytes

JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 13 2007
Fuu Sheu
Abstract This study examined how Citrus herbal medicines,Citri Reticulatae Pericarpium (CRP), Citri Reticulatae Viride Pericarpium (CRVP), Aurantii Immaturus Fructus (AIF) and Aurantii Fructus (AF),affect the differentiation of 3T3-L1 adipocytes. Eight days after induction for differentiation with 3-isobutyl-1-methylxanthine, dexamethasone and insulin (MDI) medium and simultaneously with the tested CRP, intracellular triacylglycerol accumulations of 3T3-L1 cells were significantly (P < 0.05) reduced compared with those for CRVP, AIF and AF and those of the vehicle control. This suppression affect was dose-dependent, and decreases in triacylglycerol production of 12.6, 18.7, 34.05 and 49.6% were observed for CRP at concentrations of 50, 100, 150 and 200 µg mL,1 respectively. Additionally, the expression of key transcription factors for the 3T3-L1 adipogenesis gene, including PPAR-,, C/EBP-, and SREBP-1, was markedly reduced by CRP treatment. These results suggest that dietary CRP suppresses 3T3-L1 differentiation by down-regulation of adipogenic transcription factors. Experimental data may prove useful in further medical examination of the use of CRP for body weight control. Copyright © 2007 Society of Chemical Industry [source]


Resveratrol induces apoptosis and inhibits adipogenesis in 3T3-L1 adipocytes ,

PHYTOTHERAPY RESEARCH, Issue 10 2008
Srujana Rayalam
Abstract Resveratrol, a phytoallexin, has recently been reported to slow aging by acting as a sirtuin activator. Resveratrol also has a wide range of pharmacological effects on adipocytes. In this study, we investigated the effects of resveratrol on adipogenesis and apoptosis using 3T3-L1 cells. In mature adipocytes, 100 and 200 µM resveratrol decreased cell viability dose-dependently by 23 ± 2.7%, and 75.3 ± 2.8% (p < 0.0001), respectively, after 48 h treatment, and 100 µM resveratrol increased apoptosis by 76 ± 8.7% (p < 0.0001). Resveratrol at 25 and 50 µM decreased lipid accumulation in maturing preadipocytes significantly by 43 ± 1.27% and 94.3 ± 0.3% (p < 0.0001) and decreased cell viability by 25 ± 1.3% and 70.4 ± 1.6% (p < 0.0001), respectively. In order to understand the anti-adipogenic effects of resveratrol, maturing 3T3-L1 preadipocytes were treated with 25 µM resveratrol and the change in the expression of several adipogenic transcription factors and enzymes was investigated using real-time RT-PCR. Resveratrol down-regulated the expression of PPAR,, C/EBP,, SREBP-1c, FAS, HSL, LPL and up-regulated the expression of genes regulating mitochondrial activity (SIRT3, UCP1 and Mfn2). These results indicate that resveratrol may alter fat mass by directly affecting cell viability and adipogenesis in maturing preadipocytes and inducing apoptosis in adipocytes and thus may have applications for the treatment of obesity. Copyright © 2008 John Wiley & Sons, Ltd. [source]