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Authors: | M. Hassan, J.-F. Landrier, A. Margotat, M.J. Amiot-Carlin |
Keywords: | obesity, diabetes, cardiovascular disease, adipogenesis, PPARγ, C/EBP |
DOI: | 10.17660/ActaHortic.2009.841.17 |
Abstract:
Adipose tissue, as a metabolic and endocrine organ, plays an essential role in the regulation of energy balance (Rosen and Spiegelman, 2006). Accordingly, adipocytes are emerging as a potential pharmacological target for obesity, type II diabetes, and cardiovascular diseases (Nawrocki and Sherer, 2005). Paradoxically, not only an excess of adipose tissue, but also an impaired of adipogenesis is associated with an increased risk for these complications (Bays et al., 2004; Yang et al., 2004). Adipogenesis is a complex process accompanied by coordinated changes in morphology, hormone sensitivity, and gene expression.
Several transcription factors act cooperatively and sequentially to trigger adipocyte differentiation program (Rosen et al., 2000). These include members of the CCAAT/enhancer binding protein (C/EBPs) family and peroxisome proliferator-activated receptor (PPAR ). C/EBP and C/EBP are expressed in the early stages of differentiation, and together induce the initial expression of PPAR and C/EBP (Tang and Lane, 1999). Then, PPAR and C/EBP act synergistically to activate the expression of genes involved in creating and maintaining the adipocyte phenotype (Tang and Lane, 1999; Rosen et al., 2000, 2002).
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