Molecular Regulation of Adipogenesis

Abstract

Adipogenesis, or the development of fat cells from preadipocytes, has been one of the most intensely studied models of cellular differentiation. In part this has been because of the availability of in vitro models that faithfully recapitulate most of the critical aspects of fat cell formation in vivo. More recently, studies of adipogenesis have proceeded with the hope that manipulation of this process in humans might one day lead to a reduction in the burden of obesity and diabetes. This review explores some of the highlights of a large and burgeoning literature devoted to understanding adipogenesis at the molecular level. The hormonal and transcriptional control of adipogenesis is reviewed, as well as studies on a less well known type of fat cell, the brown adipocyte. Emphasis is placed, where possible, on in vivo studies with the hope that the results discussed may one day shed light on basic questions of cellular growth and differentiation in addition to possible benefits in human health.

Grape-seed derived procyanidins interfere with adipogenesis of 3T3-L1 cells at the onset of differentiation

“…This event, called mitotic clonal expansion, ceases coincident with the expression of the key transcription factors PPARg and CCAAT/enhancer binding protein-a (C/EBPa). 15 PPARg is the regulator of many genes involved in adipose phenotype and lipid metabolism, such as fatty acid synthase and adipocyte-specific fatty acid binding protein (aP2). 15,16 After 6 days postinduction of differentiation, cells acquire adipose morphology and accumulate triglyceride droplets.…”

“…15 PPARg is the regulator of many genes involved in adipose phenotype and lipid metabolism, such as fatty acid synthase and adipocyte-specific fatty acid binding protein (aP2). 15,16 After 6 days postinduction of differentiation, cells acquire adipose morphology and accumulate triglyceride droplets. Although the transcriptional regulation of adipose differentiation has been widely studied, the intracellular signalling cascades that control this process are not fully understood.…”

JDP2 suppresses adipocyte differentiation by regulating histone acetylation

“…1,2 Adipogenesis, namely, the process whereby hormonal stimuli induce the differentiation of fibroblasts or mesenchymal cells to adipocytes, requires organized and controlled expression of a cascade of transcription factors and the modification of the chromatin within preadipocytes. [3][4][5] The factors involved in adipocyte differentiation include a nuclear receptor known as peroxisome proliferation-activated receptor gamma (PPARg) and a group of CCAAT/enhancer-binding proteins (C/ EBPs). 6,7 The rapid and transient induction of the expression of C/EBPb and C/EBPd is one of the earliest events in adipogenesis.…”

“…[3][4][5] The factors involved in adipocyte differentiation include a nuclear receptor known as peroxisome proliferation-activated receptor gamma (PPARg) and a group of CCAAT/enhancer-binding proteins (C/ EBPs). 6,7 The rapid and transient induction of the expression of C/EBPb and C/EBPd is one of the earliest events in adipogenesis. 4 These transcription factors bind to specific sequences in the promoters of the C/EBPa gene and the PPARg2 gene, inducing their expression, which, in turn, activates the full adipogenic program of gene expression.…”

“…6,7 The rapid and transient induction of the expression of C/EBPb and C/EBPd is one of the earliest events in adipogenesis. 4 These transcription factors bind to specific sequences in the promoters of the C/EBPa gene and the PPARg2 gene, inducing their expression, which, in turn, activates the full adipogenic program of gene expression. [8][9][10] Expression of PPARg2 is also induced via an SREBP-1c-dependent pathway.…”