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Review
. 2008 May 15;22(10):1269-75.
doi: 10.1101/gad.1681308.

Molecular determinants of brown adipocyte formation and function

Affiliations
Review

Molecular determinants of brown adipocyte formation and function

Stephen R Farmer. Genes Dev. .

Abstract

Humans contain essentially two types of adipose tissue: brown adipose tissue (BAT) and white adipose tissue (WAT). The function of WAT is to store fat while that of BAT is to burn fat for heat production. A potential strategy to combat obesity and its related disorders is to induce the conversion of WAT into BAT. In this issue of Genes & Development, Kajimura and colleagues (pp. 1397-1409) have identified a mechanism by which PRDM16, the principal regulator of brown adipocyte formation and function, can simultaneously induce BAT gene expression, while suppressing WAT gene expression. The studies suggest that PRDM16 and its associated coregulators PPARgamma coactivator-1alpha (PGC-1alpha) and C-terminal-binding protein 1/2 (CtBP1/2), which control the switch from WAT to BAT, are potential targets for development of obesity-related therapeutics.

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Figures

Figure 1.
Figure 1.
Mechanisms controlling the switch from white to brown phenotype. Studies by Kajimura et al. (2008) demonstrate that PRDM16 can interact with either PGC-1α/β or CtBPs to activate brown genes or to suppress white gene expression, respectively. Studies by Parker and colleagues (Christian et al. 2006; Parker et al. 2006; Powelka et al. 2006) have also shown that RIP140 in association with CtBPs can suppress mitochondrial gene expression in white adipocytes. It will be interesting to determine additional functions for PRDM16 and RIP140 coregulator complexes in controlling other features of the brown versus white fat cell phenotype including angiogenesis and adipokine production. Furthermore, knowledge of the involvement of changes in redox state (i.e., hypoxia and nutrients) in controlling these processes will be very informative for the development of therapeutics for obesity-associated disorders.

Comment on

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