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Review
. 2017 Sep 9;31(2):/j/hmbci.2017.31.issue-2/hmbci-2017-0036/hmbci-2017-0036.xml.
doi: 10.1515/hmbci-2017-0036.

Modulation of transforming growth factor-β/follistatin signaling and white adipose browning: therapeutic implications for obesity related disorders

Shehla Pervin  1 , Vineeta Singh  1 , Alexandria Tucker  1 , Javier Collazo  1 , Rajan Singh  1
Affiliations
Review

Modulation of transforming growth factor-β/follistatin signaling and white adipose browning: therapeutic implications for obesity related disorders

Shehla Pervin et al. Horm Mol Biol Clin Investig. .

Abstract

Obesity is a major risk factor for the development of diabetes, insulin resistance, dyslipidemia, cardiovascular disease and other related metabolic conditions. Obesity develops from perturbations in overall cellular bioenergetics when energy intake chronically exceeds total energy expenditure. Lifestyle interventions based on reducing total energy uptake and increasing activities including exercise have proved ineffective in the prevention and treatment of obesity because of poor adherence to such interventions for an extended period of time. Brown adipose tissue (BAT) has an extraordinary metabolic capacity to burn excess stored energy and holds great promise in combating obesity and related diseases. This unique ability to nullify the effects of extra energy intake of these specialized tissues has provided attractive perspectives for the therapeutic potential of BAT in humans. Browning of white adipose tissue by promoting the expression and activity of key mitochondrial uncoupling protein 1 (UCP1) represents an exciting new strategy to combat obesity via enhanced energy dissipation. Members of the transforming growth factor-beta (TGF-β) superfamily including myostatin and follistatin have recently been demonstrated to play a key role in regulating white adipose browning both in in-vitro and in-vivo animal models and thereby present attractive avenues for exploring the therapeutic potential for the treatment of obesity and related metabolic diseases.

Keywords: adipocyte; adipose browning; follistatin; myostatin; transforming growth factor beta.

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Conflict of interest statement

Conflict of interest: The authors state no conflict of interest.

Figures

Figure 1
Figure 1
Schematic diagram showing that antagonizing TGF-β/myostatin (Mst) signaling components lead to activation of adipose browning and provides resistance from obesity and metabolic diseases.
Figure 2
Figure 2
Follistatin regulation of white adipose tissue (WAT) browning and induction of classical brown adipose tissue (BAT) via targeting Myf5− and Myf5+ precursor pools, respectively.
See this image and copyright information in PMC

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