Brown Adipose Tissue In Humans: A New Target for Anti-Obesity Therapy

Enerbäck, Sven

doi:10.1007/978-3-642-13517-0_5

Cited by 2 publications

(2 citation statements)

References 22 publications

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“…Obesity and related metabolic diseases are recognized as global health problem and have been described as ''the plague of our time'' (25). Obesity develops when energy intake exceeds total energy expenditure.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of in vitro and in vivo brown fat differentiation program by myostatin

Braga

Pervin

Norris

et al. 2013

Obesity

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Obesity arises mainly due to the imbalance between energy storage and its expenditure. Metabolically active brown adipose tissue (BAT) has recently been detected in humans and has been proposed as a new target for anti-obesity therapy because of its unique capacity to regulate energy expenditure. Myostatin (Mst), a negative regulator of muscle mass, has been identified as a potential target to regulate overall body composition. While the beneficial effects of Mst inhibition on muscle mass are well known, its role in the regulation of lipid metabolism, and energy expenditure is not very clear. We tested the effects of Mst inhibition on the gene regulatory networks that control BAT differentiation using both in vivo and in vitro model systems. PRDM16 and UCP1, two key regulators of brown fat differentiation were significantly up regulated in levator-ani (LA) and gastrocnemius (Gastroc) muscles as well as in epididymal (Epi) and subcutaneous (SC) fat pads isolated from Mst knock out (Mst KO) male mice compared to wild type (WT) mice. Using mouse embryonic fibroblast (MEFs) primary cultures obtained from Mst KO group compared to the WT group undergoing adipogenic differentiation, we also demonstrate a significant increase in select genes and proteins that improve lipid metabolism and energy expenditure. Furthermore, treatment of Mst KO MEFs with recombinant Mst protein significantly inhibited the gene expression levels of UCP1, PRDM16, PGC1-α/β as well as BMP7. Future studies to extend these findings and explore the therapeutic potential of Mst inhibition on metabolic disorders are warranted.

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Section: Discussionmentioning

confidence: 99%

Inhibition of in vitro and in vivo brown fat differentiation program by myostatin

Braga

Pervin

Norris

et al. 2013

Obesity

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“…In addition, the fact that short-chain fatty acids mediate a wide range of metabolic functions in white adipocytes and white adipose tissues via the GPR43 receptors [ 8 , 19 , 22 ] strongly supports the hypothesis that GPR43 acts as sensor that regulates energy metabolism in white adipose tissue. Brown adipose tissue also can regulate the metabolism and energy homeostasis by heat production when the body is exposed to cold temperature [ 23 , 24 ]. Indeed, brown adipose tissue plays an important role in maintaining body temperature in rodentine mammals and infants.…”

Section: Discussionmentioning

confidence: 99%

Expression of GPR43 in Brown Adipogenesis Is Enhanced by Rosiglitazone and Controlled by PPARγ/RXR Heterodimerization

Zhou

Cheung

et al. 2018

PPAR Research

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GPR43, a G-protein coupled receptor recognizing short-chain fatty acids, has been reported to participate in many biological functions of white adipocytes, such as adipogenesis and lipolysis. However, the functional role of GPR43 in brown adipocytes is still not clear. In this study, we investigated the effects of the PPARγ agonist rosiglitazone on GPR43 expression in brown adipogenesis. The results demonstrated that GPR43 was expressed during the late phase of brown adipocyte differentiation, which could be further augmented by adipogenic agent rosiglitazone treatment. The PPARγ/RXR heterodimerization was found to be the key transcription factor for this enhancing effect of rosiglitazone on GPR43 expression. Taken together, these results suggested GPR43 levels might be regulated by PPARγ-activated events during brown adipocytes differentiation and reflect the adipogenesis status of brown adipocytes.

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Brown Adipose Tissue In Humans: A New Target for Anti-Obesity Therapy

Cited by 2 publications

References 22 publications

Inhibition of in vitro and in vivo brown fat differentiation program by myostatin

Inhibition of in vitro and in vivo brown fat differentiation program by myostatin

Expression of GPR43 in Brown Adipogenesis Is Enhanced by Rosiglitazone and Controlled by PPARγ/RXR Heterodimerization

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