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Endocrinology. 2015 Jun;156(6):2074-86. doi: 10.1210/en.2014-1831. Epub 2015 Mar 16.

Activation of transient receptor potential vanilloid 3 channel suppresses adipogenesis.

Author information

1
Food and Nutritional Sciences (S.Y.C., H.Y.C.), School of Life Sciences, Chinese University of Hong Kong, Hong Kong, China; Li Ka Shing Institute of Health Sciences and School of Biomedical Sciences (Y.H., X.Y.), Chinese University of Hong Kong, Hong Kong, China; and Centre for Cancer and Inflammation Research (H.Y.K.), School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.

Abstract

The present study shows that activation of the transient receptor potential vanilloid 3 channel (TRPV3) suppresses adipocyte differentiation. We also found that a major functional catechin compound in green tea and cocoa, (-)-epicatechin, exerts antiadipogenic effects in the adipocytes through direct activation of TRPV3. TRPV3 was detected in the 3T3-L1 adipocytes using immunohistochemistry and semiquantitative PCR. TRPV3 activation by activators (-)-epicatechin and diphenylborinic anhydride was determined using live cell fluorescent Ca(2+) imaging and patch-clamp electrophysiology. Using RNA interference, immunoblotting, and Oil red O staining, we found that the TRPV3 agonists prevented adipogenesis by inhibiting the phosphorylation of insulin receptor substrate 1, the downstream phosphoinositide 3-kinase/Akt/forkhead box protein O1 axis, and the expression of the adipogenic genes peroxisome proliferator-activated receptor γ and CCAAT/enhancer-binding protein α. TRPV3 overexpression hindered adipogenesis in the 3T3-L1 cells. In vivo studies showed that chronic treatment with the TRPV3 activators prevented adipogenesis and weight gain in the mice fed on high-fat diets. Moreover, TRPV3 expression was reduced in the visceral adipose tissue from mice fed on high-fat diets and obese (ob/ob) and diabetic (db/m(+)) mice. In conclusion, our study illustrates the antiadipogenic role of TRPV3 in the adipocytes.

PMID:
25774551
DOI:
10.1210/en.2014-1831
[Indexed for MEDLINE]

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