| First Author | Cheung SY | Year | 2015 |
| Journal | Endocrinology | Volume | 156 |
| Issue | 6 | Pages | 2074-86 |
| PubMed ID | 25774551 | Mgi Jnum | J:222171 |
| Mgi Id | MGI:5644088 | Doi | 10.1210/en.2014-1831 |
| Citation | Cheung SY, et al. (2015) Activation of transient receptor potential vanilloid 3 channel suppresses adipogenesis. Endocrinology 156(6):2074-86 |
| abstractText | 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 gamma and CCAAT/enhancer-binding protein alpha. 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. |
