| First Author | Zhao S | Year | 2016 |
| Journal | Cell Rep | Volume | 14 |
| Issue | 12 | Pages | 2872-88 |
| PubMed ID | 26997277 | Mgi Jnum | J:234876 |
| Mgi Id | MGI:5791035 | Doi | 10.1016/j.celrep.2016.02.076 |
| Citation | Zhao S, et al. (2016) alpha/beta-Hydrolase Domain 6 Deletion Induces Adipose Browning and Prevents Obesity and Type 2 Diabetes. Cell Rep 14(12):2872-88 |
| abstractText | Suppression of alpha/beta-domain hydrolase-6 (ABHD6), a monoacylglycerol (MAG) hydrolase, promotes glucose-stimulated insulin secretion by pancreatic beta cells. We report here that high-fat-diet-fed ABHD6-KO mice show modestly reduced food intake, decreased body weight gain and glycemia, improved glucose tolerance and insulin sensitivity, and enhanced locomotor activity. ABHD6-KO mice also show increased energy expenditure, cold-induced thermogenesis, brown adipose UCP1 expression, fatty acid oxidation, and white adipose browning. Adipose browning and cold-induced thermogenesis are replicated by the ABHD6 inhibitor WWL70 and by antisense oligonucleotides targeting ABHD6. Our evidence suggests that one mechanism by which the lipolysis derived 1-MAG signals intrinsic and cell-autonomous adipose browning is via PPARalpha and PPARgamma activation, and that ABHD6 regulates adipose browning by controlling signal competent 1-MAG levels. Thus, ABHD6 regulates energy homeostasis, brown adipose function, and white adipose browning and is a potential therapeutic target for obesity and type 2 diabetes. |
