| First Author | Huang C | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 473 |
| Issue | 2 | Pages | 435-41 |
| PubMed ID | 26972253 | Mgi Jnum | J:234823 |
| Mgi Id | MGI:5790918 | Doi | 10.1016/j.bbrc.2016.03.026 |
| Citation | Huang C, et al. (2016) CMKLR1 deficiency influences glucose tolerance and thermogenesis in mice on high fat diet. Biochem Biophys Res Commun 473(2):435-41 |
| abstractText | Obesity has become a global epidemic disease, contributing to increases in the prevalence of type 2 diabetes. CMKLR1, one of the receptors for chemerin, has a wide range of functions in physiological and pathological activity, including innate and adaptive immunity, inflammation, metabolism and reproduction. In our study, CMKLR1 deficiency did not influence the gain of body weight but did exacerbate glucose intolerance, increase serum insulin level, and promote insulin resistance in mice on high fat diets. The expression of thermogenesis related genes was examined and indicated to decrease in CMKLR1 knockout (KO) mice in both normal and cold environments, which indicated CMKLR1 influence the thermogenesis process. Cold exposure induced significant body mass decrease and improved glucose tolerance and insulin resistance in wild type HFD mice but had no obvious effect on CMKLR1 KO HFD mice. In vitro, loss of CMKLR1 did not significantly influence the differentiation of stromal vascular fibroblasts (SVFs) derived from adipose tissue, but did suppress the expression of thermogenesis related genes. Collectively, these data demonstrate that CMKLR1 deficiency induces inbalance of glucose metabolism and impairs the cold induced-thermogenesis process in high diet models. |
