| First Author | Loro E | Year | 2015 |
| Journal | Am J Physiol Regul Integr Comp Physiol | Volume | 309 |
| Issue | 8 | Pages | R835-44 |
| PubMed ID | 26269523 | Mgi Jnum | J:227357 |
| Mgi Id | MGI:5700273 | Doi | 10.1152/ajpregu.00505.2014 |
| Citation | Loro E, et al. (2015) IL-15Ralpha is a determinant of muscle fuel utilization, and its loss protects against obesity. Am J Physiol Regul Integr Comp Physiol 309(8):R835-44 |
| abstractText | IL-15Ralpha is the widely expressed primary binding partner for IL-15. Because of the wide distribution in nonlymphoid tissues like skeletal muscle, adipose, or liver, IL-15/IL-15Ralpha take part in physiological and metabolic processes not directly related to immunity. In fast muscle, lack of IL-15Ralpha promotes an oxidative switch, with increased mitochondrial biogenesis and fatigue resistance. These effects are predicted to reproduce some of the benefits of exercise and, therefore, improve energy homeostasis. However, the direct effects of IL-15Ralpha on metabolism and obesity are currently unknown. We report that mice lacking IL-15Ralpha (IL-15Ralpha(-/-)) are resistant to diet-induced obesity (DIO). High-fat diet-fed IL-15Ralpha(-/-) mice have less body and liver fat accumulation than controls. The leaner phenotype is associated with increased energy expenditure and enhanced fatty acid oxidation by muscle mitochondria. Despite being protected against DIO, IL-15Ralpha(-/-) are hyperglycemic and insulin-resistant. These findings identify novel roles for IL-15Ralpha in metabolism and obesity. |
