| First Author | Liu S | Year | 2014 |
| Journal | J Biol Chem | Volume | 289 |
| Issue | 19 | Pages | 13000-9 |
| PubMed ID | 24675075 | Mgi Jnum | J:214131 |
| Mgi Id | MGI:5588092 | Doi | 10.1074/jbc.M114.564658 |
| Citation | Liu S, et al. (2014) SRA gene knockout protects against diet-induced obesity and improves glucose tolerance. J Biol Chem 289(19):13000-9 |
| abstractText | We have recently shown that the non-coding RNA, steroid receptor RNA activator (SRA), functions as a transcriptional coactivator of PPARgamma and promotes adipocyte differentiation in vitro. To assess SRA function in vivo, we have generated a whole mouse Sra1 gene knock-out (SRA(-/-)). Here, we show that the Sra1 gene is an important regulator of adipose tissue mass and function. SRA is expressed at a higher level in adipose tissue than other organs in wild type mice. SRA(-/-) mice are resistant to high fat diet-induced obesity, with decreased fat mass and increased lean content. This lean phenotype of SRA(-/-) mice is associated with decreased expression of a subset of adipocyte marker genes and reduced plasma TNFalpha levels. The SRA(-/-) mice are more insulin sensitive, as evidenced by reduced fasting insulin, and lower blood glucoses in response to IP glucose and insulin. In addition, the livers of SRA(-/-) mice have fewer lipid droplets after high fat diet feeding, and the expression of lipogenesis-associated genes is decreased. To our knowledge, these data are the first to indicate a functional role for SRA in adipose tissue biology and glucose homeostasis in vivo. |
