SRA gene knockout protects against diet-induced obesity and improves glucose tolerance

J Biol Chem. 2014 May 9;289(19):13000-9. doi: 10.1074/jbc.M114.564658. Epub 2014 Mar 27.

Abstract

We have recently shown that the non-coding RNA, steroid receptor RNA activator (SRA), functions as a transcriptional coactivator of PPARγ 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 TNFα 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.

Keywords: Adipocyte; Gene Expression; Gene Knockout; Obesity; RNA.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / metabolism*
  • Adipocytes / pathology
  • Adipose Tissue / metabolism*
  • Adipose Tissue / pathology
  • Animals
  • Blood Glucose / genetics
  • Blood Glucose / metabolism*
  • Dietary Fats / adverse effects*
  • Dietary Fats / pharmacology
  • Homeostasis / genetics
  • Mice
  • Mice, Knockout
  • Obesity / chemically induced
  • Obesity / genetics
  • Obesity / metabolism*
  • Obesity / pathology
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism*
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Blood Glucose
  • Dietary Fats
  • RNA, Long Noncoding
  • Tumor Necrosis Factor-alpha
  • steroid receptor RNA activator