IRS-1 transgenic mice show increased epididymal fat mass and insulin resistance

Biochem Biophys Res Commun. 2007 Dec 14;364(2):301-7. doi: 10.1016/j.bbrc.2007.10.007. Epub 2007 Oct 12.

Abstract

Insulin receptor substrate-1 (IRS-1) is the major substrate of both the insulin receptor and the IGF-1 receptor. In this study, we created IRS-1 transgenic (IRS-1-Tg) mice which express human IRS-1 cDNA under control of the mouse IRS-1 gene promoter. In the IRS-1-Tg mice, IRS-1 mRNA expression was significantly increased in almost all tissues, but its protein expression was increased in very limited tissues (epididymal fat and skeletal muscle). IRS-1-Tg mice showed glucose intolerance and significantly enlarged epididymal fat mass, as well as elevated serum TNF-alpha concentrations. Importantly insulin signaling was significantly attenuated in the liver of IRS-1-Tg mice, which may contribute to the glucose intolerance. Our results suggest that excess IRS-1 expression may not provide a beneficial impact on glucose homeostasis in vivo.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / metabolism
  • Adipose Tissue / pathology*
  • Animals
  • Epididymis / metabolism
  • Epididymis / pathology*
  • Glucose / metabolism
  • Glucose Intolerance / genetics
  • Glucose Intolerance / metabolism
  • Insulin Receptor Substrate Proteins
  • Insulin Resistance / physiology*
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Transgenic
  • Muscle, Skeletal / metabolism
  • Phosphoproteins / biosynthesis*
  • Phosphoproteins / genetics
  • Promoter Regions, Genetic
  • RNA, Messenger / biosynthesis
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • IRS1 protein, human
  • Insulin Receptor Substrate Proteins
  • Irs1 protein, mouse
  • Phosphoproteins
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Glucose