Altered estrogen receptor expression in skeletal muscle and adipose tissue of female rats fed a high-fat diet. Academic Article uri icon

Overview

abstract

  • Estrogen receptors (ERs) are expressed in adipose tissue and skeletal muscle, with potential implications for glucose metabolism and insulin signaling. Previous studies examining the role of ERs in glucose metabolism have primarily used knockout mouse models of ERα and ERβ, and it is unknown whether ER expression is altered in response to an obesity-inducing high-fat diet (HFD). The purpose of the current study was to determine whether modulation of glucose metabolism in response to a HFD in intact and ovariectomized (OVX) female rats is associated with alterations in ER expression. Our results demonstrate that a 6-wk HFD (60% calories from fat) in female rats induces whole body glucose intolerance with tissue-specific effects isolated to the adipose tissue, and no observed differences in insulin-stimulated glucose uptake, GLUT4, or ERα protein expression levels in skeletal muscle. In chow-fed rats, OVX resulted in decreased ERα with a trend toward decreased GLUT4 expression in adipose tissue. Sham-treated and OVX rats fed a HFD demonstrated a decrease in ERα and GLUT4 in adipose tissue. The HFD also increased activation of stress kinases (c-jun NH₂-terminal kinase and inhibitor of κB kinase β) in the sham-treated rats and decreased expression of the protective heat shock protein 72 (HSP72) in both sham-treated and OVX rats. Our findings suggest that decreased glucose metabolism and increased inflammation in adipose tissue with a HFD in female rats could stem from a significant decrease in ERα expression.

publication date

  • January 13, 2011

Research

keywords

  • Adipose Tissue
  • Dietary Fats
  • Estrogen Receptor alpha
  • Muscle, Skeletal

Identity

PubMed Central ID

  • PMC3075127

Scopus Document Identifier

  • 79954463259

Digital Object Identifier (DOI)

  • 10.1152/japplphysiol.00541.2010

PubMed ID

  • 21233345

Additional Document Info

volume

  • 110

issue

  • 4