Repression of GLUT4 expression by the endoplasmic reticulum stress response in 3T3-L1 adipocytes

Ryan S. Miller, Daniel Diaczok, David W. Cooke

Research output: Contribution to journalArticle

Abstract

Expression of GLUT4 is decreased in adipocytes in obesity and type 2 diabetes, contributing to the insulin resistance of these states. Recent investigations suggest a role for activation of the ER stress response in the pathophysiology of type 2 diabetes. We investigated activation of the ER stress response in 3T3-L1 adipocytes. We show that activation of the ER stress response decreased GLUT4 expression at the level of gene transcription. Activation of the ER stress response also increased the expression of CHOP10, an inhibitor of the activity and expression of C/EBPα. As expected, activation of the ER stress response decreased expression of C/EBPα, an activator of GLUT4 expression, providing a mechanism to account for the repression of GLUT4 by ER stress activation. Our studies identify repression of GLUT4 expression as another potential mechanism for obesity-induced activation of the ER stress response to contribute to the insulin resistance of obesity.

Original languageEnglish (US)
Pages (from-to)188-192
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume362
Issue number1
DOIs
StatePublished - Oct 12 2007

Keywords

  • C/EBP
  • CHOP10
  • Diabetes
  • ER stress
  • Gadd153
  • Insulin resistance
  • UPR
  • Unfolded protein response

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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