Insulin and dexamethasone induce GLUT4 gene expression in foetal brown adipocytes: synergistic effect through CCAAT/enhancer-binding protein alpha

Biochem J. 2003 Jun 1;372(Pt 2):617-24. doi: 10.1042/BJ20030325.

Abstract

Treatment of foetal brown adipocytes in primary culture with either dexamethasone or insulin, at physiological concentrations, for 24 h up-regulates the expression of the GLUT4 gene, producing a synergistic effect on mRNA accumulation (20-fold increase), in the amount of protein in the total membrane fraction (8-fold increase) and in the transactivation of a full-promoter GLUT4 -chloramphenicol acetyltransferase gene ( CAT ) construct (7-fold increase). However, GLUT1 expression remains essentially unmodified regardless of the presence of the hormones. As a consequence, exposure of brown adipocytes to dexamethasone and insulin results in a dramatic increase of glucose uptake (12-fold). Dexamethasone induces the expression of CCAAT/enhancer-binding protein (C/EBP) alpha, insulin promotes myocyte enhancer factor-2 DNA-binding activity and both combined produces a significant increase in C/EBPalpha DNA-binding activity. Moreover, co-transfection with a wild-type C/EBPalpha construct transactivates a full-promoter GLUT4 - CAT fusion gene, whereas a dominant-negative C/EBPalpha expression vector impairs the hormonal effects. Our results show that the synergism between insulin and glucocorticoids on glucose uptake is a consequence of the activation of the GLUT4 promoter by the transcription factor C/EBPalpha.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / drug effects*
  • Adipocytes / metabolism
  • Adipose Tissue, Brown / cytology
  • Animals
  • CCAAT-Enhancer-Binding Protein-alpha / genetics
  • CCAAT-Enhancer-Binding Protein-alpha / metabolism*
  • Cell Line
  • Chloramphenicol O-Acetyltransferase / genetics
  • DNA-Binding Proteins / metabolism
  • Dexamethasone / pharmacology*
  • Drug Synergism
  • Gene Expression Regulation*
  • Genes, Dominant
  • Glucocorticoids / pharmacology*
  • Glucose / metabolism
  • Glucose Transporter Type 4
  • Hypoglycemic Agents / pharmacology*
  • Insulin / pharmacology*
  • Kinetics
  • MEF2 Transcription Factors
  • Monosaccharide Transport Proteins / genetics*
  • Monosaccharide Transport Proteins / metabolism
  • Muscle Proteins*
  • Myogenic Regulatory Factors
  • Promoter Regions, Genetic
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar
  • Transcription Factors / metabolism
  • Transcription, Genetic
  • Transcriptional Activation
  • Transfection
  • Up-Regulation

Substances

  • CCAAT-Enhancer-Binding Protein-alpha
  • DNA-Binding Proteins
  • Glucocorticoids
  • Glucose Transporter Type 4
  • Hypoglycemic Agents
  • Insulin
  • MEF2 Transcription Factors
  • Monosaccharide Transport Proteins
  • Muscle Proteins
  • Myogenic Regulatory Factors
  • RNA, Messenger
  • Slc2a4 protein, rat
  • Transcription Factors
  • Dexamethasone
  • Chloramphenicol O-Acetyltransferase
  • Glucose