Interferon-gamma-induced regulation of peroxisome proliferator-activated receptor gamma and STATs in adipocytes

J Biol Chem. 2001 Mar 9;276(10):7062-8. doi: 10.1074/jbc.M007894200. Epub 2000 Dec 5.

Abstract

Interferon-gamma (IFN-gamma) is known primarily for its roles in immunological responses but also has been shown to affect fat metabolism and adipocyte gene expression. To further investigate the effects of IFN-gamma on fat cells, we examined the effects of this cytokine on the expression of adipocyte transcription factors in 3T3-L1 adipocytes. Although IFN-gamma regulated the expression of several adipocyte transcription factors, IFN-gamma treatment resulted in a rapid reduction of both peroxisome proliferator-activated receptor (PPAR) protein and mRNA. A 48-h exposure to IFN-gamma also resulted in a decrease of both CCAAT/enhancer-binding alpha and sterol regulatory element binding protein (SREBP-1) expression. The short half-life of both the PPARgamma mRNA and protein likely contributed to the rapid decline of both cytosolic and nuclear PPARgamma in the presence of IFN-gamma. Our studies clearly demonstrated that the IFN-gamma-induced loss of PPARgamma protein is partially inhibited in the presence of two distinct proteasome inhibitors. Moreover, IFN-gamma also inhibited the transcription of PPARgamma, which was accompanied by a decrease in PPARgamma mRNA accumulation. In addition, exposure to IFN-gamma resulted in a substantial increase in STAT 1 expression and a small increase in STAT 3 expression. IFN-gamma treatment of 3T3-L1 adipocytes (48-96 h) resulted in a substantial inhibition of insulin-sensitive glucose uptake. These data clearly demonstrate that IFN-gamma treatment results in the development of insulin resistance, which is accompanied by the regulation of various adipocyte transcription factors, in particular the synthesis and degradation of PPARgamma.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adipocytes / metabolism
  • Animals
  • Biological Transport
  • CCAAT-Enhancer-Binding Protein-alpha / metabolism
  • CCAAT-Enhancer-Binding Proteins / biosynthesis
  • Cell Nucleus / metabolism
  • Cells, Cultured
  • Cytosol / metabolism
  • DNA-Binding Proteins / biosynthesis
  • DNA-Binding Proteins / metabolism*
  • Dactinomycin / pharmacology
  • Deoxyglucose / metabolism
  • Dose-Response Relationship, Drug
  • Electrophoresis, Polyacrylamide Gel
  • Gene Expression Regulation, Enzymologic
  • Immunoblotting
  • Insulin / metabolism
  • Insulin Resistance
  • Interferon-gamma / metabolism*
  • Ligands
  • Mice
  • Promoter Regions, Genetic
  • RNA, Messenger / metabolism
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • STAT1 Transcription Factor
  • STAT3 Transcription Factor
  • Sterol Regulatory Element Binding Protein 1
  • Time Factors
  • Trans-Activators / metabolism*
  • Transcription Factors / metabolism*
  • Transcription, Genetic

Substances

  • CCAAT-Enhancer-Binding Protein-alpha
  • CCAAT-Enhancer-Binding Proteins
  • DNA-Binding Proteins
  • Insulin
  • Ligands
  • RNA, Messenger
  • Receptors, Cytoplasmic and Nuclear
  • STAT1 Transcription Factor
  • STAT3 Transcription Factor
  • Srebf1 protein, mouse
  • Stat1 protein, mouse
  • Stat3 protein, mouse
  • Sterol Regulatory Element Binding Protein 1
  • Trans-Activators
  • Transcription Factors
  • Dactinomycin
  • Interferon-gamma
  • Deoxyglucose