Adiponectin gene activation by thiazolidinediones requires PPAR gamma 2, but not C/EBP alpha-evidence for differential regulation of the aP2 and adiponectin genes

Biochem Biophys Res Commun. 2003 Sep 5;308(4):933-9. doi: 10.1016/s0006-291x(03)01518-3.

Abstract

We examined the role of PPAR gamma 2 and C/EBP alpha for adiponectin and aP2 gene activation in C/EBP alpha(-/-) fibroblasts by stably expressing PPAR gamma 2 or C/EBP alpha. PPAR gamma 2, but not PPAR gamma 1, mRNA markedly increased during the differentiation to adipocytes in cells expressing C/EBP alpha. Both infected cell lines differentiated to an adipocyte phenotype and the mRNA for both aP2 and adiponectin increased in parallel. However, adiponectin mRNA was considerably higher when C/EBP alpha was present, suggesting that this transcription factor is important for full gene activation. Thiazolidinediones markedly activated the gene in PPAR gamma 2-expressing cells in the absence of C/EBP alpha, suggesting that the adiponectin promoter may have functional PPAR gamma-response elements. Several observations showed that the adiponectin and aP2 genes can be differentially regulated in adipocytes: (1) Topiramate, an anti-epileptic agent with weight-reducing properties, increased adiponectin mRNA levels and secretion, but did not, like the thiazolidinediones, increase aP2 expression; (2) IL-6 reduced adiponectin, but significantly increased, aP2 expression; and (3) TNFalpha inhibited adiponectin, but paradoxically increased, aP2 expression in PPAR gamma 2-infected C/EBP alpha null cells. These data show that activation of the adiponectin gene can be separated from effects on adipogenic genes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Adipocytes / metabolism
  • Adiponectin
  • Animals
  • Anticonvulsants / pharmacology
  • CCAAT-Enhancer-Binding Protein-alpha / metabolism*
  • Cell Differentiation
  • Cell Line
  • Culture Media / pharmacology
  • Cytokines / metabolism
  • Fibroblasts / metabolism
  • Fructose / analogs & derivatives*
  • Fructose / pharmacology
  • Gene Expression Regulation*
  • Genes, Reporter
  • Intercellular Signaling Peptides and Proteins*
  • Interleukin-6 / metabolism
  • Ligands
  • Luciferases / metabolism
  • Mice
  • Phenotype
  • Promoter Regions, Genetic
  • Proteins / genetics*
  • Proteins / metabolism*
  • RNA, Messenger / metabolism
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • Thiazoles / pharmacology*
  • Thiazolidinediones*
  • Time Factors
  • Topiramate
  • Transcription Factors / metabolism*
  • Transcription, Genetic
  • Transcriptional Activation
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Adiponectin
  • Anticonvulsants
  • CCAAT-Enhancer-Binding Protein-alpha
  • Culture Media
  • Cytokines
  • Intercellular Signaling Peptides and Proteins
  • Interleukin-6
  • Ligands
  • Proteins
  • RNA, Messenger
  • Receptors, Cytoplasmic and Nuclear
  • Thiazoles
  • Thiazolidinediones
  • Transcription Factors
  • Tumor Necrosis Factor-alpha
  • Topiramate
  • Fructose
  • 2,4-thiazolidinedione
  • Luciferases