[Molecular mechanism of switching adipocyte / osteoblast differentiation through regulation of PPAR-gamma function]

Clin Calcium. 2008 May;18(5):656-61.
[Article in Japanese]

Abstract

Adipocytes and osteoblasts are derived from mesenchymal stem cells, and some adipocyte differentiation regulators suppress osteoblast differentiation. PPAR-gammaplays a pivotal role for adipocyte differentiation and glucose tolerance. PPAR-gammais a member of nuclear receptor super family and regulates mRNA expression level of target genes by binding to fatty acid derivatives and thiazolidinediones. Recently, it was found that PPAR-gammainhibits osteoblast differentiation and regulates bone metabolism. In this report, we show recent studies about the extracellular signals regulating the transactivation function of PPAR-gamma.

Publication types

  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing / physiology
  • Adipocytes / cytology*
  • Animals
  • Bone and Bones / metabolism
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / physiology
  • Cell Differentiation
  • Humans
  • MAP Kinase Kinase Kinases / physiology
  • Mesenchymal Stem Cells / cytology
  • Mice
  • Osteoblasts / cytology*
  • PPAR gamma / genetics*
  • PPAR gamma / physiology*
  • Signal Transduction / genetics*
  • Signal Transduction / physiology*
  • Transcriptional Activation
  • Wnt Proteins / physiology
  • Wnt-5a Protein

Substances

  • Adaptor Proteins, Signal Transducing
  • PPAR gamma
  • Tab2 protein, mouse
  • Wnt Proteins
  • Wnt-5a Protein
  • Wnt5a protein, mouse
  • Wnt5a protein, rat
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • MAP Kinase Kinase Kinases
  • MAP kinase kinase kinase 7