Differential regulation of gene expression and insulin-induced activation of phosphodiesterase 3B in adipocytes of lean insulin-resistant IRS-1 (-/-) mice

Masaaki Hasegawa, Yan Tang, Haruhiko Osawa, Hiroshi Onuma, Tatsuya Nishimiya, Masaaki Ochi, Yasuo Terauchi, Takashi Kadowaki, Hideichi Makino

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

Phosphodiesterase (PDE) 3B, a major isoform of PDE in adipocytes, mediates the antilipolytic action of insulin. PDE3B gene expression is generally reduced in adipocytes of either monogenic or polygenic rodent models of obese, insulin-resistance. An increased fat cell size, a common feature of obesity, could account for this reduction. Insulin receptor substrate-1 (IRS-1) (-/-) mice are lean with a reduced fat cell size and have insulin resistance due to a primary defect of insulin signaling. To determine whether the regulation of PDE3B gene expression is correlated with fat cell size, we examined this gene expression in adipose tissues of IRS-1 (-/-) mice. In IRS-1 (-/-) mice, PDE3B mRNA and protein levels were increased 1.24- and 1.35-fold those in C57BL/6J control mice, respectively. Independently, the fold induction of PDE activity by insulin (insulin-induced/basal) was 1.7-fold in control mice, but was reduced to 1.35-fold in IRS-1 (-/-) mice. Thus, PDE3B gene expression may be inversely correlated with a fat cell size, whereas insulin-induced PDE3B activation is mediated through IRS-1.

Original languageEnglish (US)
Pages (from-to)79-85
Number of pages7
JournalDiabetes Research and Clinical Practice
Volume58
Issue number2
DOIs
StatePublished - Nov 1 2002
Externally publishedYes

Keywords

  • Adipocyte
  • Gene expression
  • IRS-1
  • Insulin resistance
  • Phosphodiesterase 3B

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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