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Pioglitazone improves insulin signaling defects in skeletal muscle from Wistar fatty (fa/fa) rats.

Abstract：

:The effects of pioglitazone, a novel antidiabetic insulin-sensitizing agent, on insulin signaling in skeletal muscles from genetically obese Wistar fatty rats and their lean littermates were studied. Increased tyrosine phosphorylation levels of insulin receptors (IRs) and insulin receptor substrate 1 (IRS-1) in response to insulin were not observed in fatty rats. Insulin-stimulated phosphatidylinositol (PI) 3-kinase activity was reduced in fatty rats. Administration of pioglitazone (3 mg/kg/day) to fatty rats for 10 or 18 days reversed the decline in the insulin-stimulated tyrosine phosphorylated IR and IRS-1 levels and the reduced insulin-stimulated PI 3-kinase activities. In contrast, insulin-stimulated tyrosine phosphorylation of IR and IRS-1 and PI 3-kinase activity in lean rats was not changed by pioglitazone. IR expression in fatty rats was down-regulated, which was not affected by pioglitazone. There was no difference between the PI 3-kinase expression levels in fatty and lean rats and pioglitazone did not change these expression levels. These results indicate that pioglitazone can correct the insulin signaling defects of Wistar fatty rats, thereby ameliorating insulin resistance.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Hayakawa T,Shiraki T,Morimoto T,Shii K,Ikeda H

doi

10.1006/bbrc.1996.0912

subject

Has Abstract

pub_date

1996-06-14 00:00:00

pages

439-44

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(96)90912-2

journal_volume

223

pub_type

杂志文章

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