Insulin action impaired by deficiency of the G-protein subunit G ialpha2.

Abstract:

:Integration of information between tyrosine kinase and G-protein-mediated pathways is necessary, but remains poorly understood. Here we use cells from transgenic mice harbouring inducible expression of RNA antisense to the gene encoding G ialpha2 to show that G ialpha2 is critical for insulin action. G ialpha2 deficiency in adipose tissue and liver produces hyperinsulinaemia, impaired glucose tolerance and resistance to insulin in vivo. Insulin resistance affects glucose-transporter activity and recruitment, counterregulation of lipolysis, and activation of glycogen synthase, all of which are cardinal responses to insulin. G ialpha2 deficiency increases protein-tyrosine phosphatase activity and attenuates insulin-stimulated tyrosine phosphorylation of IRS (insulin-receptor substrate 1) in vivo. G ialpha2 deficiency creates a model for insulin resistance characteristic of noninsulin-dependent diabetes mellitus (NIDDM), implicating G ialpha2 as a positive regulator of insulin action.

journal_name

Nature

journal_title

Nature

authors

Moxham CM,Malbon CC

doi

10.1038/379840a0

subject

Has Abstract

pub_date

1996-02-29 00:00:00

pages

840-4

issue

6568

eissn

0028-0836

issn

1476-4687

journal_volume

379

pub_type

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