Disruption of IRS-2 causes type 2 diabetes in mice View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1998-02

AUTHORS

Dominic J. Withers, Julio Sanchez Gutierrez, Heather Towery, Deborah J. Burks, Jian-Ming Ren, Stephen Previs, Yitao Zhang, Dolores Bernal, Sebastian Pons, Gerald I. Shulman, Susan Bonner-Weir, Morris F. White

ABSTRACT

Human type 2 diabetes is characterized by defects in both insulin action and insulin secretion. It has been difficult to identify a single molecular abnormality underlying these features. Insulin-receptor substrates (IRS proteins) may be involved in type 2 diabetes: they mediate pleiotropic signals initiated by receptors for insulin and other cytokines1. Disruption of IRS-1 in mice retards growth, but diabetes does not develop because insulin secretion increases to compensate for the mild resistance to insulin2,3. Here we show that disruption of IRS-2 impairs both peripheral insulin signalling and pancreatic β-cell function. IRS-2-deficient mice show progressive deterioration of glucose homeostasis because of insulin resistance in the liver and skeletal muscle and a lack of β-cell compensation for this insulin resistance. Our results indicate that dysfunction of IRS-2 may contribute to the pathophysiology of human type 2 diabetes. More... »

PAGES

900-904

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/36116

DOI

http://dx.doi.org/10.1038/36116

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1019591506

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9495343


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