Shouhong Xuan, Tadahiro Kitamura, Jun Nakae, Katerina Politi, Yoshiaki Kido, Peter E. Fisher, Manrico Morroni, Saverio Cinti, Morris F. White, Pedro L. Herrera, Domenico Accili, Argiris Efstratiadis
J Clin Invest.
2002;
110(7):1011–1019
doi:10.1172/JCI15276
This article Copyright © 2002, The American Society for Clinical Investigation
Abstract
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D
efective insulin secretion is a feature of type 2 diabetes that results from inadequate compensatory increase of β cell mass and impaired glucose-dependent insulin release. β cell proliferation and secretion are thought to be regulated by signaling through receptor tyrosine kinases. In this regard, we sought to examine the potential proliferative and/or antiapoptotic role of IGFs in β cells by tissue-specific conditional mutagenesis ablating type 1 IGF receptor (IGF1R) signaling. Unexpectedly, lack of functional IGF1R did not affect β cell mass, but resulted in age-dependent impairment of glucose tolerance, associated with a decrease of glucose- and arginine-dependent insulin release. These observations reveal a requirement of IGF1R-mediated signaling for insulin secretion.
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