Defective insulin secretion in pancreatic beta cells lacking type 1 IGF receptor.
Defective insulin secretion is a feature of type 2 diabetes that results from inadequate compensatory increase of beta cell mass and impaired glucose-dependent insulin release. beta 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 beta cells by tissue-specific conditional mutagenesis ablating type 1 IGF receptor (IGF1R) signaling. Unexpectedly, lack of functional IGF1R did not affect beta 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.
Published In/Presented At
Xuan, S., Kitamura, T., Nakae, J., Politi, K., Kido, Y., Fisher, P. E., Morroni, M., Cinti, S., White, M. F., Herrera, P. L., Accili, D., & Efstratiadis, A. (2002). Defective insulin secretion in pancreatic beta cells lacking type 1 IGF receptor. The Journal of clinical investigation, 110(7), 1011–1019. https://doi.org/10.1172/JCI15276
Medicine and Health Sciences
Department of Pathology and Laboratory Medicine