INSULIN-LIKE GROWTH FACTOR 1 RECEPTOR KNOCKOUT IN MICE LEADS TO ALTERED GLUCOSE-INSULIN HOMEOSTASIS AND INCREASED ENDOTHELIAL NITRIC OXIDE PRODUCTION

摘要

IGF1RKO mice have impaired whole-body glucose handling, enhanced insulin sensitivity and increased basal NO production in the vasculature. These data raise the possibility that reduced IGF-1 receptor action in the endothelium may have a favourable effect on NO bioavailability, possibly by a novel interaction with insulin signalling.