Global, neuronal or β cell-specific deletion of inceptor improves glucose homeostasis in male mice with diet-induced obesity.

ABSTRACT: Insulin resistance is an early complication of diet-induced obesity (DIO)¹, potentially leading to hyperglycaemia and hyperinsulinaemia, accompanied by adaptive β cell hypertrophy and development of type 2 diabetes². Insulin not only signals via the insulin receptor (INSR), but also promotes β cell survival, growth and function via the insulin-like growth factor 1 receptor (IGF1R)^3-6. We recently identified the insulin inhibitory receptor (inceptor) as the key mediator of IGF1R and INSR desensitization⁷. But, although β cell-specific loss of inceptor improves β cell function in lean mice⁷, it warrants clarification whether inceptor signal inhibition also improves glycaemia under conditions of obesity. We assessed the glucometabolic eff

SUBMITTER: Grandl G 

PROVIDER: S-EPMC10963260 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature