Glucose Sensing by Skeletal Myocytes Couples Nutrient Signaling to Systemic Homeostasis.

ABSTRACT: Skeletal muscle is a major site of postprandial glucose disposal. Inadequate insulin action in skeletal myocytes contributes to hyperglycemia in diabetes. Although glucose is known to stimulate insulin secretion by β cells, whether it directly engages nutrient signaling pathways in skeletal muscle to maintain systemic glucose homeostasis remains largely unexplored. Here we identified the Baf60c-Deptor-AKT pathway as a target of muscle glucose sensing that augments insulin action in skeletal myocytes. Genetic activation of this pathway improved postprandial glucose disposal in mice, whereas its muscle-specific ablation impaired insulin action and led to postprandial glucose intolerance. Mechanistically, glucose triggers K_ATP channel-dependent calcium signaling, which promotes HDA

SUBMITTER: Meng ZX 

PROVIDER: S-EPMC5489118 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature