Agonist-independent Gα_z activity negatively regulates beta-cell compensation in a diet-induced obesity model of type 2 diabetes.

ABSTRACT: The inhibitory G protein alpha-subunit (Gα_z) is an important modulator of beta-cell function. Full-body Gα_z-null mice are protected from hyperglycemia and glucose intolerance after long-term high-fat diet (HFD) feeding. In this study, at a time point in the feeding regimen where WT mice are only mildly glucose intolerant, transcriptomics analyses reveal islets from HFD-fed Gα_z KO mice have a dramatically altered gene expression pattern as compared with WT HFD-fed mice, with entire gene pathways not only being more strongly upregulated or downregulated versus control-diet fed groups but actually reversed in direction. Genes involved in the "pancreatic secretion" pathway are the most strongly differentially regulated: a finding that correlates with enhanced i

SUBMITTER: Schaid MD 

PROVIDER: S-EPMC7948463 | biostudies-literature | 2021 Jan-Jun

REPOSITORIES: biostudies-literature