Systemic Metabolic Alterations Correlate with Islet-Level Prostaglandin E₂ Production and Signaling Mechanisms That Predict β-Cell Dysfunction in a Mouse Model of Type 2 Diabetes.

ABSTRACT: The transition from β-cell compensation to β-cell failure is not well understood. Previous works by our group and others have demonstrated a role for Prostaglandin EP3 receptor (EP3), encoded by the Ptger3 gene, in the loss of functional β-cell mass in Type 2 diabetes (T2D). The primary endogenous EP3 ligand is the arachidonic acid metabolite prostaglandin E₂ (PGE₂). Expression of the pancreatic islet EP3 and PGE₂ synthetic enzymes and/or PGE₂ excretion itself have all been shown to be upregulated in primary mouse and human islets isolated from animals or human organ donors with established T2D compared to nondiabetic controls. In this study, we took advantage of a rare and fleeting phenotype in which a subset of Black and Tan BRachyury (B

SUBMITTER: Schaid MD 

PROVIDER: S-EPMC7830513 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature