Joshua C Neuman, Austin Reuter, Kathryn A Carbajal, Michael D Schaid, Grant Kelly, Kelsey Connors, Cecilia Kaiser, Joshua Krause, Liam D Hurley, Angela Olvera, Dawn Belt Davis, Jaclyn A Wisinski, Maureen Gannon, Michelle E Kimple
Signaling through Prostaglandin E2 EP3 receptor (EP3) actively contributes to the β-cell dysfunction of type 2 diabetes (T2D). In T2D models, full-body EP3 knockout mice have a significantly worse metabolic phenotype than wild-type controls due to hyperphagia and severe insulin resistance resulting from loss of EP3 in extra-pancreatic tissues, masking any potential beneficial effects of EP3 loss in the β-cell. We hypothesized β-cell-specific EP3 knockout (EP3 βKO) mice would be protected from high-fat diet (HFD)-induced glucose intolerance, phenocopying mice lacking the EP3 effector, Gɑz , which is much more limited in its tissue distribution...
March 13, 2024: American Journal of Physiology. Endocrinology and Metabolism