Casp1 and Ripk3 are required for homeostatic insulin secretion in mice
Objectives- Cell death and inflammatory pathways play important roles in adaptations to nutrient overload and metabolic dysfunction. This study investigates the metabolic consequences that arise from the dual disruption of both caspase 1 (Casp1) and receptor interacting protein kinase 3 (Ripk3) in mice fed a control or obesity-inducing diet. Methods- Male and female wild-type (WT), Casp1/11…
Casp1 and Ripk3 play crucial roles in maintaining insulin secretion balance in mice, according to a study. When both proteins were deleted or inhibited in mice on a low-fat diet, the animals showed reduced glucose levels after glucose consumption due to higher insulin levels in the bloodstream. This increased insulin secretion was also observed in isolated islets outside the body and was not influenced by alterations in the proportion of various islet cells.
However, the presence of urocortin-3 (Ucn3)-positive beta cells decreased in the double knockout mice, indicating a change in Ucn3-Sst signaling. Although exogenous Sst (Octreotide) could revert the decreased glucose response, Ucn3 alone was not effective. The study concludes that Casp1 and Ripk3 independently regulate normal glucose-stimulated insulin release in islets.
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