Sodium butyrate prevents cytokine-induced β-cell dysfunction through restoration of stromal interaction molecule 1 expression and activation of store-operated calcium entry.

ABSTRACT: Sodium butyrate (NaB) improves β-cell function in preclinical models of diabetes; however, the mechanisms underlying these beneficial effects have not been fully elucidated. In this study, we investigated the impact of NaB on β-cell function and calcium (Ca²⁺) signaling using ex vivo and in vitro models of diabetes. Our results show that NaB significantly improved glucose-stimulated insulin secretion in islets from human organ donors with type 2 diabetes and in cytokine-treated INS-1 β cells. Consistently, NaB improved glucose-stimulated Ca²⁺ oscillations in mouse islets treated with proinflammatory cytokines. Because the oscillatory phenotype of Ca²⁺ in the β cell is governed by changes in endoplasmic reticulum (ER) Ca²⁺ levels, we explored the

SUBMITTER: Lee CC 

PROVIDER: S-EPMC11607631 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature