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Dapansutrile preserves pancreatic beta-cell function by regulating insulin vesicle membrane fusion and mitochondrial homeostasis

ABSTRACT: DAPA improved pancreatic beta-cell function in diabetic mice by inhibiting NLRP3-Caspase-1 signaling, enhancing insulin vesicle fusion, and modulating mitochondrial homeostasis, indicating its potential as a novel treatment for diabetes.

ORGANISM(S): Mus Musculus

SUBMITTER: Jiaqiang Zhou

PROVIDER: PXD054615 | iProX | Tue Aug 06 00:00:00 BST 2024

REPOSITORIES: iProX

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Dapansutrile preserves pancreatic beta-cell function by regulating insulin vesicle membrane fusion and mitochondrial homeostasis.

Wu Ying Y Fu Hongxing H Zhu Min M Yao Yuanfa Y Jin Luhong L Lin Xihua X Zhou Jiaqiang J

Diabetes, obesity & metabolism 20260128

<h4>Aims/hypothesis</h4>Pancreatic beta-cell dysfunction is pivotal in diabetes pathogenesis, with the NOD-like receptor protein 3 (NLRP3) inflammasome playing a crucial role. Dapansutrile (DAPA), a novel NLRP3 inhibitor, demonstrates promise in diabetes management.<h4>Methods</h4>The diabetic model of high-fat diet (HFD) + streptozotocin (STZ) mice was utilized to assess glucose metabolism indicators following DAPA intervention. Experiments involving pancreatic islets from normal mice or humans ...[more]

PMID: 41605812

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