Loss of β-cell identity in human islets treated with glibenclamide.

ABSTRACT:

Aims

Loss of β-cell identity can contribute to the reduction of functional β-cell mass in type 2 diabetes. Sulfonylureas show shorter durability of antihyperglycaemic action and higher rates of secondary failure compared to other antihyperglycaemic agents, suggesting that they could accelerate the decline of β-cell functional mass in type 2 diabetes. We aimed to investigate the impact of chronic exposure to sulfonylureas on β-cell identity.

Materials and methods

Islets from human multi-organ donors were cultured for 4-7 days at 5.6 mM glucose with or without glibenclamide. β-cell function (glucose stimulated insulin secretion, GSIS), apoptosis (TUNEL) and gene (RT-qPCR) and protein expression (immunofluorescence, genetic β-cell tracing and Western Blot) were determined.

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SUBMITTER: Fernandez C 

PROVIDER: S-EPMC12409205 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature