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Mitochondrial glucose metabolism is essential for the initiation of insulin release from pancreatic {beta}-cells. Fusion of mitochondria is supported by mitofusin 1 (MFN1) and mitofusin 2 (MFN2). Whether this process is important for glucose sensing by {beta}-cells is unclear. Here, we generated mice with {beta}-cell-selective, adult-restricted deletion of Mfn1 and Mfn2 (betaMfn1/2-KO), and explored the impact on insulin secretion and glucose homeostasis. betaMfn1/2-KO mice displayed higher glycaemia and a >five-fold decrease in plasma insulin post-intraperitoneal glucose injection. Mitochondrial length, glucose-induced hyperpolarization, ATP synthesis and Ca2+ accumulation were significantly reduced in betaMfn1/2-KO mouse islets. Ca2+ dynamics and mitochondrial membrane potential changes were also suppressed in vivo. Defective glucose-stimulated insulin secretion in islets isolated from betaMfn1/2-KO mice was nevertheless normalised by the addition of GLP-1 receptor agonists. Mitochondrial fusion and fission cycles are thus essential in the {beta}-cell to maintain normal mitochondrial bioenergetics and glucose sensing both in vitro and in vivo.

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