Cell Commun Signal 2017 Nov 13;15(1):47. Epub 2017 Nov 13.
Department of Medicine, Albert Einstein College of Medicine, New York, NY, USA.
Background: One of the most common side effects of the immunosuppressive drug tacrolimus (FK506) is the increased risk of new-onset diabetes mellitus. However, the molecular mechanisms underlying this association have not been fully clarified.
Methods: We studied the effects of the therapeutic dose of tacrolimus on mitochondrial fitness in beta-cells.
Results: We demonstrate that tacrolimus impairs glucose-stimulated insulin secretion (GSIS) in beta-cells through a previously unidentified mechanism. Indeed, tacrolimus causes a decrease in mitochondrial Ca uptake, accompanied by altered mitochondrial respiration and reduced ATP production, eventually leading to impaired GSIS.
Conclusion: Our observations individuate a new fundamental mechanism responsible for the augmented incidence of diabetes following tacrolimus treatment. Indeed, this drug alters Ca fluxes in mitochondria, thereby compromising metabolism-secretion coupling in beta-cells.
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