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Mitochondrial function in normal and diabetic beta-cells

Published in Nature. 2001, vol. 414, no. 6865, p. 807-12
Abstract The aetiology of type 2, or non-insulin-dependent, diabetes mellitus has been characterized in only a limited number of cases. Among these, mitochondrial diabetes, a rare subform of the disease, is the consequence of pancreatic beta-cell dysfunction caused by mutations in mitochondrial DNA, which is distinct from the nuclear genome. The impact of such mutations on beta-cell function reflects the importance of mitochondria in the control of insulin secretion. The beta-cell mitochondria serve as fuel sensors, generating factors that couple nutrient metabolism to the exocytosis of insulin-containing vesicles. The latter process requires an increase in cytosolic Ca2+, which depends on ATP synthesized by the mitochondria. This organelle also generates other factors, of which glutamate has been proposed as a potential intracellular messenger.
Keywords AnimalsDNA, MitochondrialDiabetes Mellitus, Type 2/drug therapy/genetics/physiopathologyExocytosisHumansInsulin/secretionIslets of Langerhans/physiology/physiopathologyMitochondria/physiologyMitochondrial Diseases/drug therapy/genetics/physiopathologyMutationSignal Transduction
PMID: 11742413
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MAECHLER, Pierre, WOLLHEIM, Claes. Mitochondrial function in normal and diabetic beta-cells. In: Nature, 2001, vol. 414, n° 6865, p. 807-12. https://archive-ouverte.unige.ch/unige:47616

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Deposited on : 2015-03-06

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