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Mitochondrial signals in glucose-stimulated insulin secretion in the beta cell

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Published in The Journal of Physiology. 2000, vol. 529 Pt 1, p. 49-56
Abstract Glucose-induced insulin secretion is determined by signals generated in the mitochondria. The elevation of ATP is necessary for the membrane-dependent increase in cytosolic Ca2+, the main trigger of insulin exocytosis. Beta cells depleted of mitochondrial DNA fail to respond to glucose while still secreting insulin in response to membrane depolarisation. This cell model resembles the situation of defective insulin secretion in patients with mitochondrial diabetes. On the other hand, infants with activating mutations in the mitochondrial enzyme glutamate dehydrogenase are characterised by hyperinsulinism and hypoglycaemia. We have recently proposed that glutamate, generated by this enzyme, participates in insulin secretion as a glucose-derived metabolic messenger. In this model, glutamate acts downstream of the mitochondria by sensitising the exocytotic process to Ca2+. The evidence in favour of such a role for glutamate is discussed in the present review.
Keywords AnimalsExocytosis/drug effectsGlucose/pharmacologyHumansInsulin/metabolismIslets of Langerhans/drug effects/metabolismMitochondria/drug effects/physiologySignal Transduction/drug effects/physiologyStimulation, Chemical
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PMID: 11080250
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MAECHLER, Pierre, WOLLHEIM, Claes. Mitochondrial signals in glucose-stimulated insulin secretion in the beta cell. In: The Journal of Physiology, 2000, vol. 529 Pt 1, p. 49-56. https://archive-ouverte.unige.ch/unige:35094

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Deposited on : 2014-03-28

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