Mitochondrial function in normal and diabetic β-cells

Pierre Maechler () and Claes B. Wollheim ()
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Pierre Maechler: University Medical Centre
Claes B. Wollheim: University Medical Centre

Nature, 2001, vol. 414, issue 6865, 807-812

Abstract: 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 β-cell dysfunction caused by mutations in mitochondrial DNA, which is distinct from the nuclear genome. The impact of such mutations on β-cell function reflects the importance of mitochondria in the control of insulin secretion. The β-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.

Date: 2001
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DOI: 10.1038/414807a

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