Scientific article
Open access

Mitochondrial function in normal and diabetic beta-cells

Published inNature, vol. 414, no. 6865, p. 807-812
Publication date2001

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.

  • Animals
  • DNA, Mitochondrial
  • Diabetes Mellitus, Type 2/drug therapy/genetics/physiopathology
  • Exocytosis
  • Humans
  • Insulin/secretion
  • Islets of Langerhans/physiology/physiopathology
  • Mitochondria/physiology
  • Mitochondrial Diseases/drug therapy/genetics/physiopathology
  • Mutation
  • Signal Transduction
Citation (ISO format)
MAECHLER, Pierre, WOLLHEIM, Claes. Mitochondrial function in normal and diabetic beta-cells. In: Nature, 2001, vol. 414, n° 6865, p. 807–812. doi: 10.1038/414807a
Main files (1)
Article (Published version)
ISSN of the journal0028-0836

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