Mitochondrial function in normal and diabetic beta-cells

[摘要] 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.

[关键词] STIMULATED INSULIN-SECRETION;METABOLIC COUPLING FACTORS;TRNA(LEU(UUR)) MUTATION;GUANINE-NUCLEOTIDES;GENE-TRANSCRIPTION;PANCREATIC-ISLETS;GLUCOSE;DNA;EXOCYTOSIS;MELLITUS