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betes in combination with deafness. This high percentage confirms previous reports indicating that the prevalence of the 3243 nt mutation is increased in diabetic populations with sensory hearing loss [7, 8]. Until now, mitochondrial diabetes has probably been underestimated because of heteroplasmy and difficulty of searching for all mutations in the mitochondrial genome for each patient, despite the use of different techniques [9]. Moroever, it is likely that in some families, mitochondrial diabetes is secondary to mutations in nuclear genes coding for proteins belonging to the respiratory chain or important for the stability of the mitochondrial genome. In conclusion, these results demonstrate that clinical criteria are most important to improve the detection of diabetes secondary to a respiratory chain defect. A mitochondrial origin might be evocated when diabetes is associated with other symptoms, especially with nerve deafness.

Effect of angiotensin II and bradykinin on insulin-stimulated tyrosine kinase activity of insulin receptor