Mitochondrial transhydrogenase--a key enzyme in insulin secretion and, potentially, diabetes.
Two recent studies have shown that the glucose intolerance and impaired insulin secretion of the C57BL/6J mouse strain results from oxidative stress due to a mutated nicotinamide nucleotide transhydrogenase. Reproduction of this phenotype, by mutating the same enzyme in another strain with normal glucose tolerance, suggests that the mechanism of the transhydrogenase-dependent inhibition of insulin secretion involves a partial uncoupling by the UCP2 protein. These exciting findings raise important questions, not least their potential relevance for human diabetes.
Rydström
Jan
J
Department of Biochemistry and Biophysics, Göteborg University, 405-30 Göteborg, Sweden. jan.rydstrom@chem.gu.se
D000375:Aging / Q000502:physiology; D000818:Animals; D003920:Diabetes Mellitus / Q000209:etiology; D018149:Glucose Intolerance / Q000201:enzymology*; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D051379:Mice; D009250:NADP Transhydrogenases / Q000235:genetics / Q000502:physiology*
D007328:Insulin; D009250:NADP Transhydrogenases