期刊
TRENDS IN BIOCHEMICAL SCIENCES
卷 31, 期 7, 页码 355-358出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tibs.2006.05.003
关键词
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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.
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