期刊
CURRENT DIABETES REVIEWS
卷 5, 期 2, 页码 120-144出版社
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/157339909788166800
关键词
Diabetes; Mitochondria; Nitric Oxide; Oxygen; Uncoupling proteins; Oxidative stress
资金
- Swedish Research Council [9940, 10840]
- Marcus and Amalia Wallenberg Foundation
- Linne Foundation for Medical Research
- Swedish Diabetes Association
- Swedish Society for Medical Research
- National Institutes of Health (NIH/NIDDK) [R00DK077858]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R00DK077858] Funding Source: NIH RePORTER
The role of altered mitochondria function has recently emerged as an important mechanism for the development of diabetic complications. Altered mitochondria function has also been implicated in the ageing process, defective insulin secretion, hypertension, arteriosclerosis, ischemia-reperfusion injury and apoptosis. Normally, the mitochondria are associated with ATP production using primarily pyruvate as the substrate, but recent reports indicate that tissue specific preferences exist. Also, the mitochondria are a substantial source of superoxide production, preferentially during states of elevated intracellular glucose concentrations. The mitochondria function is regulated by several factors including nitric oxide, oxidative stress, mammalian target of rapamycin, ADP and Pi availability, which result in a complex regulation of ATP production and oxygen consumption, but also superoxide generation. These factors seem to be tissue specific, which warrants a more diverse mechanistic model applying to that specific tissue or cell type. This review presents the basic functions of the mitochondria and focuses on the complex interplay between oxidative stress, nitric oxide and uncoupling proteins in regulating mitochondria function with special focus on diabetes-induced alterations occurring on the mitochondria level.
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