Prevention of mitochondrial oxidative damage as a therapeutic strategy in diabetes.

TitlePrevention of mitochondrial oxidative damage as a therapeutic strategy in diabetes.
Publication TypeJournal Article
Year of Publication2004
AuthorsGreen, K, Brand, MD, Murphy, MP
JournalDiabetes
Volume53 Suppl 1
PaginationS110-8
Date Published2004 Feb
ISSN0012-1797
KeywordsAnimals, Antioxidants, Diabetes Mellitus, Humans, Mitochondria, Oxidative Stress, Oxygen Consumption, Reactive Oxygen Species, Superoxides
Abstract

Hyperglycemia causes many of the pathological consequences of both type 1 and type 2 diabetes. Much of this damage is suggested to be a consequence of elevated production of reactive oxygen species by the mitochondrial respiratory chain during hyperglycemia. Mitochondrial radical production associated with hyperglycemia will also disrupt glucose-stimulated insulin secretion by pancreatic beta-cells, because pancreatic beta-cells are particularly susceptible to oxidative damage. Therefore, mitochondrial radical production in response to hyperglycemia contributes to both the progression and pathological complications of diabetes. Consequently, strategies to decrease mitochondrial radical production and oxidative damage may have therapeutic potential. This could be achieved by the use of antioxidants or by decreasing the mitochondrial membrane potential. Here, we outline the background to these strategies and discuss how antioxidants targeted to mitochondria, or selective mitochondrial uncoupling, may be potential therapies for diabetes.

DOI10.2337/diabetes.53.2007.s110
Alternate JournalDiabetes
Citation Key10.2337/diabetes.53.2007.s110
PubMed ID14749275