Abstract
Insulin resistant individuals manifest multiple disturbances in free fatty acids metabolism and have excessive lipid accumulation in insulin-target tissues. A wide range of evidence suggests that defective muscle mitochondrial metabolism, and subsequent impaired ability to oxidize fatty acids, may be a causative factor in the accumulation of intramuscular lipid and the development of insulin resistance. Such mitochondrial dysfunction includes loss of mitochondria, defects in the mitochondrial OXPHOS system and decreased rate of ATP synthesis. Stimulation of mitochondrial biogenesis appears as a strategy for the clinical management of the metabolic syndrome, by enhancing mitochondrial activity and protecting the cell against the increased flux of reduced substrates to the electron transport chain and thus reducing metabolic inflammation.
Keywords: Metabolic diseases, SIRT1, AMPK, PGC-1α, mitochondria, biogenesis, oxidative phosphorylation, cellular metabolism, high-fat diets, obesity
Current Drug Targets
Title: Regulation of Mitochondrial Biogenesis in Metabolic Syndrome
Volume: 12 Issue: 6
Author(s): Anabela P. Rolo, Ana P. Gomes and Carlos M. Palmeira
Affiliation:
Keywords: Metabolic diseases, SIRT1, AMPK, PGC-1α, mitochondria, biogenesis, oxidative phosphorylation, cellular metabolism, high-fat diets, obesity
Abstract: Insulin resistant individuals manifest multiple disturbances in free fatty acids metabolism and have excessive lipid accumulation in insulin-target tissues. A wide range of evidence suggests that defective muscle mitochondrial metabolism, and subsequent impaired ability to oxidize fatty acids, may be a causative factor in the accumulation of intramuscular lipid and the development of insulin resistance. Such mitochondrial dysfunction includes loss of mitochondria, defects in the mitochondrial OXPHOS system and decreased rate of ATP synthesis. Stimulation of mitochondrial biogenesis appears as a strategy for the clinical management of the metabolic syndrome, by enhancing mitochondrial activity and protecting the cell against the increased flux of reduced substrates to the electron transport chain and thus reducing metabolic inflammation.
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Cite this article as:
P. Rolo Anabela, P. Gomes Ana and M. Palmeira Carlos, Regulation of Mitochondrial Biogenesis in Metabolic Syndrome, Current Drug Targets 2011; 12 (6) . https://dx.doi.org/10.2174/138945011795529056
DOI https://dx.doi.org/10.2174/138945011795529056 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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