Current Drug Targets

Francis J. Castellino
Kleiderer-Pezold Professor of Biochemistry
Director, W.M. Keck Center for Transgene Research
Dean Emeritus, College of Science
230 Raclin-Carmichael Hall, University of Notre Dame
Notre Dame, IN 46556


Regulation of Mitochondrial Biogenesis in Metabolic Syndrome

Author(s): Anabela P. Rolo, Ana P. Gomes and Carlos M. Palmeira

Affiliation: Center for Neurosciences and Cell Biology, Department of Life Sciences, University of Coimbra, 3001-401 Coimbra, Portugal.


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

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Article Details

Page: [872 - 878]
Pages: 7
DOI: 10.2174/138945011795529056