Document Detail


Mitochondrial function and dysfunction in exercise and insulin resistance.
MedLine Citation:
PMID:  19448712     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fatty acid translocase (FAT/CD36) represents a novel flexible regulatory system, influencing rates of mitochondrial fatty acid metabolism in both human and rodent skeletal muscle. During exercise, the subcellular redistribution of FAT/CD36 provides a mechanism to increase not only plasma membrane fatty acid transport, but also mitochondrial fatty acid oxidation. This FAT/CD36-mediated coordination of long chain fatty acid (LCFA) transport and oxidation is an intriguing model in the context of insulin resistance. It was believed for almost a decade that reductions in fatty acid oxidation increased intramuscular lipids, thereby contributing to insulin resistance. A reduction in mitochondrial content may reduce the capacity of skeletal muscle LCFA oxidation; however, work from my laboratory has shown that, in some insulin-resistant muscles, mitochondrial content and fatty acid oxidation are both increased, yet these muscles accumulate lipids because of a considerably greater increase in fatty acid transport. Therefore, an alternative model is being considered, in which the balance between LCFA uptake and oxidation is a determining factor in the development of insulin resistance. A permanent redistribution of the LCFA transport protein FAT/CD36 to the sarcolemmal has been consistently found, which results in an increased rate of LCFA transport. This work suggests that the accumulation of skeletal muscle lipids, regardless of changes in mitochondria, is attributable to an increased rate of LCFA transport that exceeds the capacity for oxidation.
Authors:
Graham P Holloway
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Applied physiology, nutrition, and metabolism = Physiologie appliquée, nutrition et métabolisme     Volume:  34     ISSN:  1715-5312     ISO Abbreviation:  -     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-05-18     Completed Date:  2009-07-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101264333     Medline TA:  Appl Physiol Nutr Metab     Country:  Canada    
Other Details:
Languages:  eng     Pagination:  440-6     Citation Subset:  IM    
Affiliation:
Department of Human Health & Nutritional Sciences, University of Guelph, Guelph, ON N1G 2W1, Canada. ghollowa@uoguelph.ca
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MeSH Terms
Descriptor/Qualifier:
Energy Metabolism
Exercise / physiology*
Fatty Acids / metabolism
Humans
Insulin Resistance / physiology*
Mitochondria / physiology*
Signal Transduction
Chemical
Reg. No./Substance:
0/Fatty Acids

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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