NDLI: Mitochondrial function and dysfunction in exercise and insulin resistance.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Holloway, Graham P.
Description	Country affiliation: Canada Author Affiliation: Holloway GP ( Department of Human Health & Nutritional Sciences, University of Guelph, Guelph, ON N1G 2W1, Canada. ghollowa@uoguelph.ca)
Abstract	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.
File Format	HTM / HTML
ISSN	17155312
Issue Number	3
Volume Number	34
e-ISSN	17155320
Journal	Applied Physiology, Nutrition, and Metabolism
Language	English
Publisher	Canadian Science Publishing
Publisher Date	2009-06-01
Publisher Place	Canada
Access Restriction	Subscribed
Subject Keyword	Discipline Physiology Discipline Metabolism Discipline Nutritional Sciences Discipline Sports Medicine Exercise Physiology Insulin Resistance Mitochondria Energy Metabolism Fatty Acids Metabolism Humans Signal Transduction Journal Article Research Support, Non-u.s. Gov't Review
Content Type	Text
Resource Type	Article
Subject	Nutrition and Dietetics Physiology Endocrinology, Diabetes and Metabolism Physiology (medical) Sports Science

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