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Current Pharmaceutical Design

Eiditor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Effects of Dietary Polyunsaturated Fatty Acids on Mitochondria

Author(s): S. Rohrbach

Volume 15 , Issue 36 , 2009

Page: [4103 - 4116] Pages: 14

DOI: 10.2174/138161209789909692

Price: $58

Abstract

Type and quantity of ingested dietary fat contribute to the onset and progression of chronic diseases such as diabetes, obesity or arteriosclerosis. Attention is increasingly focussing on effective therapies for these diseases as well as functional foods that impede the development of insulin resistance and obesity. Studies provided evidence showing polyunsaturated fatty acids of the omega-3 and the omega-6 families play beneficial roles in prevention and treatment of diseases as diverse as Alzheimers disease, cancer and cardiovascular diseases such as myocardial infarction, arrhythmia, atherosclerosis and hypertension. Strongest evidence is derived from in vitro experiments on cultured cells and animalbased studies, while the results from clinical studies are inconclusive. After ingestion, polyunsaturated fatty acids are distributed to cells and enriched in cellular membranes, where they influence cellular metabolism and survival. Polyunsaturated fatty acids are involved in various mitochondrial processes including mitochondrial calcium homeostasis, gene expression, respiratory function, ROS production and mitochondrial apoptosis. Therefore, mitochondria play a central role in the mechanisms underlying the protective effects of polyunsaturated fatty acids. The complex mechanisms involved in the effects of polyunsaturated fatty acid on mitochondrial actions depend on structural properties, cellular uptake, shuttling and metabolism, competition with intracellular stores as well as inherent properties of fatty acid metabolites. This review will summarize recent findings on the effects of various types of polyunsaturated fatty acids on mitochondria.

Keywords: n-3 PUFA, n-6 PUFA, calcium homeostasis, gene expression, mitochondrial function, reactive oxygen species, apoptosis


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