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Update on lipids andmitochondrialfunction William C. StanleyRamzi J. KhairallahErinne R. Dabkowski2012 год

Update on lipids and mitochondrial function
review

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Аннотация: Purpose of review Recent evidence has linked n-3 polyunsaturated fatty acid (PUFA) supplementation with dramatic alterations of mitochondrial phospholipid membranes and favorable changes in mitochondrial function. In the present review, we examine the novel effects of n-3 PUFA on mitochondria, with an emphasis on cardiac mitochondrial phospholipids. Recent findings There is growing evidence that dietary n-3 PUFA, particularly docosahexaenoic acid (DHA), has profound effects on mitochondrial membrane phospholipid composition and mitochondrial function. Supplementation with n-3 PUFA increases membrane phospholipid DHA and depletes arachidonic acid, and can increase cardiolipin, a tetra-acyl phospholipid that is unique to mitochondrial and essential for optimal mitochondrial function. Recent studies show that supplementation with DHA decreases propensity for cardiac mitochondria to undergo permeability transition, a catastrophic event often leading to cell death. This finding provides a potential mechanism for the cardioprotective effect of DHA. Interestingly, other n-3 PUFAs that modify membrane composition to a lesser extent have substantially less of an effect on mitochondria and do not appear to directly protect the heart. Summary Current data support a role for n-3 PUFA supplementation, particularly DHA, on mitochondria that are strongly associated with changes in mitochondrial phospholipid composition.
Год издания: 2012
Авторы: William C. Stanley, Ramzi J. Khairallah, Erinne R. Dabkowski
Издательство: Lippincott Williams & Wilkins
Источник: Current Opinion in Clinical Nutrition & Metabolic Care
Ключевые слова: Fatty Acid Research and Health, Lipid metabolism and biosynthesis, Mitochondrial Function and Pathology
Другие ссылки: Current Opinion in Clinical Nutrition & Metabolic Care (HTML)
Europe PMC (PubMed Central) (PDF)
Europe PMC (PubMed Central) (HTML)
PubMed Central (HTML)
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