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Abstract:
Dietary fatty acids and cholesterol have been associated with the development of atherosclerosis. This paper suggest metabolic pathways involved in this process. Specific fatty acids (DGLA, GLA) with high specificity for cholesterol transport enzymes give a high efficiency for transport of cholesterol to the liver. Arachidonic acid (AA) is proposed to block the endogenous conversion of dietary linoleic acid to GLA and DGLA, which results in impared cholesterol transport to the liver and increased serum levels. Increased levels of cholesterol and its oxygenation products promote the release of AA from membrane phospholipids and its conversion to thromboxane, resulting in a positive feedback reaction of thrombus formation and ischemia.