Exchange of unsaturated fatty acids between adipose tissue and atherosclerotic plaque studied with artificial neural networks.

摘要

The linoleic C18:2 (n-6) and linolenic C18:3 (n-3) are recognized as essential components of the diet. Free radical peroxidation of essential fatty acids (EFAs) present in lipoproteins produces oxidized low-density lipoproteins which play a critical role in the development of atherosclerosis. The accumulation of EFAs in the vascular wall and correlations between their content in the adipose tissue and atherosclerotic plaque have been confirmed. The present study was undertaken to determine the usefulness of a neural network for studying the exchange between tissues of linoleic, alpha-linolenic, and arachidonic acids-three fatty acids with a well-understood metabolism. Atheromatous plaques, adipose tissue, and serum were obtained from 31 patients who underwent surgery due to atherosclerotic stenosis of the abdominal aorta, iliac or femoral arteries. Fatty acids were extracted and separated as methyl esters using gas chromatography. Statistical analysis was done with STATISTICA neural networks package. Several correlations reported previously were corroborated and factors modifying the content of individual EFAs in adipose tissue and atherosclerotic plaque were revealed. Artificial neural networks (ANNs) were used to determine factors modifying the content of linoleic, alpha-linolenic, and arachidonic acids in human atheromatous plaques. The mechanism of exchange of some fatty acids between the adipose tissue, atheromatous plaque, and plasma is discussed. The results provide evidence for an effective mechanism of tissue uptake and turnover of linoleic acid. Reduced plasma levels of this acid are compensated by release from adipose tissue and atheromatous plaque. While alpha-linolenic acid is continuously taken up by the plaque, adipose tissue absorbs this acid to a certain level only. The dynamics of exchange of arachidonic acid between adipose tissue and atheromatous plaque reflects a minor role for adipose tissue in determining plaque content of this acid, suggesting that "de novo" synthesis is the chief source of arachidonic acid in plaques.