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Quantification of Monocyte Transmigration and Foam Cell Formation from Individuals with Chronic Inflammatory Conditions
Published on: October 17, 2017
Dietary trans fatty acids and composition of human atheromatous plaques
Ewa Stachowska1, Barbara Dołegowska, Dariusz Chlubek
1Dept. of Biochemistry & Chemistry, Pomeranian Medical University, al. Powstancow Wlkp 72, 70-111 Szczecin, Poland. ewast@sci.pam.szczecin.pl.
Abstract:
Dietary fatty acids are incorporated into atheromatous plaques mainly in the form of cholesterol esters. Physicochemical properties of the plaque (e. g. mechanical strength) depend on its fatty acid composition. Trans isomers of unsaturated fatty acids (TFA) are known to reduce the availability of fatty acid precursors for the synthesis of anticoagulant PG(1) and PG(3) prostaglandins. The present study was undertaken to determine the content of trans isomers in atheromatous plaques and to search for correlations between trans isomers in the plaque and adipose tissue. Atheromatous plaques 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 (GC) with an internal standard. Correlations were searched for with statistical methods, taking the level of significance as p < 0.05. We found spatial and positional isomers of sixteen- and eighteen-carbon fatty acids in plaques and adipose tissue, with elaidic acid (C18:1 trans-9) being the most abundant. Every plaque and adipose tissue sample contained linolelaidic acid (C18:2 trans-9 trans-12) which is derived exclusively from linoleic acid, as well as conjugated dienes of linoleic acid (CLA) produced during oxidative processes. The presence of trans isomers of fatty acids in the atheromatous plaque seems to be of relevance to plaque formation. Of much concern is the detection of elaidic and linolelaidic acids which adversely affect the physiologically important metabolism of eicosanoids. The TFA pool in adipose tissue has little effect on the amount of these acids in the atheromatous plaque. Apparently, the presence of TFA in atheromatous plaques is the result of processes taking place during plaque formation and maturation.
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