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№2' 2015

CARDIOLOGY

International Medical Journal, Vol. 21., Iss. 2, 2015, P. 5−14.


THE ROLE OF PALMITIC FATTY ACID IN INITIATION OF HYPERTRIGLYCERIDEMIA, HYPERCHOLESTEROLEMIA, ATHEROSCLEROSIS, AND ATHEROMATOSIS


Titov V. N., Rozhkova T. A., Amelyushkina V. A., Kukharchuk V. V.

Russian Cardiology Research−and−Production Center, Ministry of Health, Moscow, Russian Federation

Phylogenetically, at early stages high density lipoproteins (HDL) are initial transporters of all fatty acids (FA) to cells, later unsaturated and polyenic FA (PFA) are transported by low density lipoproteins (LDL). Insulin−dependent cells absorb palmitic saturated acid (SFA), oleic monounsaturated FA (MFA) and oleic triglycerides (TG) in very low density lipoproteins (VLDL). Hepatocytes separately secrete palmitic, oleic and linolenic VLDL. After hydrolysis of TG in the circulation, cells uptake ligand palmitic and oleic VLDL by apoЕ/В−100 endocytosis, i.e., these TG are not converted into LDL. Under the effect of cholesteryl ester transfer protein, PFA from HDL are transported to linoleic VLDL as cholesterol (CL) polyesters and convert VLDL into linolenic LDL which are taken up by cells via apoВ−100 endocytosis. Physiologically, the amount of oleic VLDL is always greater than that of palmitic VLDL. In insulin resistance (IR) syndrome, palmitic SFA produced de novo from glucose is not converted into oleic MFA. Hepatocyte secrete predominantly palmitic VLDL, the amount of which is greater than that of oleic VLDL. As a result of slow hydrolysis in the blood the major proportion of palmitic VLDL is converted into palmitic LDL. These LDL initiate hyperlipidemia, lower HDL−CL, reduce bioavailability of PFA, and trigger atherosclerosis with formation of atheromatosis in arterial intima. Nonphysiological effect of excessive palmitic acid and palmitic TG in vivo cannot be abolished by statins and increased dietary ?−3 PFA content, which can be effective only in prevention of hyperlipidemia, atherosclerosis, coronary atheromatosis, coronary heart disease and myocardial infarction.

Key words: palmitic fatty acid, hypertriglyceridemia, low density lipoprotein cholesterol, atherosclerosis, atheromatosis.


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