LIPOLYSIS IN VERY LOW DENSITY LIPOPROTEINS - LOCUS MINORIS RESISTENTIAE - IN THE PATHOGENESIS OF HYPERTRIGLYCERIDEMIA. POSITIVE EFFECTS OF DIET, POLYENIC FATTY ACIDS, STATINS AND FIBRATES
Autor: | V V Kukharchuk, M Yu Kotlovsky, V A Amelyshkina, T A Rozhkova, A V Yakimenko, V N Titov, E V Kurdoyak |
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Rok vydání: | 2019 |
Předmět: |
Very low-density lipoprotein
medicine.medical_specialty Lipolysis Probucol Lipoproteins VLDL Endocytosis Palmitic acid 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine In vivo Internal medicine medicine Humans Triglycerides Hypertriglyceridemia Chemistry Fatty Acids Biochemistry (medical) Fibric Acids General Medicine medicine.disease Diet Medical Laboratory Technology Endocrinology Thromboxanes lipids (amino acids peptides and proteins) Hydroxymethylglutaryl-CoA Reductase Inhibitors 030215 immunology medicine.drug |
Zdroj: | Russian Clinical Laboratory Diagnostics. 64:388-396 |
ISSN: | 0869-2084 |
Popis: | Inhibition of hydrolysis of palmitic and oleic triglycedires (TG) in very low density lipoproteins (VLDL), slow formation of active apoВ-100 conformation, blockade of апоЕ/В-100 ligand formation in VLDL and their reduced uptake by insulin-dependent cells cause hypertriglyceridemia (HTG). Palmitic and oleic VLDL (>80% total VLDL) are not converted in low density lipoproteins (LDL). Atherosclerosis is not an alimentary deficiency of polyenic fatty acids (PFA), but results from low in vivo bioavailability of PFA in LDL against the background of high dietary palmitic FA and palmitic LDL. Plasma PFA content and cellular PFA deficiency are as high as LDL cholesterol (CL). Primary prevention of atherosclerosis should be based on a decrease in dietary content of palmitic saturated FA, trans FA and a moderate increase in PFA. It seems highly unlikely that the xeobiotics statins, fibrates and probucol produce pleiotropic biological effects in vivo. These effects are brought about by phylogenetically early humoral mediators eicosanoids: prostacyclins, prostaglandins, thromboxanes, leukotrienes, and resolvins. It is reasonable to suggest that all preparations which act according to the same algorithm activate TG hydrolysis in VLDL and normalize cellular uptake of PFA in linoleic and linolenic LDL via apoВ-100 endocytosis. Atherosclerosis is a syndrome of cellular deficiency of essential polyenic FA. |
Databáze: | OpenAIRE |
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