title: [THE LIPOLYSIS IN PHYLOGENETICALLY EARLY LIPOPROTEINS OF LOW DENSITY AND MORE LATER LIPOPROTEINS OF VERY LOW DENSITY: FUNCTION AND DIAGNOSTIC VALUE OF APOE AND APOC-III].
abstract: According to phylogenetic theory of general pathology, the function of low density lipoproteins (LDL) and hydrolysis of triglycerides (TG) in them under the effect of hepatic glycerol hydrolase apoC-III (HGH) developed at much earlier stages of phylogenesis than functioning of insulin-dependent phylogenetically late very low density lipoproteins (VLDL). For millions ofyears, lipolysis and HGH+apoC-III have activated transfer of polyenic fatty acids (FA) in the form of cholesteryl polyesters (CLE) from high density lipoproteins (HDL) to linoleic and linolenic LDL under the effect of cholesteryl ester transfer protein. It is reasonable to suggest that hepatocytes physiologically secrete oleic and palmitic VLDL and linoleic and linolenic LDL. Cells uptake ligand oleic and palmitic VLVL by apoE/B-100 receptor-mediated endocytosis. Physiologically, VLDL are not converted to LDL. If hepatocytes secrete palmitic VLDL in greater amounts than oleic VLDL upon slow hydrolysis ofpalmitic TG and under the effect of postheparinic lipoprotein lipase+apoC-II, only some proportion of palmitic TG is uptaken by cells as VLDL, and the rest is converted in ligand-free palmitic LDL These LDL increase plasma contents of TG and LDL-cholesterol and form small dense palmitic LDL. Expression of HGH+apoC-III synthesis compensates TG hydrolysis in nonphysiological palmitic LDL. In vivo, apoC-III is neither physiological no pathological inhibitor of lipolysis. Increase in plasma apoC-III content is an indicator of accumulation of non-physiological palmitic LDL and atherosclerosis-atheromatosis risk factor ApoE content ofpalmitic LDL increases together with apoC-III, i.e., apoE in ligand VLDL is not internalized via apoE/B-100 endocytosis. An increase in apoC-III and apoE contents are reliable in vivo tests for the rise inpalmitic FA, palmitic TG and excessive secretion of palmitic VLDL by hepatocytes. ApoC-III and apoE contents in LDL are additional tests to evaluate the efficiency of atherosclerosis prevention when physiological function of trophology and biological reaction of exotrophy are normalized.
authors.forename: T A
authors.initials: TA
authors.lastname: Rozhkova
authors.forename: V N
authors.initials: VN
authors.lastname: Titov
authors.forename: V A
authors.initials: VA
authors.lastname: Amelyushkina
authors.forename: S I
authors.initials: SI
authors.lastname: Kaba
authors.forename: V V
authors.initials: VV
authors.lastname: Kukhartchuk
mesh_terms: D053305:Apolipoprotein C-III / Q000097:blood*; D001057:Apolipoproteins E / Q000097:blood*; D050197:Atherosclerosis / Q000097:blood / Q000175:diagnosis*; D005075:Biological Evolution; D005227:Fatty Acids / Q000097:blood; D022781:Hepatocytes / Q000378:metabolism; D006801:Humans; D008066:Lipolysis; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood*; D008079:Lipoproteins, VLDL / Q000097:blood*; D008099:Liver / Q000378:metabolism; D008994:Monoacylglycerol Lipases / Q000378:metabolism; D010802:Phylogeny; D014280:Triglycerides / Q000097:blood
chemical_list: D053305:Apolipoprotein C-III; D001057:Apolipoproteins E; D005227:Fatty Acids; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; D014280:Triglycerides; D008994:Monoacylglycerol Lipases