title: [THE SPIRIT CHOLESTEROL, BIOLOGICA L ROLE AT STAGES OF PHYLOGENESIS, MECHANISMS OF INHIBITION OF SYNTHESIS OF STEROL BY STATINS, FACTORS OF PHARMACOGENOMICS AND DIAGNOSTIC SIGNIFICANCE OF CHOLESTEROL OF LIPOPROTEINS OF LOW DENSITY].
abstract: The hypolipidemic effect of statins is realized by inhibition of synthesis of local pool of cholesterol spirit in endoplasmic net of hepatocytes. The cholesterol spirit covers all hydrophobic medium of triglycerides with polar mono layer of phosphatidylcholines and cholesterol spirit prior to secretion of lipoproteins of very low density into hydrophilic medium. The lesser mono layer between lipase enzyme and triglycerides substrate contains of cholesterol spirit the higher are the parameters of hydrolysis of palmitic and oleic lipoproteins of very low density. The sequence of effect of statins is as follows: blocking of synthesis in hepatocytes and decreasing of content of unesterified cholesterol spirit in blood plasma; activation of hydrolysis of triglycerides in palmitic and oleic lipoproteins of very low density; formation of ligand lipoproteins of very low density and their absorption by cells by force of apoB-100 endocytosis; decreasing in blood of content of polyenoic fatty acids, equimolar esterified by cholesterol spirit, polyethers of cholesterol spirit and decreasing of level of cholesterol spirit-lipoproteins of very low density. There is no way to eliminate aphysiological effect of disordered biological function of trophology (nutrition) on metabolism of fatty acids in population by means of pharmaceuticals intake. It is necessary to eliminate aphysiological effect of environment. To decrease rate of diseases of cardiovascular system one has to decrease in food content of saturated fatty acids and in the first instance palmitic saturated fatty acid, trans-form fatty acid, palmitoleic fatty acids up to physiological values and increase to the same degree the content of polyenoic fatty acids. The saturated fatty acids block absorption of polyenoic fatty acids by cells. The atherosclerosis is a deficiency of polyenoic fatty acids under surplus of palmitic saturated fatty acid.
authors.forename: V N
authors.initials: VN
authors.lastname: Titov
authors.forename: M Yu
authors.initials: MY
authors.lastname: Kotlovskii
authors.forename: A A
authors.initials: AA
authors.lastname: Pokrovskii
authors.forename: O S
authors.initials: OS
authors.lastname: Kotlovskaia
authors.forename: A V
authors.initials: AV
authors.lastname: Osedko
authors.forename: N M
authors.initials: NM
authors.lastname: Titova
authors.forename: Yu V
authors.initials: YV
authors.lastname: Kotlovskii
authors.forename: A M
authors.initials: AM
authors.lastname: Digaii
mesh_terms: D000818:Animals; D008078:Cholesterol, LDL / Q000096:biosynthesis / Q000737:chemistry / Q000235:genetics; D005227:Fatty Acids / Q000737:chemistry / Q000378:metabolism; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000493:pharmacokinetics / Q000494:pharmacology; D010597:Pharmacogenetics
chemical_list: D008078:Cholesterol, LDL; D005227:Fatty Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors