title: [The carrier protein of cholesterol ethers: the physical chemical characteristics, functions, role in pathogenesis of atherosclerosis and grounds for inhibition (a lecture)].
abstract: The first function of carrier protein of cholesterol ethers in phylogenesis was passive transfer of polar diglycerides from lipoproteins of very low density to lipoproteins of very high density to proceed with hydrolysis. At the later degrees, carrier protein of cholesterol ethers initiated reverse transfer of polyenoic fatty acids from lipoproteins of very high density to lipoproteins of very low density in form of polyenoic ethers with spirit cholesterol. This occurrence became a stage of transfer and active absorption by cells polyenoic fatty acids using apoB-100 receptor endocytosis in lipoproteins of very low density. Later on, in phylogenesis under mutation of carrier protein of cholesterol ethers null cells began compensatory absorb polyenoic fatty acids in lipoproteins of very high density by force of apoE/A-I endocytosis. In certain percentage of species of animals (primates, rabbits) and humans the cells absorb polyenoicfatty acids byforce of apoB-100 endocytosis. In other species (rats and mice) the cells absorb polyenoic fatty acids through apoE/A = I receptors. In animals, under first receptor absorption of polyenoic fatty acids by cells it is easy to reproduce atherosclerosis and atheromatosis on the model of exogenous hypercholesterolemia and it is practically impossible in second case. The absence in vivo of lipoproteins of very high density and triple associate of lipoproteins of very high density + carrier protein of cholesterol ethers + lipoproteins of very low density is followed by increasing of spirit cholesterol-lipoproteins of very high density and decreasing of content of spirit cholesterol-lipoproteins of very low density as risk factors of human atherosclerosis. This occurrence served as foundation for proposal to apply blockers of action of carrier protein of cholesterol ethers in patients with atherosclerosis. The main function of lipoproteins of very high density as of all lipoproteins is to transfer fatty acids to cells and only in second instance to transfer from all cells spirit cholesterol in the form of mono-ethers cholesterol. Only results of clinical studies will demonstrate the effectiveness of compensatory apoE/A-I receptor endocytosis of lipoproteins of very low density in comparison with physiological apoB-100 endocytosis.
authors.forename: V N
authors.initials: VN
authors.lastname: Titov
mesh_terms: D053299:Apolipoprotein B-100 / Q000378:metabolism*; D050197:Atherosclerosis / Q000378:metabolism* / Q000473:pathology; D002784:Cholesterol / Q000378:metabolism*; D005227:Fatty Acids / Q000378:metabolism*; D006801:Humans; D006937:Hypercholesterolemia / Q000378:metabolism / Q000473:pathology; D008074:Lipoproteins / Q000378:metabolism*; D008075:Lipoproteins, HDL / Q000378:metabolism; D008079:Lipoproteins, VLDL / Q000378:metabolism
chemical_list: D053299:Apolipoprotein B-100; D005227:Fatty Acids; D008074:Lipoproteins; D008075:Lipoproteins, HDL; D008079:Lipoproteins, VLDL; C030104:lipoprotein cholesterol; C026277:very high density lipoproteins; D002784:Cholesterol