title: [THE BECOMING IN PHYLOGENESIS OF TRANSFER IN INTERCELLULAR MEDIUM AND ACTIVE ABSORPTION OF POLYENOIC FATTY ACIDS BY CELLS SEQUENTIALLY OF HIGH DENSITY LIPOPROTEINS, LOW DENSITY LIPOPROTEINS AND HIGH DENSITY APOE-LIPOPROTEINS].
abstract: After more than half-century of different conceptions, the theory of general pathology was used to substantiate that all lipoproteins are bi-layer:lipid by their structure. The main function of high density lipoproteins as of all lipoproteins is transfer of fatty acids to cells and only in second turn taking away of spirit cholesterol from cells. At the stages of phylogenesis high density lipoproteins, low density lipoproteins and very low density lipoproteins began to function in a subsequent way. The fatty acids were transferred by low density lipoproteins in polar lipids at passive absorption by cells. Later on, lipoproteins transfer fatty acids in non-polar ethers with spirits glycerin and spirit cholesterol. The cells absorb them by receptor endocytosis. The hepatocytes secret in blood palmitic, oleic, linoleic and linoleic very low density lipoproteins. The palmitic and oleic very low density lipoproteins absorb physiologically insulin-dependent cells apoE/B-100 = endocytosis. The linoleic and linoleic very low density lipoproteins after transition of polyethers cholesterol from high density lipoproteins turn into low density lipoproteins. The cells absorb them by apoB-100 = endocytosis. The formation of chylomicrons occurs in blood and hepatocytes absorb them by the way of apoB/E-48 = endocytosis. The absorption of poly-unsaturated fatty acids by cells with apoB-100 = endocytosis form sensitivity of animals to exogenous hyper spirit cholesterol and absorption of poly-unsaturated fatty acids by apoE/A-I = receptors form corresponding resistance. The ApoE in lipoproteins form cooperative ligands--apoE/B-48 for chylomicrons, apoE/B-100 for very low density lipoproteins and apoE/A-I for high density lipoproteins. The chylomicrons in blood form apoB-48 from complexes of triglycerides secreted by enterocytes. These views change conceptions of pathogenesis and prevention of atherosclerosis, metabolic syndrome and resistance to insulin whose pathogenesis is unified by disorder of transfer in intercellular medium and absorption of fatty acids by cells.
authors.forename: V N
authors.initials: VN
authors.lastname: Titov
mesh_terms: D000818:Animals; D001055:Apolipoproteins B / Q000737:chemistry / Q000378:metabolism; D001057:Apolipoproteins E / Q000737:chemistry / Q000378:metabolism*; D050197:Atherosclerosis / Q000378:metabolism* / Q000473:pathology; D001692:Biological Transport; D002784:Cholesterol / Q000378:metabolism; D002788:Cholesterol Esters / Q000378:metabolism; D004705:Endocytosis; D020895:Enterocytes / Q000166:cytology / Q000378:metabolism; D005231:Fatty Acids, Unsaturated / Q000378:metabolism; D022781:Hepatocytes / Q000166:cytology / Q000378:metabolism; D006801:Humans; D007333:Insulin Resistance; D008075:Lipoproteins, HDL / Q000737:chemistry / Q000378:metabolism*; D008077:Lipoproteins, LDL / Q000737:chemistry / Q000378:metabolism*; D024821:Metabolic Syndrome / Q000378:metabolism* / Q000473:pathology; D014280:Triglycerides / Q000737:chemistry / Q000378:metabolism
chemical_list: D001055:Apolipoproteins B; D001057:Apolipoproteins E; D002788:Cholesterol Esters; D005231:Fatty Acids, Unsaturated; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D014280:Triglycerides; D002784:Cholesterol