RESUMO
The earlier insulin-independent low-density lipoproteins and more late insulin-dependent very low-density lipoproteins implement different functions at the stages of phylogenesis. The disorder of biological function of trophology, alteration of fatty acids in triglycerides, prevalence of palmitic very low-density lipoproteins over oleic very low-density lipoproteins supply mitochondria of cells with non-optimal substrate - palmitic saturated fatty acid for gaining energy, ATP synthesis. Physiologically, cells implement oleic alternative of fatty acids metabolism, oxidizing mainly ω-9 endogenous oleic mono-unsaturated fatty acid. The pathology of low density lipoproteins is primary deficiency of poly-unsaturated fatty acids in cells, atherosclerosis and atheromotosis of intima of arteries of elastic type with development of dense plaques from poly-unsaturated fatty acids in the form of polyethers of cholesterol. The pathology of very low-density lipoproteins includes: a) syndrome of resistance to insulin; b) pathology of phylogenetically earlier insulin-independent visceral fatty tissue - metabolic syndrome; c) pathology of phylogenetically later insulin-dependent subcutaneous adipocytes - obesity; d) secondary atherosclerosis, under cumulation of palmitic low-density lipoproteins in blood with development of atherothrombosis of intima of arteries, soft plaques rich with triglycerides. As for the prevention of disorders of transfer of fatty acids to very low-density lipoproteins and low-density lipoproteins is common in many ways - minimization of aphysiological effect of surplus amount of food, biological function of diet. The prevention at the level of population includes: a) maximal limitation of content of palmitic saturated fatty acid in food; b) moderate increasing of polysaturated fatty acids, ω-3 poly-saturated fatty acids predominantly; c) increasing of physical activity. The pharmaceuticals are not provided by biology in primary prevention of metabolic pandemics under aphysiological impact of environment factors.
RESUMO
It is supposed that the main cause of insulin synthesis at late stages of phylogenesis became discrepancy between increase in vivo need in energy and physical chemical parameters of palmitic saturated fatty acid; its transportation to cells in composition of lipoproteins in optimal quantity (more than 15% of all fatty acids) became in vivo unfeasible. The biological role of insulin consists in supporting of insulin-dependent cells (skeletal miocytes in the first place) with substrates for gaining energy. The hormone transforms all palmitic saturated fatty acid endogenously synthesized from glucose into specific for animal cells rn-9 C18:1 oleic mono unsaturated fatty acid. The endogenous mono unsaturated fatty acid is oxidized by mitohondria with the highest constant of reaction velocity gaining for cells optimal quantity of biotransforming energy in the form of ATP. The insulin expresses in hepatocytes synthesis of oleic triglycerides and formation of oleic lipoproteins of very low density that only insulin-dependent cells absorb using apoE/B-100-endocytosis. The insulin expresses synthesis of Palmitoyl-KoA-elongase, stearyl-KoA-desaturase and glucose transporters 4, activates glucose absorption by cells with the purpose of synthesis endogenous oleic saturated fatty acid. The insulin substitutes in vivo ineffective palmitic alternative of metabolism of fatty acids for potentially more effective oleic metabolism of fatty acids. The insulin increases unsaturation of fatty acids and number of double binds in them. This can be established by direct titration of double binds by ozone on the basis of quantitative detection of fatty acids using technique of gas chromatography and calculating ratio C16:1/C16:0, C18:1/C18:0 and C18:1/C16:0. The diabetes mellitus is a disorder of metabolism of mono unsaturated fatty acid in the first place and only in the second place pathology of glucose absorption by cells.
