[Formation in the phylogenesis of three pulls of cells with expressed different absorption and metabolism of fatty acids. Insulin and medium chains fatty acids.]

Somatic cells at the early stages of phylogenesis realized the metabolism of long-chain fatty acids (FA), primarily palmitic saturated FA. It dominated the construction of a bilayer cell membrane and as a substrate for oxidation in mitochondria during energy production. Later, polyene FAs became involved in the construction of the cell membrane, the membranes of intracellular organelles, and became the substrate for the synthesis of biologically active eicosanoids. At later stages of phylogenesis, the metabolism of medium-chain FAs is activated and the formation of ketone bodies as a substrate, which is available for oxidation by the mitochondria of the formed cells of the nervous tissue in the absence of first substrate glucose. In the later stages of phylogenesis, insulin initiated: a) the transformation of carnivorous ancestors of the species Homo sapiens in the ocean into a herbivorous species while living on land; b) the formation of the new biological function of locomotion and c) the dominance of the oleic variant of the metabolism of long-chain fatty acids with higher kinetic parameters of mitochondria oxidation. Metabolites of medium chain FA have become humoral mediators of metabolism and the formation of feedback mechanisms in the function of trophology and cognitive biological function. The formation of an oleic variant of the metabolism of fatty acids under the action of insulin led to the improvement of the energy supply of cells and the high kinetic parameters of many species of herbivorous mammals, including Homo sapiens. The species Homo sapiens was not omnivorous (Omnivores); the insulin's regulatory action during life on land has turned it into a herbivorous species (Herbivore), but with a carnivorous (Carnivore) (fish-eating) past. Seven metabolic pandemics (1. atherosclerosis and atheromatosis; 2. metabolic arterial hypertension; 3. metabolic syndrome; 4. insulin resistance syndrome; 5. obesity; 6. nonalcoholic fatty liver disease and 7. endogenous hyperuricemia) are only functional disorders and can be, in most cases, eliminated. From the standpoint of the phylogenetic theory of general pathology, atherosclerosis and atheromatosis of the arteries have no great future. As soon, as the majority of individuals of the Homo sapiens species realize that in phylogenesis they have formed as herbivores and stop eating excessive amounts of meat food, exogenous palmitic FA, the incidence in the population will begin to decrease. Patients are still obliged to justify the binary, biological name of the species - reasonable man. Prevention and other metabolic pandemics, diseases of civilization, can be discussed. It takes time, an understanding of what happens by the doctors, diligence and the desire of patients to be healthy.

[The insulin initiates "kinetic perfection" of biologic function of locomotion. The glucose as substratum for synthesis of ω-9 oleic fatty acid by cross-striated miocytes.]

The phylogenesis theory affords ground for the following propositions. 1. There is no absorption of glucose from intercellular medium by cells in vivo until there is possibility to absorb polar fatty acids from associates with albumin. 2. The late in phylogenesis humoral insulin regulates no stages of glucose metabolism; they are completed a billion years before hormone synthesis. 3. The phylogenetically late insulin is "hostage" of biological function of trophology, function of nutrition, biological reaction of exotrophy; it has no possibility to decrease in food excessed amount of physiologic palmitic saturated fatty acids with low kinetic parameters of ß-oxidation in mitochondria. 4. The early in phylogenesis, resistant organizational to insulin pool of visceral fatty cells of omentum and late pool of insulin-dependent adipocytes are different in many functional parameters. 5. All "metabolic pandemics" such as syndrome of resistance to insulin, atherosclerosis, metabolic arterial hypertension, metabolic syndrome and obesity are primarily pathologies of fatty acids. 6. All "metabolic pandemics" are pathologies of one biological function, function of locomotion under single algorithm of formation of their pathogenesis. 7. The etiological factor of "metabolic pandemics" is uniform - effect of environmental factors in form of disorder of biological function of trophology, function of nutrition; aphysiological excess content in food of palmitic saturated fatty acid, aphysiological trans-forms of fatty acids and ω-7-palmitoleic mono unsaturated fatty acid. The insulin activates absorption by myocytes, cardiomyocytes of glucose as substrate of synthesis out of it in situ de novo ω-9 oleic mono unsaturated fatty acid. With such physical chemical parameters that mitochondria oxidize it with the most high constant of velocity of reaction and high effectiveness of formation of ATP.

[The difference of conformation of apoB-100 in lipoproteins of low and very low density. The modified lipoproteins and destructive inflammation in intima of arteries: a lecture].

The formation of ligand occurs in phylogenetically earlier lipoproteins of very low density and later lipoproteins of very low density when apoB- 100 takes active conformation in association with essential polyenoic fatty acids, in form of ethers with alcohol cholesterol, palmitic and oleic triglycerides. In lipoproteins of low density apoB-100-domain-ligand is formed, in lipoproteins of very low density apoE/B-100-ligand is formed. The ligand lipoproteins absorb cells using apoE/B-100 and apoB-100 receptor endocytosis. In cases of excess of palmitic triglycerides. and lipoproteins of very low density of the same name in blood, damage of primary structure of post-heparin, hepatic lipoprotein lipase and co-enzymes apoC-II and apoC-II, phenotype E2/E2 blood accumulates pre-ligand lipoproteins rich in triglycerides. In case of pathology of apoB-100-receptor post-ligand lipoproteins of low density with low content of triglycerides are cumulated. All non-ligand lipoproteins in a physiological way denature neutrophils. The presence of pathology induces modification in case of action of other agents (glyco-toxins). The pre-lipoproteins form in the intima of arteries soft voluminous plaques and such destructive inflammatory process as athero-thrombosis. The post-lipoproteins form flat plaques and destructive inflammatory atheromatosis. The atherosclerosis can be labeled as disease ofconformation. The surplus of palmitic saturated fatty acids in food, phenotype E2/E2 and deletion of gene apoB-100-receptor are causes of intima lesion. The non-ligand lipoproteins form destructive process, dying foam cells and macrophages--inflammatory component. The atheromatosis is a result of realization of biological function of endoecology, support of "purity" of intercellular medium.