Является ли человек всеядным? Биологически это невозможно; Homo sapiens - травояден. В филогенезе же предки человека при жизни в океане, были плотоядными, рыбоядными. В филогенезе, мы полагаем, последовательно с интервалами в миллионы лет сформировались 3 системы переноса к клеткам жирных кислот в форме неполярных триглицеридов в составе апоВ липопротеинов.1. У плотоядных (Carnivore) в океане и на суше: энтероциты, апоЕ/В-48 ХМ→ гепатоциты→ апоВ-100 ЛПОНП→ ЛПНП→ апоВ-100 эндоцитоз. 2. У травоядных (Herbivore), до синтеза инсулина: перенос химически инертной пальмитиновой насыщенных жирных кислот по пути: гепатоциты→ пальмитиновые ЛПОНП→ ЛПНП→ апоВ-100 поглощение клетками. 3. У травоядных (Herbivore) при действии инсулина, перенос химически активной олеиновой мононенасыщенной жирной кислоты наиболее короткий: гепатоциты→ олеиновые ЛПОНП→ апоЕ/В-100 эндоцитоз инсулинзависимыми клетками. На ступенях филогенеза; 1. у плотоядных, 2. у травоядных до синтеза инсулина и 3. у травоядных при действии инсулина: 1. ХМ→ пальмитиновые ЛПОНП→ ЛПНП→ апоВ-100 эндоцитоз; 2. пальмитиновые ЛПОНП→ ЛПНП→апоВ-100 эндоцитоз и 3. олеиновые ЛПОНП→ апоЕ/В-100 эндоцитоз, видно, почему олеиновые ЛПОНП не могут переносить пальмитиновые ЛПОНП с иными физико-химическими свойствами. В инсулинзависимой системе переноса олеиновой мононенасыщенной жирной кислоты, триглицериды задействованы только ЛПОНП и нет ЛПНП. При избытке плотоядной (мясной) пищи и пальмитиновой насыщенной жирной кислоты НЖК клетки не поглощают безлигандные пальмитиновые ЛПОНП→ЛПНП путем апоЕ/В-100 эндоцитоза. Формирование у пациента переноса насыщенных жирных кислот до действия инсулина объективизирует гиперлипопротеинемия (ГЛП) типа IIб. При избыточном потреблении мясной пищи и формировании переноса насыщенных жирных кислот, что характерно для плотоядных, у пациентов выявляется методом электрофореза гиперлипопротеинемия типа V. Атеросклероз и атероматоз, хотя и имеют общие звенья патогенеза, являются биологически разными, последовательными процессами, нарушением биологической функции трофологии и функции эндоэкологии.

Является ли человек всеядным? Биологически это невозможно; Homo sapiens - травояден. В филогенезе же предки человека при жизни в океане, были плотоядными, рыбоядными. Предполагается, что в филогенезе последовательно с интервалами в миллионы лет сформировались 3 системы переноса к клеткам жирных кислот в форме неполярных триглицеридов в составе апоВ липопротеинов. 1. У плотоядных (Carnivore) в океане и на суше: энтероциты, апоЕ/В-48 хиломикроны → гепатоциты→ апоВ-100 ЛПОНП→ ЛПНП→ апоВ-100 эндоцитоз. 2. У травоядных (Herbivore), до синтеза инсулина перенос химически инертной пальмитиновой насыщенных жирных кислот осуществлялся по пути: гепатоциты→ пальмитиновые ЛПОНП→ ЛПНП→ апоВ-100 поглощение клетками. 3. У травоядных (Herbivore) при действии инсулина перенос химически активной олеиновой мононенасыщенной жирной кислоты представлял наиболее короткий путь: гепатоциты→ олеиновые ЛПОНП→ апоЕ/В-100 эндоцитоз инсулинзависимыми клетками. На ступенях филогенеза; 1. у плотоядных, 2. у травоядных до синтеза инсулина и 3. у травоядных при действии инсулина: 1. хиломикроны → пальмитиновые ЛПОНП→ ЛПНП→ апоВ-100 эндоцитоз; 2. пальмитиновые ЛПОНП→ ЛПНП→апоВ-100 эндоцитоз и 3. олеиновые ЛПОНП→ апоЕ/В-100 эндоцитоз, видно, почему олеиновые ЛПОНП не могут переносить пальмитиновые ЛПОНП с иными физико-химическими свойствами. В инсулинзависимой системе переноса олеиновой мононенасыщенной жирной кислоты, триглицериды задействованы только ЛПОНП и нет ЛПНП. При избытке плотоядной (мясной) пищи и пальмитиновой насыщенной жирной кислоты НЖК клетки не поглощают безлигандные пальмитиновые ЛПОНП→ЛПНП путем апоЕ/В-100 эндоцитоза. Формирование у пациента переноса насыщенных жирных кислот до действия инсулина объективизируется по уровню гиперлипопротеинемии (ГЛП) типа IIб. При избыточном потреблении мясной пищи и формировании переноса насыщенных жирных кислот, что характерно для плотоядных, у пациентов методом электрофореза выявляется гиперлипопротеинемия типа V. Атеросклероз и атероматоз, хотя и имеют общие звенья патогенеза, являются биологически разными, последовательными процессами, отражающими нарушение биологической функции трофологии и функции эндоэкологии. Is the human being an omnivore? Biologically, this is impossible. Homo sapiens is the herbivore. However phylogenetically, ocean-living ancestors of people were fish-eating carnivores. We suggest that three systems of fatty acid (FA) transport to cells have formed successively, at several million-year intervals, in the form of nonpolar triglycerides (TG) as constituents of apoB lipoproteins (LP): i) in the carnivores, both in the ocean and on land: enterocytes → apoВ-100 VLDL → LDL → apoВ-100 endocytosis; ii) in herbivores prior to insulin production: transport of chemically inert palmitic FA along the hepatocytes → palmitic VLDL→ LDL→ apoВ-100 cellular uptake pathway; iii) in herbivores under the action of insulin, the transport pathway for chemically active oleic FA is the shortest: hepatocytes→ oleic VLDL→ apoЕ/В-100 endocytosis by insulin-dependent cells. Thus, oleic VLDL cannot transport palmitic TG that have different physico-chemical parameters. In the insulin-dependent transport of oleic FA, TG are associated only with VLDL but not with LDL. When the diet is rich in meat and palmitic saturated FA cells do not internalize nonligand palmitic VLDL→LDL via apoЕ/В-100 endocytosis; physiologically, this endocytosis does not exist. In type IIb hyperlipoproteinemia, saturated FA are transported before the effect of insulin. If a patient eats excessive meat, transport of saturated FA follows the pathway typical of carnivore animals, which results in type V hyperproteinemia as detected by LP electrophoresis. Although atherosclerosis and atheromatosis share some pathogenetic features they are biologically different processes associated with impaired biological functions of trophology and endoecology.

The effect of statins occur in several stages: 1) inhibition in hepatocytes of synthesis of functionally specific pool of spirit cholesterol, polar mono-layer of lipoproteins of very low density; 2)activation of hydrolysis of triglycerides in lipoproteins of very low density, formation of apoE/B-100-ligand and absorption of lipoproteins of very low density by insulin-depended cells; 3) decreasing of content of and spirit cholesterol-lipoproteins of very low density in blood plasma; 4) activation of hydrolysis of triglycerides in lipoproteins of low density, formation of apoB-100-ligand and absorption of lipoproteins of low density by insulin-independent cells; 5) decreasing of level of and increasing of content of lipoproteins of high density. During first weeks of effect of statins occurs decreasing of concentration of triglycerides and unesterified spirit cholesterol-lipoproteins of very low density in blood plasma. Then, slower and more durational decreasing of level of spirit cholesterol-lipoproteins of low density occurs. The value of spirit cholesterol-lipoproteins of low density is primarily determined by content of palmitic saturated fatty acid in food, its endogenous synthesis from glucose and concentration of palmitic triglycerides and lipoproteins of very low density of the same name in blood plasma. The effect of preparations is biologically valid and corresponds to alternative hypolipidemic preparations. All these preparations have an effect following a common algorithm: they activate, using different mechanisms, receptor absorption of lipoproteins of very low density or lipoproteins of low density by cells. The level of spirit cholesterol-lipoproteins of low density in full measure depends on content of triglycerides in blood. The concentration ofspirit cholesterol in blood plasma has a reliable diagnostic significance only under physiological content of triglycerides. The main criterion of diagnostic and control of hypolipidemic therapy biologically is content of triglycerides. The comprehension of differences in effect of hypolipidemic preparations within framework of common algorithm permits rationally combine them under treatment of both primary inheritable phenotypes of glucolipoproteins and secondary symptomatic types of glucolipoproteins under obligatory observation of strict dietary treatment.

The study was carried out to determine risk factors of false positive and false negative results under polymerase chain reaction-analysis of clinical material. The samples with high viral load can be the source of false positive results. The contamination with nucleic acids can occur at any section of polymerase chain reaction analysis. The study data permitted to establish that the most sensitive stage is isolation and purification of nucleic acids especially under manual mode of operation. The detection of positive signal in most samples of one setting indicates total contamination. The cases when only several samples are polluted are special challenge. The presence of sample with high concentration of viral nucleic acid and several samples with low concentration in one setting means necessity of repeated analysis beginning with stage of isolation of nucleic acid. The analysis of curves of accumulation of products of amplification, their forms and positioning on chart is the obligatory stage of polymerase chain reaction study in real time regimen. These actions permit to exclude the readouts of false negative testing results to departments. The study conclusions are equipotent for polymerase chain reaction testing of any nucleic acid targets.

The regulation of metabolism of glucose is billions years older than system of insulin and biological function of locomotion (function of motion). Hence hypoglycemic effect of hormone is mediated by alteration of metabolism of fatty acids. The insulin in physiological way deprives mitochondrions a possibility to metabolize ketone bodies, short chain, medium chain and long chain fatty acids and 'forces" them to oxidize glucose which phylogenetically is not an optimal substrate. The relationships between fatty acids and glucose in the Rendle cycle have an effect only on autocrine level (in cell) determining alternation of biological reactions of exotrophia (after food intake) and endotrophia (beyond food intake) in biological function of alimentation (trophology). The most anti-diabetic pharmaceuticals are as insulin hyperlipemic by their mechanism of action. The decrease content of lipid substrates of oxidation in cytosol of cells and mitochondrions "are forced" to oxidize glucose. In these conditions, insulin enhances absorption of glucose by cells through glucose carriers--GLUT4. The derivatives of sulfonil-urea increase secretion of insulin by beta-cells of islets. The biguanidines bond in cytosol covalently and irreversibly ketone bodies taking them away from oxidation in mitochondrions. The fibrates, glitazones, flavonoids and flavones, lipoic tio-fatty acids. The endogenous eicosanoids, derivatives omega-3 and omega-6 of essential polyolefinic fatty acids and conjugated unsaturated fatty acids are the antagonists of receptors of activation of proliferation of peroxisomes. In peroxisomes, they enhance alpha-, beta- and omega-oxidation of all exogenous a physiological fatty acids and excess of palmitic saturated fatty acid forming hypolipidemia in cytozol. The hypolipidemic pharmaceuticals with effect of beta-blocker of oxidation stop absorption of fatty acids by mitochondrions. The omega-3 essential polvolefinic fatty acids, simultaneously with hypolipidemic effect, activate function of GLUT4. In patients of middle age, the diabetes mellitus type II is a symptom of syndrome of atherosclerosis. The reason is that in cells the deficiency of essential polyolefinic fatty acids and is determined by derangement of synthesis of phospholipids and function of GLUT4. It is valid to consider diabetes mellitus primarily as a pathology of metabolism of fatty acids and secondly as a pathology of content of glucose. It is necessary to take into account both under treatment (tactic activities) and strategic program of prevention of diabetes mellitus in population.

ApoE vector protein in association with apoB-100 directly transferring saturated and monounsaturated FA (SFA and MFA) in triglyceride form (composed of very low density lipoproteins (L)) to the cells which are assimilating FA by cooperative receptors of apoE. Only insulin dependent cells have apoe/B-l00 receptors on the cell membrane (skeletal myocytes, cardiac myocytes, periportal hepatocytes, adipocytes of subcutaneous fat and Kupffer's macrophages). Phylogenetically late apoE has a domain for protein-protein interaction unlike the other apos. Apo forms cooperative ligands: apoE/A-l, apoE/B-48 and apoE/B-100 while using this domain. At later stages of phylogenesis while apoE forms cooperative ligands it is also involved in cell transfer and absorption of polyunsatured essential fatty acids in high density L, SFA +MFA +unsatured FA in chylomicrons, SFA+MFA in very low density L. Phenotype E 33 appears to be regular. Phenotypes E2/2 and E4/4 are cause of hypertriglyceridemia of I and V types, which call destructive inflammation of arterial intima with atherothrombosis.

The regulation of metabolism of glucose is billions years older than system of insulin and biological function of locomotion (function of motion). Hence hypoglycemiс effect of hormone is mediated by alteration of metabolism of fatty acids. The insulin in physiological way deprives mitochondrions a possibility to metabolize ketone bodies, short chain, medium chain and long chain fatty acids and forces them to oxidize glucose which phylogenetically is not an optimal substrate. The relationships between fatty acids and glucose in the Rendle cycle have an effect only on autocrine level (in cell) determining alternation of biological reactions of exotrophia (after food intake) and endotrophia (beyond food intake) in biological function of alimentation (trophology). The most anti-diabetic pharmaceuticals are as insulin hyperlipemiс by their mechanism of action. The decrease content of lipid substrates of oxidation in cytosol of cells and mitochondrions “are forced” to oxidize glucose. In these conditions, insulin enhances absorption of glucose by cells through glucose carriers GLUT4. The derivatives of sulfonil-urea increase secretion of insulin by β-cells of islets. The biguanidines bond in cytosol covalently and irreversibly ketone bodies taking them away from oxidation in mitochondrions. The fibrates, glitazones, flavonoids and flavones, lipoic tio-fatty acids. The endogenous eicosanoids, derivatives ω-3 and ω-6 of essential polyolefinic fatty acids and conjugated unsaturated fatty acids are the antagonists of receptors of activation of proliferation of peroxisomes. In peroxisomes, they enhance α-, βand ω-oxidation of all exogenous aphysiological fatty acids and excess of palmitic saturated fatty acid forming hypolipidemia in cytozol. The hypolipidemic pharmaceuticals with effect of β-blocker of oxidation stop absorption of fatty acids by mitochondrions. The Ω-3 essential polyolefinic fatty acids, simultaneously with hypolipidemic effect, activate function of GLUT4. In patients of middle age, the diabetes mellitus type II is a symptom of syndrome of atherosclerosis. The reason is that in cells the deficiency of essential polyolefinic fatty acids and is determined by derangement of synthesis of phospholipids and function of GLUT4. It is valid to consider diabetes mellitus primarily as a pathology of metabolism of fatty acids and secondly as a pathology of content of glucose. It is necessary to take into account both under treatment (tactic activities) and strategic program of prevention of diabetes mellitus in population.

The cells’ malabsorption of three classes of lipoproteins chylomicrons and lipoproteins of low and very low density, form under electrophoresis six phenotypes of hyperlipoproteinemia. In phylogenesis, cells absorb lipoproteins in a consecutive way by apoE/B-48, apoB-100 and apoE/B-100 receptor endocytosis. The domain-ligand in lipoproteins of very low density is forming when apoB-100 takes active conformation “deformed bilayer apoprotein-lipid” in association with domain apoE apoE/B-100 ligand is formed. Another active conformation apoB-100 in domain is globule with lipids in “pocket” forming apoB-100 ligand. In blood 9 subclasses are formed: pre-ligand and post-ligand chylomicrons, lipoproteins with low density and lipoproteins with very low density. The ligand lipoproteins bind receptors of membrane and absorb cells. Both pre-chylomicrons, pre-lipoproteins with low density, pre-lipoproteins with very low density and post-chylomicrons, post-lipoproteins with low density, post-lipoproteins with very low density remain in blood. The sub-classes of lipoproteins form at electrophoregram 6phenotypes of hyperlipoproteinemia: phenotype I pre-chylomicrons + pre-lipoproteins with very low density; phenotype IIa post-lipoproteins with low density; phenotype IIb pre-lipoproteins with very low density; phenotype III post-chylomicrons + pre-lipoproteins with very low density; phenotype IV pre-lipoproteins with very low density; phenotype V pre-chylomicrons + post-chylomicrons + pre-lipoproteins with very low density + post-lipoproteins with very low density. The formation under electrophoresis of primary phenotypes and secondary types of hyperlipoproteinemia occurs according single algorithm. In a physiological sense, the major mass of palmitic and oleic lipoproteins with very low density absorb cells without transformation into lipoproteins with low density. Only linoleic and linolenic lipoproteins with very low density which are formed after binding of apoB-100 of triglycerides the same name and which are not much in blood acquire density of lipoproteins with low density physiologically. Under high content of triglycerides in blood main mass of lipoproteins with low density consists of aphysiologic palmitic lipoproteins with very low density with hydrated density lipoproteins with low density, the cause of hyperlipoproteinemia of phenotype III is genotype e2\e2 apoE; hyperlipoproteinemia of phenotype V genotype e4/e4 and probably toxic inhibition of activity (synthesis) phylogenetically late stearil-KoA-desaturase-2.

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 (glyсo-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 of conformation. 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.

Objective. The objective of the work was to evaluate importance of some genetic-related parameters determination such as serum apolipoproteins (apo) A-I, B, C-III, E, and Lp(a) in patients with hypertriglyceridemia (HTG) who were consulted by a lipidologist. Patients and methods. The study group consisted of 96 patients (48 men and 48 women) from 17 to 70 years old, with serum triglycerides (TG) exceeding 2,3 mmol/l. Fasting plasma TG, cholesterol, apo A-I, B, C-III, E, and Lp(a) were measured. Lipid electrophoresis was also performed. Results. We found the significant correlations of serum TG levels with apo E and C-III, and apo E with apo C-III in patients with HTG that points out the receptor defect of VLDL uptake by some cells that is one of some causes developing HTG. Apo B level was higher in patients with type IIb hyperlipidemia in comparison to types III, IV and V. As to apo A-I and Lp(a) levels, we have found no difference between patients with moderate and severe HTG. The elevated levels of serum apo E and C-III were determined in 68,8 % and 76 % patients, accordingly. ~ Conclusion. The evaluation of genetic-related parameters of serum apo C-III and apo E is an additional — diagnostic tool for the identification of primary HTG patients.

LDLP and VLDLP have different biological functions: phylogenetically older LDLP transfer FA that serve as substrates for intracellular production of energy and ATP while VLDLP transfer FA--precursors of cell membranes and eicosanoids. The cells absorb LDLP via apoB-100 endocytosis and VLDLP through apoE/B-100 receptors. VLDLP consist of palmitic and oleic VLDLP and LDLP of linoleic and linolenic LDLP. The contribution of LDLP to the development of HLP atherosclerosis and atheromatosis is negligible. LDLP form palmitic and oleic VLDLP with hydrated LDLP density. Blockade of LDLP absorption by apoB endocytosis and deficit of poly-FA constitute the etiological basis of atherosclerosis. Its pathogenetic basis is the excess of palmitic VLDLP with LDPL density in the intercellular space that block absorption of linoleic LDLP with all transferred SC poly-FA. Atheromatosis is clinically and prognostically most significant symptom of atherosclerosis associated with accumulation of ligand-free VLDLP and LDLP in arterial intima of the elastic type as the local pool of interstitial tissue for intravascular pool of intercellular medium. Type 2 diabetes mellitus in aged patients is a symptom of atherosclerosis resulting from SC poly-FA deficit and GLUT4 incompetence. Insulin-dependent cells differ in the degree of insulin resistance. Non-alcoholic fatty liver disease, synthesis of a physiological palmitic TG by hepatocytes and excessive formation of palmitic VLDLP in liver integrate pathogenesis of atherosclerosis and hepatic steatosis. The main pathogenetic factor is the excess of palmitic s-FA and palmitic TG.