Titov V P, Sazhina N N, Aripovskiy A V, Evteeva N M
The Russian cardiologic R&D production complex of Minzdrav of Russia, 121552, Moscow, Russia.
The N.M. Emmanuel institute of biochemical physics, Moscow, Russia.
Klin Lab Diagn. 2016;61(5):260-270. doi: 10.18821/0869-2084-2016-61-5-260-270.
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 β-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.
系统发生学理论为以下命题提供了依据。1. 在体内细胞能够从与白蛋白结合的物质中吸收极性脂肪酸之前，细胞不会从细胞间介质中吸收葡萄糖。2. 系统发生后期的体液胰岛素并不调节葡萄糖代谢的任何阶段；这些阶段在激素合成前数十亿年就已完成。3. 系统发生后期的胰岛素是营养生物学功能、营养功能、外营养生物反应的“人质”；它无法在食物中过量的生理棕榈酸饱和脂肪酸（线粒体β氧化动力学参数低）时减少其含量。4. 系统发生早期对胰岛素有抗性的网膜内脏脂肪细胞池和后期胰岛素依赖的脂肪细胞池在许多功能参数上有所不同。5. 所有“代谢大流行”，如胰岛素抵抗综合征、动脉粥样硬化、代谢性动脉高血压、代谢综合征和肥胖，主要都是脂肪酸的病理学问题。6. 所有“代谢大流行”都是单一生物功能（运动功能）在其发病机制形成的单一算法下的病理学问题。7. “代谢大流行”的病因是一致的——环境因素以营养生物学功能、营养功能紊乱的形式产生影响；食物中棕榈酸饱和脂肪酸的非生理过量含量、脂肪酸的非生理转化形式以及ω-7-棕榈油酸单不饱和脂肪酸。胰岛素激活心肌细胞、心肌对葡萄糖的吸收，葡萄糖作为原位从头合成ω-9油酸单不饱和脂肪酸的底物。在这样的物理化学参数下，线粒体以最高的反应速度常数和最高的ATP形成效率对其进行氧化。
