Titov V N, Shoibonov B B
Klin Lab Diagn. 2016 Feb;61(2):93-101.
The high content of palmitic saturated fatty acid, palmitic triglycerides in food, the large amount of lipoproteins of very low density of the same name in blood, obvious insufficient amount of unesterified fatty acids releasing under lipolysis in blood to meet in vivo requirements in biotransforming energy of ATP are the causes of biological malfunction of homeostasis. As a rule, for every cell in vivo everything is always to be enough. The deficiency of synthesis of ATP by reason of non-optimal substratum for acquirement of ATP by mitochondria is followed by activation also phylogenetically earlier biological function of adaptation, biological reaction of stress. Thus, surplus of palmitic unesterified fatty acid after every food intake forms in vivo biological reaction of "metabolic" stress, deficiency of energy by reason of realization by mitochondria in vivo non-optimal exogenous substratum-palmitic unesterified fatty acid, deficiency of acyl- and acetyl-KoA and prognostically formation of potentially ineffective palmitic alternative of metabolism of fatty acids. The deficiency of palmitic unesterified fatty acids in biological reaction of exotrophy after every intake of food compensates biological reaction of stress, activation of releasing of palmitic unesterified fatty acids from visceral fatty cells of gland as it physiologically occurs in biological reaction of endotrophy. At that, adrenalin increases lipolysis in visceral fatty cells of gland and physiologically late insulin can't inhibit lipolysis in phylogenetically early visceral fatty cells. Increasing of content of unesterifed fatty acids in blood plasma, as it always occurs in vivo, stops absorption of glucose by cells initiating hyperglycemia, hyperinsulinemia, and syndrome of resistance to insulin. The result of such a compensation of biological reaction of exotrophy is biological reaction of endotrophy, condition of "metabolic" stress, depletion of function of β-cells of islets with formation of diabetes mellitus type I, deficiency in vivo of insulin synthesis. The biological role of albumin - transfer of fatty acids in intercellular medium inform of unesterifed fatty acids and prevention of formation of pool of free fatty acids effecting aphysiologically.
食物中棕榈酸饱和脂肪酸、棕榈酸甘油三酯含量高，血液中大量同名极低密度脂蛋白，血液中脂解时释放的未酯化脂肪酸量明显不足，无法满足体内生物转化ATP能量的需求，是体内稳态生物功能紊乱的原因。通常，体内每个细胞的一切都应始终充足。由于线粒体获取ATP的底物不理想，导致ATP合成不足，进而激活了进化上更早的适应生物功能，即应激生物反应。因此，每次进食后，棕榈酸未酯化脂肪酸过剩在体内形成“代谢”应激生物反应，由于线粒体在体内利用不理想的外源性底物——棕榈酸未酯化脂肪酸，导致能量不足，酰基辅酶A和乙酰辅酶A缺乏，且预后形成潜在无效的棕榈酸脂肪酸代谢替代物。每次进食后外营养生物反应中棕榈酸未酯化脂肪酸的缺乏，补偿了应激生物反应，激活了腺体内脏脂肪细胞中棕榈酸未酯化脂肪酸的释放，就像在营养生物反应中生理上发生的那样。此时，肾上腺素增加腺体内脏脂肪细胞的脂解作用，而生理上较晚出现的胰岛素无法抑制进化上较早的内脏脂肪细胞的脂解作用。血浆中未酯化脂肪酸含量增加，就像体内总是发生的那样，会阻止细胞吸收葡萄糖，引发高血糖、高胰岛素血症和胰岛素抵抗综合征。这种外营养生物反应补偿的结果是内营养生物反应、“代谢”应激状态、胰岛β细胞功能耗竭并形成I型糖尿病、体内胰岛素合成不足。白蛋白的生物学作用——以未酯化脂肪酸的形式在细胞间介质中转运脂肪酸，并防止形成非生理性影响的游离脂肪酸池。
