Titov V N
Klin Lab Diagn. 2012 May(5):3-12.
The becoming at the late stages of phylogeny of the biologic function of locomotion, insulin system and the earliest formed function of mitochondria make it possible to align all oxidized substrates in the following sequence: a) fatty acid metabolites C4 - ketone bodies; b) butyric fatty acid short-chained metabolites C6-C10; c) palmitic fatty acid with specific carrier; d) glucose. The mitochondria will begin to oxidize glucose if there will be no ketone bodies in cytosol and no remains of short-chained fatty acids and palmitic fatty acid. According to "the biologic subordination principle" philogenically late insulin can't change the functional characteristics of the phylogeny earliest mitochondria. To "force" the mitochondria starting to oxidize glucose first of all the insulin is to inhibit the biochemical reactions in all cells where releasing of polar non-etherified fatty acids and formation of their polar metabolites occurs. As in case of insulin, the same marked and prolonged hypoglycemia is induced by DL-aminocarnitine. This substance specifically inhibits both activity of carnitine-palmitoilacylaminotrsansferase and flux of acyl-KoA in mitochondria. The pronounced decrease of fatty acids content and their metabolites in matrix force mitochondria to oxidize glucose. It is possible to be validly of opinion that the same philogenically ancient principles as inhibition of activity of carnitine-palmitoilacylaminotrsansferase, decrease of formation of fatty acid metabolites C4 (ketone bodies), short-chained metabolites of palmitic fatty acid and olein mono fatty acid are applied in realization of philogenically late insulin effect. The first insulin effect in the hypoglycemia and biologic exotrophy reaction conditions is targeted to the regulation of fatty acids metabolism. Only second insulin effect is targeted to the glucose metabolic transformation. Therefore, there is a background to consider the diabetes mellitus primarily as a disorder of metabolism of unsaturated and mono fatty acids and only secondary and only then as a disorder of glucose metabolism. If insulin will not be able to decrease in cytosol the content of lipid substances of oxidation of insulin the mitochondria will not oxidize glucose. At that, a pathogenesis uniform syndrome of resistance to insulin is formed independently of etiologic factors. Under these conditions the mitochondria physiologically "don't want" to oxidize glucose a possibility exists to oxidize fatty acids and their polar metabolites.
在系统发育后期，运动生物功能、胰岛素系统以及线粒体最早形成的功能的出现，使得所有氧化底物能够按以下顺序排列：a）脂肪酸代谢产物C4 - 酮体；b）丁酸短链脂肪酸代谢产物C6 - C10；c）带有特定载体的棕榈酸；d）葡萄糖。如果细胞溶质中没有酮体，也没有短链脂肪酸和棕榈酸的残留，线粒体将开始氧化葡萄糖。根据“生物从属原则”，系统发育后期的胰岛素无法改变系统发育最早的线粒体的功能特性。要“迫使”线粒体首先开始氧化葡萄糖，胰岛素首先要抑制所有细胞中释放极性非酯化脂肪酸及其极性代谢产物的生化反应。与胰岛素的情况一样，DL - 氨基肉碱也会引发同样显著且持久的低血糖。这种物质特异性地抑制肉碱 - 棕榈酰氨基转移酶的活性以及线粒体中酰基辅酶A的通量。基质中脂肪酸含量及其代谢产物的显著减少迫使线粒体氧化葡萄糖。可以合理地认为，在实现系统发育后期胰岛素效应时，应用了与抑制肉碱 - 棕榈酰氨基转移酶活性、减少脂肪酸代谢产物C4（酮体）、棕榈酸短链代谢产物和油酸单脂肪酸形成相同的系统发育古老原则。在低血糖和生物外向反应条件下，胰岛素的第一个作用是针对脂肪酸代谢的调节。只有胰岛素的第二个作用是针对葡萄糖代谢转化。因此，有理由将糖尿病主要视为不饱和脂肪酸和单脂肪酸代谢紊乱，只是次要的，然后才是葡萄糖代谢紊乱。如果胰岛素无法降低细胞溶质中胰岛素氧化的脂质物质含量，线粒体将不会氧化葡萄糖。此时，无论病因如何，都会形成一种统一的胰岛素抵抗发病机制综合征。在这些条件下，线粒体在生理上“不想”氧化葡萄糖，存在氧化脂肪酸及其极性代谢产物的可能性。
