title: [The insulin regulation of metabolism of fat acids and glucose next in the realization of biologic function of locomotion].
abstract: 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.
authors: V N
authors: VN
authors: Titov
mesh_terms: D000818:Animals; D004734:Energy Metabolism / Q000502:physiology*; D005227:Fatty Acids / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D008124:Locomotion / Q000502:physiology*; D008928:Mitochondria / Q000378:metabolism; D010084:Oxidation-Reduction
chemical_list: D005227:Fatty Acids; D007328:Insulin; D005947:Glucose