[Phylogeny, development of processes of cellular fatty acid transfer and absorption, biological locomotion function, and insulin function. Pathogenesis of insulin resistance syndrome].
Passive cellular absorption of first glucose (Glu) and then fatty acids (FA) as substrate for energy generation formed during phylogeny. Glucose transporters ensure Glu absorption; the cells absorb FA as polar unetherified FA from the associates with albumin and oxidize them at once. Later there was an active cell absorption of saturated and unsaturated (with one-three double bonds) FAs as nonpolar triglycerides as part of very low-density lipoproteins via apoB-100 receptor-mediated endocytosis. When the biological function of locomotion was established, there was an insulin (Ins) system; the latter initiated apoE vector synthesis and targeted FA transfer mainly to skeletal myocytes and formed apoE/B-100 endocytosis. The major role of Ins is energy provision for the biological function of locomotion. Ins blocks the lipolysis and oxidation of FA in the myocytes until the cytosol contains sufficient Glu, and activates its absorption from the intercellular medium. FA lipolysis and oxidation begin only in glycopenia. Activation of myocytic FA oxidation with normal Glu levels and blocked lipolysis underlies Ins resistance. This occurs with: a) activated biological function of adaptation, a biological stress reaction, and the elevated intercellular levels of unetherified FAs that are passively absorbed and oxidized by cells; b) impaired biological function in exotrophy--high dietary palmitinic FA levels, a biological reaction of FA transfer to the cells, and blockade of apoE/B-100 endocytosis; c) impaired biological function of endoecology, purity of the intercellular medium, biological function of inflammation, and synthesis of lipid transfer C-reactive protein that as a vector redirects a flux of FA from myocytes to interstitial cells that realize the systemic inflammatory response syndrome. Since the formation of biological functions of adaptation, exotrophy, and endoecology occurred earlier than that of biological function of locomotion, Ins resistance is the enhanced passive cell absorption of FA, as this took place before the function of locomotion was formed. According to our described principle of biological subordination, phylogenetically later Ins cannot regulate the processes formed in earlier steps of phylogeny.
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D000818:Animals; D001692:Biological Transport; D004734:Energy Metabolism; D005227:Fatty Acids / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000502:physiology*; D007333:Insulin Resistance; D008124:Locomotion / Q000502:physiology*; D024821:Metabolic Syndrome / Q000209:etiology*; D010802:Phylogeny
D005227:Fatty Acids; D007328:Insulin; D005947:Glucose