The phylogenetic theory of general pathology. The becoming of function of at mitochondria at symbiosis of bacterial cells and archaea. Inconsistency of Randle cycle, regulation metabolism of fatty acids and glucose by insulin.

Abstract

The implementation of Randle rule is not a cycle; fatty acids C4 - ketone bodies at interrelationships with glucose metabolite - pyruvate regulate production of mitochondria of acetyl-KoA by induction of substrate and its conversion in Krebs cycle, reactions of respiratory chain, oxidative phosphorylation and formation of ATP. In phylogenesis, the early substrate for formation of ATP by mitochondria is acetyl-KoA from C4 fatty acids 4; this is alternative A of induction by substrate adopted from archaea. The alternative B of induction in bacteria is based on synthesis of acetyl-KoA by mitohondria from pyruvate developed in cytosol from exogenous glucose. The insulin is late activator of absorption by glucose cells in phylogenesis; using induction by substrate, insulin inhibits absorption of fatty acids by cells and specifically activates absorption of glucose by them. The insulin activates absorption of glucose only by insulin-dependent cells by force of decreasing of "bioavailability" of fatty acids. These cells are preferred to be metabolize by mitochondria from times of archaea. The insulin, blocking lipolysis in insulin-dependent adipocytes "forces" mitochondria, instead of formation of acetyl-KoA from fatty acids, to produce it from pyruvate at activation of glycolysis and pyruvate-dehydrogenased complex. Under effect of insulin, mitochondria form acetyl-KoA and synthesize ATP from oleic mono-saturated fatty acids but not from palmitic saturated fatty acids. The kinetic parameters of second reaction and formation of ATP per unit of time (effectiveness) are much higher than in first reaction. The effectiveness of i9mplementation of alternative A in synthesis of ATP, kinetic parameters of production of acetyl-KoA in mitochondria in alternative A are more effective than in case of alternative B and metabolic conversion of glucose. The syndrome of resistance to insulin is, at the first place, pathology of metabolism of fatty acids and only in the second place metabolism of glucose. The incapacity of insulin to block lipolysis in the phylogenetically earlier visceral fatty cells is the basis of resistance.