title: [Insulin: initiation of pool of insulin-dependent cells, targeted transfer of triglycerides and increase of kinetic parameters of oxidation of fatty acids].
abstract: The insulin, to provide with energy the biological function of locomotion, formed: a) pool of phylogenetically late insulin-dependent cells; b) highly productive vector variant of transfer of saturated and mono unsaturated fatty acids only to insulin-dependent cells; c) new variant of active absorption of substrates for acquiring energy by cells--apoE/B-100-receptor endocytosis; d) transformation of all endogenically synthesized palmitic saturated fatty acid in oleic mono saturated fatty acid and e) replacement of potentially ineffective palmitic variant of formation of energy in vivo with potentially high-performance oleic variant of metabolism of substrates for turning out of ATP. The insulin expressed synthesis of apoE glucose carrier 4 and stearyl-KoA-desaturase. These occurrences confirm that syndrome of insulin resistance primarily is the pathology of metabolism of fatty acids and only secondary the pathology metabolism of glucose. The multi-functional fatty cells of visceral areolar tissue and specialized adipocytes of subcutaneous fat depots are phylogenetically, regulatory and functionally different cells. They are formed under development of different biological functions: the first ones under realization of biological function of trophology and second ones under realization of biological function of locomotion. At the level of organism, the mechanisms of hypothalamus-fatty cells feedback are realized by peptide leptin and in case of hypothalamus-adipocytes feedback--peptide adiponectin. The potential possibilities of mitochondria in synthesis of ATP are high and are conditioned only by amount of substrate of mitochondria acetyl-KoA. This shortage can be chronic as in cases of disorder of insulin function and palmitic variant of metabolism of substrates for acquiring energy by cells. The deficiency of acetyl-KoA can be acute as is the case of diabetic coma when surplus amount of ketonic bodies follows the expressed deficiency of acetyl-KoA formed from glucose and fatty acids. Can the intravenous injection of acetyl-KoA be effective under diabetic ketoacidosic coma?
authors: V N
authors: VN
authors: Titov
mesh_terms: D000105:Acetyl Coenzyme A / Q000378:metabolism / Q000627:therapeutic use; D000255:Adenosine Triphosphate / Q000378:metabolism; D017667:Adipocytes; D000273:Adipose Tissue / Q000378:metabolism; D001692:Biological Transport; D003926:Diabetic Coma / Q000188:drug therapy / Q000378:metabolism; D005227:Fatty Acids / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007031:Hypothalamus / Q000378:metabolism; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance; D050356:Lipid Metabolism; D010084:Oxidation-Reduction; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D005227:Fatty Acids; D007328:Insulin; D014280:Triglycerides; D000105:Acetyl Coenzyme A; D000255:Adenosine Triphosphate; D005947:Glucose