Seven etiologic factors of insulin resistance syndrome development

Biological role of insulin is metabolic processes regulation of, firstly, fatty acids (FA) and, secondly, of glucose. Insulin is known to regulate phylogenetic transformation of sarcophagous (ichthyophagous) animals of the ocean to herbivorous animals on land. Seven etiologic factors of insulin resistance syndrome: 1) somatic cells do not absorb glucose while they are able to absorb FA; FA absorption is always more active. To force cells to absorb glucose insulin deprives them of FA in non-esterified FA form (NEFA) absorption opportunity; 2) insulin warrants the highest mitochondria productivity in adenosine triphosphate (ATP) production and high animal unit kinetics parameters. Insulin indirectly regulates glucose metabolism; glucose is a substrate for olein monounsaturated FA synthesis. Among long chain FA mitochondria oxidize it most actively, producing ATP; 3) insulin cannot block NEFA release if lipolysis in visceral fatty omentum cells was activated by phylogenetically earlier hormone. Isulin blocks lipolysis only in subcutaneous adipocytes; 4) biochemical activity of palmitic saturated FA (SFA) is low; it is high in olein monounsaturated FA (MFA). In such biological function as locomotion development insulin expresses de novo synthesis of two enzymes: palmytoil-CoA-elongase and stearoyl-CoA-desaturase. These enzymes turn all hepatocyte synthesized palmitate SFA to highly active olein MFA; 5) insulin turns to olein MFA only palmitate SFA which was synthesized from glucose de novo but not from meat food SFA; 6) cells absorb FA in olein triglycerides form by apoE/В-100-endocytosis more actively than palmitate triglycerides by apoВ-100-endocytosis; 7) lack of ATP mitochondria production in trophology biologic function in mitochondria oxidation of palmitate SFA is to be compensated by biologic adaptation function activation, biologic endotrophy reaction, lypolysis in visceral fatty omentum cells and NEFA release. High NEFA serum level is the most common reason for insulin resistance syndrome.

insulin, fatty acids, glucose, insulin resistance, phylogenesis