[Leptin and adiponectin in pathogenesis of metabolic syndrome]

Metabolic syndrome, hypernutrition syndrome is a phylogenetically determined sequence of symptoms having common pathogenesis. Etiologically, it is due to excessive intake of adequate food. Enterocytes and omental adipose cells form an early phylogenetically unified and paracrinically regulated community that alternately realize exo- and endotrophic biological reactions. Visceral obesity high level of non-esterified fatty acids (FA), formation of plasma FA pool and their integration into the endothelial membrane, and enlargement of enterocytes are the main cause of increased hydrodynamic pressure. Toll-like receptors perceive albumin associates containing a supraphysiological number of FA as aliens and initiate the inflammatory reaction. Lipid-overloaded cells undergo "endoplasmic stress", abnormal protein synthesis (folding), and apoptosis-like death. Visceral fat serves as phylogenetically early FA depot for the realization of biological functions of homeostasis, trophology endoecology, and adaptation; it is anatomically confined and regulated at the level of paracrine communities. The subcutaneous depot realizes the phylogenetically late locomotor function; its size is not anatomically restricted. Visceral adipose cells have no receptors for phylogenetically late insulin (INS). Cells of the subcutaneous FA depot are specialized adipocytes having INS and GLUT4 receptors. They are regulated by the phylogenetically late humoral mechanisms at the total body level. Leptin initiates in vivo humoral, hypothalamic regulation of the size of INS-insensitive visceral adipose cells quantitatively programmed in ontogenesis; also, it prevents "endoplasmic stress" and apoptosis, regulates food consumption. Leptin initiates switching FA storage from the visceral adipocyte pool to the subcutaneous one. Adiponectin is a phylogenetically late humoral inducer of regulation of the optimal in vivo number of cells from the hypothalamus level. It is biologically predetermined to regulate the number (proliferation) of INS-dependent adipocytes in subcutaneous fat.