Abstract

Metabolic syndrome (overeating) is a phylogenetically-determined sequence of symptoms with the same pathogenesis. There is only one etiological factor, namely, increased consumption of physiologically optimal food. Enterocytes and omentum fat cells are phylogenetically paracrine-regulated cell community that realizes the biological reactions of exo- and endotrophy. Visceral obesity, high level of unesterified fatty acids (FA), formation of a pool of micellar FA in the blood, integration of these FA into endothelial cell plasma membrane and enlargement of adipocytes are the causes of hydrodynamic hypertension. Toll-like receptors recognize the albumin associates with greater amount of FA than physiologically required as non- self and initiate inflammatory process. Endoplasm stress forms in lipid-laden cells, protein synthesis (folding) impairs and induces apoptosis-like cell death. Visceral fat is a phylogenetically repository of FA to fulfill the biological function of homeostasis, trophology, endoecology and adaptation; it is regulated at the early level of paracrine communities and is anatomically limited. The subcutaneous fat repository fulfills the phylogenetically late function of locomotion; the repository size is not anatomically limited. Visceral fat cells don't have receptors for phylogenetically late insulin (INS); specialized adipoсytes laden with INS and GLUT4 receptors are cells that form the subcutaneous repository. These cells are regulated by phylogenetically late humoral factors at the body level. Leptin is the initiator of humoral hypothalamic regulation of in vivo sized ontogenetically programmed number of visceral INS-insensitive fat cells. It prevents endoplasm stress and apoptosis, being designed to regulate the amount of consumed food. Leptin initiates transformation of FA storing from visceral repository into subcutaneous repository. Adiponectin is phylogenetically late humoral hypothalamic regulatory factor that controls optimal number of fat cells in vivo. Its biological role is to regulate the number (proliferation) of insulin- dependent adipocytes in subcutaneous fatty tissue.

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