title: [THE FATTY CELL. THE VISCERAL FATTY TISSUE, EFFECT OF HUMORAL MEDIATOR LEPTIN IN AUTOCRINE WAY AND IN PARACRIN CENOSISES OF CELLS. TWO PHYLOGENETICALLY, FUNCTIONALLY AND REGULATORY DIFFERENT POOLS OF FATTY TISSUE IN VIVO].
abstract: Every cell reserves fatty acids in cytozol in drops of lipids in the form of non-polar triglycerides for itself andfor oxidation in mitochondria. The specialized visceral fatty cells ofomentum and adipocytes ofsubcutaneous fat are the cells absorbing saturated and mono unsaturated fatty acids in form of triglycerides in apoB-48 chylomicrons, apoB-100 lipoproteins of low and very low density. They deposit their physiological time and liberate fatty acids in intercellular medium in the form ofpolar unesterified fatty acids bound by albumin. According phylogenetic theory of general pathology, in biological function of trophology (nutrition) fatty cells sequentially implement biological reaction of exotrophy (external nutrition), deposition and endotrophy (internal nutrition). The humoral regulator offeedback in visceral fatty cells is leptin acting in autocrine way, in paracrin cenosises of cells and on the level of organism. The biological role of leptin is in preventing a) deposition of surplus amount of non-polar triglycerides in fatty cells; b) formation of endoplasmic "stress"; c) death of fatty cells in apoptosis way, formation of corpuscles of apoptosis and failure of biological function of endoecology; d) formation of biological reaction of inflammation in visceral fatty tissue; e) high level of unsaturated fatty acids in intercellular medium and f) development of metabolic syndrome. The leptin prevents aphysiological deposit ofnon-polar triglycerides in insulin-dependent cells that are not intended to deposit non-polar triglycerides and also in β-cells of islands. The main cause of high level ofleptin in blood plasma is overeating offood physiological by content of nutrients.
authors.forename: V N
authors.initials: VN
authors.lastname: Titov
mesh_terms: D017667:Adipocytes / Q000145:classification / Q000378:metabolism* / Q000473:pathology; D052242:Adiponectin / Q000235:genetics / Q000378:metabolism; D002001:Adipose Tissue, Brown / Q000378:metabolism* / Q000473:pathology; D002914:Chylomicrons / Q000378:metabolism; D005227:Fatty Acids / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D006963:Hyperphagia / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D050152:Intra-Abdominal Fat / Q000378:metabolism* / Q000473:pathology; D020738:Leptin / Q000235:genetics / Q000378:metabolism; D050356:Lipid Metabolism; D024821:Metabolic Syndrome / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D008928:Mitochondria / Q000378:metabolism; D015398:Signal Transduction; D014280:Triglycerides / Q000378:metabolism
chemical_list: D052242:Adiponectin; D002914:Chylomicrons; D005227:Fatty Acids; D020738:Leptin; D014280:Triglycerides