title: [The unity of pathogenesis of insulin resistance syndrome and non-alcoholic fatty disease of liver. The metabolic disorder of fatty acids and triglycerides].
abstract: The pathogenesis of non-alcoholic fatty disease of liver (steatosis) is still as unclear as a loss of hepatocytes similar to apoptosis, development of biological reaction of inflammation, its transformation into steatohepatitis with subsequent fibrosis and formation of atrophic cirrhosis. The article suggests that steatosis is developed due to higher concentration of palmitic saturated fatty acid (C 16:0) in food, intensification of its endogenic synthesis from food carbohydrates and glucose and development of insulin resistance. It is displayed in in hormone ability to activate both oxidation in cells of glucose and synthesis of oleic monoene fatty acid from palmitic saturated fatty acid (C 18:1). The insulin resistance initiates pathologic process on the level of paracrine associations of cells resulting in permanent increase of concentration of non-etherified fatty acids in intercellular medium and intensification of their passive absorption by cells. The phylogenetically ancient mitochondrions will not to oxidize glucose until non-etherified fatty acids are present in cytosol and hence there is an opportunity to oxidize them. To eliminate undesirable action of polar saturated palmitic fatty acid, the cells etherify it by spirit glyceride into triglycerides to deposit in cytosol or to secrete into blood in a form of lipoproteins of very low density. Under insulin resistance, saturated palmitic fatty acid synthesized by hepatocytes from glucose, does not further transform into oleic monoenic fatty acid. The cells are to etherify endogenic (exogenic) palmnitic saturated fatty acid into composition of aphysiologic palmitic triglycerides (saturated palmitic fatty acid in position sn-2 of spirit glyceride). At that, triglycerides of palmitat-palmitat-oleat and even tripalmitat type are formed. The melting temperature of tripalmitat is 48 degrees C and melting temperature of physiologic trioletat is 13 degrees C. The intracellular lipases factually can't hydrolyze palmitic triglycerides. So, hepatocytes, overloaded by them, are destroyed in a way similar to apoptosis. The formed corpuscles of apoptosis disorder the biologic function of endoecology and trigger biologic reaction of inflammation. At that, steatosis changes into steato-hepatitis. The prevention of steatosis consists in dramatic restriction of concentration of palmitic saturated fatty acid in food. The treatment effect is targeted to: decreasing the formation of palmitine triglycerides by force of concurrent etherification of palmitic saturated fatty acid not into triglycerides but into phosphatidylcholine (symmetric phospholipids of soya); intensification of oxidation of palmitic saturated fatty acid in peroxisomes (glytazones and fibrates); decrease of insulin resistance (binuanide metformine).
authors.forename: V N
authors.initials: VN
authors.lastname: Titov
authors.forename: K V
authors.initials: KV
authors.lastname: Ivanova
authors.forename: P P
authors.initials: PP
authors.lastname: Malyshev
authors.forename: S I
authors.initials: SI
authors.lastname: Kaba
authors.forename: Iu K
authors.initials: IuK
authors.lastname: Shiriaeva
mesh_terms: D000818:Animals; D017209:Apoptosis; D005234:Fatty Liver / Q000378:metabolism* / Q000473:pathology; D022781:Hepatocytes / Q000378:metabolism / Q000473:pathology; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D065626:Non-alcoholic Fatty Liver Disease; D019308:Palmitic Acid / Q000378:metabolism*; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D014280:Triglycerides; D019308:Palmitic Acid