Abstract
Metabolic syndrome and non-alcoholic fatty liver disease, as its hepatic manifestation, are extremely relevant and socially significant health problems today. The article presents new data on the problem of the pathogenesis of non-alcoholic fatty liver disease from the perspective of the influence of bile acids on the state of carbohydrate and lipid metabolism, the functioning of adipose tissue, the composition and function of the intestinal microbial-tissue complex. Bile acids are ligand-binding domains involved in the activation of many receptors. The role of endogenous fructose, uric acid, chronic kidney disease, platelet dysfunction in the development of the disease is highlighted, the directions of therapeutic action are determined. An increase in oxidative stress, a violation of the intestinal microbial-tissue complex, dyslipidemia, and excessive platelet activation form a “vicious circle” that promotes the progression of liver and kidney diseases.
Highlights
Что повышенные уровни циркулирующих вторичных желчных кислот (ЖК) у больных с ХБП способствуют сосудистой кальцификации за счет уменьшения активации FXR и прямого токсичного воздействия дезоксихолевой кислоты на сосудистую стенку
Sanchez-Lozada L.G., Andres-Hernando A., Garcia-Arroyo F.E. et al Uric acid activates aldose reductase and the polyol pathway for endogenous fructose and fat production causing development of fatty liver in rats
Summary
Metabolic syndrome and non-alcoholic fatty liver disease, as its hepatic manifestation, are extremely relevant and socially significant health problems today. The article presents new data on the problem of the pathogenesis of non-alcoholic fatty liver disease from the perspective of the influence of bile acids on the state of carbohydrate and lipid metabolism, the functioning of adipose tissue, the composition and function of the intestinal microbial-tissue complex. An increase in oxidative stress, a violation of the intestinal microbial-tissue complex, dyslipidemia, and excessive platelet activation form a “vicious circle” that promotes the progression of liver and kidney diseases. Неалкогольная жировая болезнь печени (НАЖБП) возникает вследствие реализации патогенетических механизмов МС в печени и является его печеночным проявлением. Более правильным и отражающим сущность патологических процессов, лежащих в основе заболевания, является термин «метаболически ассоциированная жировая болезнь печени» (MAFLD). В связи с этим важна подробная оценка роли желчных кислот (ЖК), как универсальных регуляторных молекул, в патогенезе НАЖБП и МС в целом
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