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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">nogr</journal-id><journal-title-group><journal-title xml:lang="ru">Экспериментальная и клиническая гастроэнтерология</journal-title><trans-title-group xml:lang="en"><trans-title>Experimental and Clinical Gastroenterology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1682-8658</issn><publisher><publisher-name>«Global Media Technologies»</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.31146/1682-8658-ecg-183-11-20-24</article-id><article-id custom-type="elpub" pub-id-type="custom">nogr-1469</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ПЕРЕДОВАЯ СТАТЬЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>LEADING ARTICLE</subject></subj-group></article-categories><title-group><article-title>Роль желчных кислот в многообразии механизмов формирования печеночных проявлений метаболического синдрома</article-title><trans-title-group xml:lang="en"><trans-title>The role of bile acids in the variety of mechanisms of the formation of hepatic manifestations of metabolic syndrome</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1095-8787</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гриневич</surname><given-names>В. Б.</given-names></name><name name-style="western" xml:lang="en"><surname>Grinevich</surname><given-names>V. B.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Гриневич Владимир Борисович, заведующий 2 кафедрой (терапии усовершенствования врачей), д. м. н., профессор</p><p>194044, Санкт-Петербург, улица Академика Лебедева, д. 6</p></bio><bio xml:lang="en"><p>Vladimir B. Grinevich, Head of 2nd Therapy department of postgraduate education, DSci, professor; Scopus Author ID: 7005167197</p><p>194044, St. Petersburg, Akademika Lebedev street, 6</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-8347-0531</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Кравчук</surname><given-names>Ю. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Kravchuk</surname><given-names>Yu. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кравчук Юрий Алексеевич, д. м. н., профессор 2 кафедры (терапии усовершенствования врачей)</p><p>194044, Санкт-Петербург, улица Академика Лебедева, д. 6</p></bio><bio xml:lang="en"><p>Yuri A. Kravchuk, M.D., D. Sc. (Medicine), Professor of 2nd Therapy department of postgraduate education</p><p>194044, St. Petersburg, Akademika Lebedev street, 6</p></bio><email xlink:type="simple">kravchuk2003@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Арапханова</surname><given-names>М. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Arapkhanovа</surname><given-names>M. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Арапханова Марина Магомедовна, врач-гастроэнтеролог клиники 2 кафедры (терапии усовершенствования врачей)</p><p>194044, Санкт-Петербург, улица Академика Лебедева, д. 6</p></bio><bio xml:lang="en"><p>Marina M. Arapkhanova, gastroenterologist of 2nd Therapy department of postgraduate education</p><p>194044, St. Petersburg, Akademika Lebedev street, 6</p></bio><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Кон</surname><given-names>В. Е.</given-names></name><name name-style="western" xml:lang="en"><surname>Kon</surname><given-names>V. E.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кон Виктория Ефимовна, к. м. н., заведующая кардиологическим отделением с восстановительным лечением № 1</p><p>197341, Санкт-Петербург, ул. Аккуратова, д. 2</p></bio><bio xml:lang="en"><p>Viktoria E. Kon, MD, PhD, Head of the Cardiology Department with Rehabilitation Treatment No. 1</p><p>197341, St. Petersburg, st. Akkuratova, 2</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Михайлова</surname><given-names>Л. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Mikhailova</surname><given-names>L. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Михайлова Любовь Вячеславовна, врач-кардиолог</p><p>197341, Санкт-Петербург, ул. Аккуратова, д. 2</p></bio><bio xml:lang="en"><p>Lyubov V. Mikhailova, cardiologist</p><p>197341, St. Petersburg, st. Akkuratova, 2</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3279-6448</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ратникова</surname><given-names>А. К.</given-names></name><name name-style="western" xml:lang="en"><surname>Ratnikova</surname><given-names>A. K.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Ратникова Анна Константиновна, врач УЗД, врач-кардиолог</p><p>194044, Санкт-Петербург, улица Академика Лебедева, д. 6194291, Санкт-Петербург, пр. Культуры, д. 4 </p></bio><bio xml:lang="en"><p>Anna K. Ratnikova, sonologist, cardiologist</p><p>194044, St. Petersburg, Akademika Lebedev street, 6194291, St. Petersburg, Kultury Ave., 4 </p></bio><xref ref-type="aff" rid="aff-3"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБВОУ ВО «Военно-медицинская академия имени С. М. Кирова» МО РФ</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Military Medical Academy named after S. M. Kirov</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное учреждение «Национальный медицинский исследовательский центр имени В. А. Алмазова» Министерства здравоохранения Российской Федерации</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Almazov National Medical Research Centre</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru"><institution>ФГБВОУ ВО «Военно-медицинская академия имени С. М. Кирова» МО РФ; ФГБУ «Северо-Западный окружной научно-клинический центр имени Л. Г. Соколова Федерального медико-биологического агентства»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Military Medical Academy named after S. M. Kirov; Federal state budgetary institution “North-West District Scientific and Clinical Center named after L. G. Sokolov Federal Medical and Biological Agency”</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2020</year></pub-date><pub-date pub-type="epub"><day>13</day><month>11</month><year>2020</year></pub-date><volume>183</volume><issue>11</issue><fpage>20</fpage><lpage>24</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Гриневич В.Б., Кравчук Ю.А., Арапханова М.М., Кон В.Е., Михайлова Л.В., Ратникова А.К., 2020</copyright-statement><copyright-year>2020</copyright-year><copyright-holder xml:lang="ru">Гриневич В.Б., Кравчук Ю.А., Арапханова М.М., Кон В.Е., Михайлова Л.В., Ратникова А.К.</copyright-holder><copyright-holder xml:lang="en">Grinevich V.B., Kravchuk Y.A., Arapkhanovа M.M., Kon V.E., Mikhailova L.V., Ratnikova A.K.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.nogr.org/jour/article/view/1469">https://www.nogr.org/jour/article/view/1469</self-uri><abstract><p>Метаболический синдром и неалкогольная жировая болезнь печени, как его печеночное проявление, сегодня являются крайне актуальными и социально значимыми проблемами здравоохранения. В статье представлены новые данные по проблеме патогенеза неалкогольной жировой болезни печени с позиции влияния желчных кислот на состояние углеводного и липидного обмена, функционирование жировой ткани, состав и функции микробно-тканевого комплекса кишечника. Желчные кислоты являются лиганд-связывающими доменами, участвующими в активации многих рецепторов. Освещена роль эндогенной фруктозы, мочевой кислоты, хронической болезни почек, дисфункции тромбоцитарного звена в развитии заболевания, определены направления терапевтического воздействия. Увеличение окислительного стресса, нарушение микробно-тканевого комплекса кишечника, дислипидемия, избыточная активация тромбоцитов формируют «порочный круг», способствующий прогрессированию заболеваний печени и почек.</p></abstract><trans-abstract xml:lang="en"><p>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.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>метаболический синдром</kwd><kwd>НАЖБП</kwd><kwd>МАЖБП</kwd><kwd>желчные кислоты</kwd><kwd>фруктоза</kwd><kwd>мочевая кислота</kwd></kwd-group><kwd-group xml:lang="en"><kwd>metabolic syndrome</kwd><kwd>NAFLD</kwd><kwd>MAFLD</kwd><kwd>bile acids</kwd><kwd>fructose</kwd><kwd>uric acid</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Беленков Ю.Н., Привалова Е. В., Каплунова В. Ю. и др. Метаболический синдром: история развития, основные критерии диагностики. Рациональная фармакотерапия в кардиологии. – 2018. – № 14(5). – С. 757–764.</mixed-citation><mixed-citation xml:lang="en">Belenkov Yu. N., Privalova E. V., Kaplunova V. Yu. et al. Metabolic syndrome: history of development, the main criteria for diagnosis. Rational pharmacotherapy in cardiology, 2018, No. 14 (5), pp.757–764 (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Tilg H., Effenberger M. From NAFLD to MAFLD: when pathophysiology succeeds. Nat Rev Gastroenterol Hepatol, 2020, Vol. 17, pp. 387–388.</mixed-citation><mixed-citation xml:lang="en">Tilg H., Effenberger M. From NAFLD to MAFLD: when pathophysiology succeeds. Nat Rev Gastroenterol Hepatol, 2020, Vol. 17, pp. 387–388.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Селиверстов П.В., Джадхав С. Н., Цурцумия Д. Б. и др. Неалкогольная жировая болезнь печени: возможности диагностики. РМЖ. – 2019. – № 5. – С. 36–40</mixed-citation><mixed-citation xml:lang="en">Seliverstov P. V., Dzhadkhav S. N., Tsurtsumia D. B. et al. Diagnostic capabilities in non-alcoholic fatty liver disease. RMJ, 2019, Vol. 5, pp.36–40. (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Twisk J., Hoekman M. F., Lehmann E. M. et al. Insulin suppresses bile acid synthesis in cultured rat hepatocytes by down-regulation of cholesterol7 alpha-hydroxylase and sterol 27-hydroxylase gene transcription. Hepatology, 1995, Vol. 21, pp. 501–510.</mixed-citation><mixed-citation xml:lang="en">Twisk J., Hoekman M. F., Lehmann E. M. et al. Insulin suppresses bile acid synthesis in cultured rat hepatocytes by down-regulation of cholesterol7 alpha-hydroxylase and sterol 27-hydroxylase gene transcription. Hepatology, 1995, Vol. 21, pp. 501–510.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Ивашкин В. Т. Ядерные рецепторы и патология печени // Рос. журн. гастроэнтерол. гепатол. колопроктол. 2010. – Т. 20, № 4. – С. 7–15.</mixed-citation><mixed-citation xml:lang="en">Ivashkin V. T. Nuclear receptors and liver pathology. Rus J Gastroenterol Hepatol Coloproctol. 2010, Vol. 20, No. 4, pp. 7–15. (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Gottlieb A., Canbay A. Why Bile Acids Are So Important in Non-Alcoholic Fatty Liver Disease (NAFLD) Progression. Review. Cells, 2019, Vol. 8, 1358 P.</mixed-citation><mixed-citation xml:lang="en">Gottlieb A., Canbay A. Why Bile Acids Are So Important in Non-Alcoholic Fatty Liver Disease (NAFLD) Progression. Review. Cells, 2019, Vol. 8, 1358 P.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Zhang Y.; Lee F. Y.; Barrera G. et al. Activation of the nuclear receptor FXR improves hyperglycemia and hyperlipidemia in diabeticmice. Proc. Natl. Acad. Sci. USA. 2006, Vol. 103, pp. 1006–1011.</mixed-citation><mixed-citation xml:lang="en">Zhang Y.; Lee F. Y.; Barrera G. et al. Activation of the nuclear receptor FXR improves hyperglycemia and hyperlipidemia in diabeticmice. Proc. Natl. Acad. Sci. USA. 2006, Vol. 103, pp. 1006–1011.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Conde J.; Scotece M.; Gomez R., Lopez V. Adipokines: Biofactors from white adipose tissue. A complex hub among inflammation, metabolism, and immunity. BioFactors. 2011, Vol. 37, pp. 413–420.</mixed-citation><mixed-citation xml:lang="en">Conde J.; Scotece M.; Gomez R., Lopez V. Adipokines: Biofactors from white adipose tissue. A complex hub among inflammation, metabolism, and immunity. BioFactors. 2011, Vol. 37, pp. 413–420.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Nam J.S., Ahn C. W., Park H. J., Kim Y. S. Semaphorin 3 C is a Novel Adipokine Representing Exercise-Induced Improvements of Metabolism in Metabolically Healthy Obese Young Males, Scientific Reports. 2020, Vol. 10, 10005 P. https://doi.org/10.1038/s41598–020–67004–7</mixed-citation><mixed-citation xml:lang="en">Nam J.S., Ahn C. W., Park H. J., Kim Y. S. Semaphorin 3 C is a Novel Adipokine Representing Exercise-Induced Improvements of Metabolism in Metabolically Healthy Obese Young Males, Scientific Reports. 2020, Vol. 10, 10005 P. https://doi.org/10.1038/s41598–020–67004–7</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Ikejima K., Takei Y., Honda H. et al. Leptin receptor-mediated signaling regulates hepatic fibrogenesis and remodeling of extracellular matrix in the rat. Gastroenterology. 2002, Vol. 122, pp. 1399–1410.</mixed-citation><mixed-citation xml:lang="en">Ikejima K., Takei Y., Honda H. et al. Leptin receptor-mediated signaling regulates hepatic fibrogenesis and remodeling of extracellular matrix in the rat. Gastroenterology. 2002, Vol. 122, pp. 1399–1410.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Marra F.; Bertolani C. Adipokines in liver diseases. Hepatology. 2009, Vol. 50, pp. 957–969.</mixed-citation><mixed-citation xml:lang="en">Marra F.; Bertolani C. Adipokines in liver diseases. Hepatology. 2009, Vol. 50, pp. 957–969.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Nakahara M., Fujii H., Maloney P. R., Shimizu M., Sato R. Bile Acids Enhance LowDensity Lipoprotein Receptor Gene Expression via a MAPK Cascade-mediated Stabilization of mRNA. J. Boil. Chem. 2002, Vol. 277, pp. 37229–37234.</mixed-citation><mixed-citation xml:lang="en">Nakahara M., Fujii H., Maloney P. R., Shimizu M., Sato R. Bile Acids Enhance LowDensity Lipoprotein Receptor Gene Expression via a MAPK Cascade-mediated Stabilization of mRNA. J. Boil. Chem. 2002, Vol. 277, pp. 37229–37234.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Радченко В.Г., Селиверстов П. В., Иванова В. Ф., Ситкин С. И. Алгоритм лечения неалкогольной жировой болезни печени и роль митохондриальной дисфункции в ее развитии. Фарматека, 2017, № 6 (339), С. 12–19.</mixed-citation><mixed-citation xml:lang="en">Radchenko V. G., Seliverstov P. V., Ivanova V. F., Sitkin S. I. Algorithm for the treatment of non-alcoholic fatty liver disease and the role of mitochondrial dysfunction in its development. Farmateka. 2017, No. 6 (339), pp. 12–19. (In Russ.)</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Wirth K., Peter R. S., Saely C. H., Concin H., Nagel G. Longterm weight change: association with impaired glucose metabolism in young Austrian adults. PLoS One. 2015, Vol. 10, e 0127186.</mixed-citation><mixed-citation xml:lang="en">Wirth K., Peter R. S., Saely C. H., Concin H., Nagel G. Longterm weight change: association with impaired glucose metabolism in young Austrian adults. PLoS One. 2015, Vol. 10, e 0127186.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Mosca A., Nobili V., De Vito R. et al. Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents. J Hepatol. 2017, Vol. 66(5), pp.1031–1036.</mixed-citation><mixed-citation xml:lang="en">Mosca A., Nobili V., De Vito R. et al. Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents. J Hepatol. 2017, Vol. 66(5), pp.1031–1036.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Ouyang X., Cirillo P., Sautin Y. et al. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol, 2008;48(6):993–999.</mixed-citation><mixed-citation xml:lang="en">Ouyang X., Cirillo P., Sautin Y. et al. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. J Hepatol, 2008;48(6):993–999.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Lanaspa M.A., Ishimoto T., Li N. et al. Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome. Nat Commun. 2013, Vol. 4, 2434 P.</mixed-citation><mixed-citation xml:lang="en">Lanaspa M.A., Ishimoto T., Li N. et al. Endogenous fructose production and metabolism in the liver contributes to the development of metabolic syndrome. Nat Commun. 2013, Vol. 4, 2434 P.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">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. J Biol Chem. 2019;294(11):4272–4281.</mixed-citation><mixed-citation xml:lang="en">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. J Biol Chem. 2019;294(11):4272–4281.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Pavlovic N., Rani B., Gerwins P., Heindryckx F. Platelets as Key Factors in Hepatocellular Carcinoma. Cancers (Basel). 2019, Vol. 11(7), 1022 P.</mixed-citation><mixed-citation xml:lang="en">Pavlovic N., Rani B., Gerwins P., Heindryckx F. Platelets as Key Factors in Hepatocellular Carcinoma. Cancers (Basel). 2019, Vol. 11(7), 1022 P.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Christopher D. Byrne &amp; Giovanni Targher. What’s new in NAFLD pathogenesis, biomarkers and treatment? Nature Reviews Gastroenterology &amp; Hepatology. 2020, Vol. 17, pp. 70–71.</mixed-citation><mixed-citation xml:lang="en">Christopher D. Byrne &amp; Giovanni Targher. What’s new in NAFLD pathogenesis, biomarkers and treatment? Nature Reviews Gastroenterology &amp; Hepatology. 2020, Vol. 17, pp. 70–71.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Klisic A., Isakovic A., Kocic G. et al. Relationship between Oxidative Stress, Inflammation and Dyslipidemia with Fatty Liver Index in Patients with Type 2 Diabetes Mellitus. Exp Clin Endocrinol Diabetes. 2018;126(6):371–378.</mixed-citation><mixed-citation xml:lang="en">Klisic A., Isakovic A., Kocic G. et al. Relationship between Oxidative Stress, Inflammation and Dyslipidemia with Fatty Liver Index in Patients with Type 2 Diabetes Mellitus. Exp Clin Endocrinol Diabetes. 2018;126(6):371–378.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Jovanovich A., Isakova T., Block G. et al. Deoxycholic Acid, a Metabolite of Circulating Bile Acids, and Coronary Artery Vascular Calcification in CKD. Am J Kidney Dis, 2018;71(1):27–34.</mixed-citation><mixed-citation xml:lang="en">Jovanovich A., Isakova T., Block G. et al. Deoxycholic Acid, a Metabolite of Circulating Bile Acids, and Coronary Artery Vascular Calcification in CKD. Am J Kidney Dis, 2018;71(1):27–34.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Gargiulo R., Suhail F., Lerma E. V. Cardiovascular disease and chronic kidney disease. Dis Mon, 2015;61(9):403–413.</mixed-citation><mixed-citation xml:lang="en">Gargiulo R., Suhail F., Lerma E. V. Cardiovascular disease and chronic kidney disease. Dis Mon, 2015;61(9):403–413.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
