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<article article-type="review-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">medsovet</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинский Совет</journal-title><trans-title-group xml:lang="en"><trans-title>Meditsinskiy sovet = Medical Council</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2079-701X</issn><issn pub-type="epub">2658-5790</issn><publisher><publisher-name>REMEDIUM GROUP Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.21518/ms2022-026</article-id><article-id custom-type="elpub" pub-id-type="custom">medsovet-7561</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>ЗАБОЛЕВАНИЯ БИЛИАРНОЙ СИСТЕМЫ И ПЕЧЕНИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>DISEASES OF THE BILIARY SYSTEM AND LIVER</subject></subj-group></article-categories><title-group><article-title>Полиморфизмы генов HSD17B13, GCKR, HFE и CP как факторы развития неалкогольной жировой болезни печени и сопутствующих ее заболеваний</article-title><trans-title-group xml:lang="en"><trans-title>Polymorphisms of HSD17B13, GCKR, HFE, and CP as factors of the development of non-alcoholic fatty liver disease and comorbid diseases</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3992-9207</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Смирнова</surname><given-names>О. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Smirnova</surname><given-names>O. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Смирнова Ольга Валентиновна, д.м.н., профессор, заведующая лабораторией клинической патофизиологии, главный научный сотрудник; профессор </p><p>660022, Красноярск, ул. Партизана Железняка, д. 3 «Г»;660041, Красноярск, пр. Свободный, д. 79 </p></bio><bio xml:lang="en"><p>Olga V. Smirnova, Dr. Sci. (Med.), Professor, Head of Laboratory of Clinical Pathophysiology; Professor </p><p>3G, Partizan Zheleznyak St., Krasnoyarsk, 660022;79, Svobodnyy Ave, Krasnoyarsk, 660041</p></bio><email xlink:type="simple">ovsmirnova71@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-1295-9262</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Лагутинская</surname><given-names>Д. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Lagutinskaya</surname><given-names>D. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Лагутинская Дарья Владимировна, младший научный сотрудник; аспирант </p><p>660022, Красноярск, ул. Партизана Железняка, д. 3 «Г»;660041, Красноярск, пр. Свободный, д. 79</p></bio><bio xml:lang="en"><p>Darya V. Lagutinskaya, Juniour Research Associate; Postgraduate Student </p><p>3G, Partizan Zheleznyak St., Krasnoyarsk, 660022;79, Svobodnyy Ave, Krasnoyarsk, 660041</p></bio><email xlink:type="simple">dlagut1210@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Научно-исследовательский институт медицинских проблем Севера;&#13;
Сибирский федеральный университет</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Scientific Research Institute of medical problems of the North; &#13;
Siberian Federal University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2023</year></pub-date><pub-date pub-type="epub"><day>25</day><month>05</month><year>2023</year></pub-date><volume>0</volume><issue>8</issue><fpage>119</fpage><lpage>125</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Смирнова О.В., Лагутинская Д.В., 2023</copyright-statement><copyright-year>2023</copyright-year><copyright-holder xml:lang="ru">Смирнова О.В., Лагутинская Д.В.</copyright-holder><copyright-holder xml:lang="en">Smirnova O.V., Lagutinskaya D.V.</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.med-sovet.pro/jour/article/view/7561">https://www.med-sovet.pro/jour/article/view/7561</self-uri><abstract><p>В настоящее время неалкогольная жировая болезнь печени (НАЖБП) является одним из самых распространенных хронических заболеваний печени. Данное состояние рассматривается как печеночная манифестация метаболического синдрома, который связан с избыточным весом и нарушением обмена глюкозы и жиров. Несмотря на очевидную роль образа жизни в появлении этой болезни, все больше высказывается предположений о том, что нарушения метаболизма жиров и углеводов имеют под собой генетическую основу, которая и определяет склонность к развитию НАЖБП. Показано, что мутантные полиморфизмы генов HSD17B13, GCKR, HFE и CP оказывают влияние на течение НАЖБП, однако эти эффекты требуют дополнительного изучения. Поэтому целью данной работы явились анализ и  систематизация имеющихся данных об  их влиянии на состояние пациентов с НАЖБП из преимущественно зарубежных источников за последние 10 лет. В ходе исследования было проанализировано 573 литературных источника, в работе были использованы наиболее важные 64 источника. Мутация гена HSD17B13 связывается с более легким течением НАЖБП, тогда как полиморфизмы гена GCKR, напротив, связаны с более тяжелыми гистологическими проявлениями данного заболевания, например, стеатоз и фиброз. Гены HFE и CP, хоть и не связаны напрямую с обменом макронутриентов, тем не менее, способствуют развитию более тяжелых форм НАЖБП, что может быть связано с развитием воспаления и оксидативного стресса, вызванного избыточным накоплением железа в гепатоцитах.</p></abstract><trans-abstract xml:lang="en"><p>Currently, non-alcoholic fatty liver disease is one of the most common chronic liver diseases. In recent years, this condition has been considered as a hepatic manifestation of the metabolic syndrome, which is associated with overweight and impaired glucose and fat metabolism. Despite the obvious role of lifestyle in the development of this disease, it is increasingly being suggested that disorders in the metabolism of fats and carbohydrates have a genetic basis, which determines the tendency to develop NAFLD. Mutant polymorphisms of the HSD17B13, GCKR, HFE, and CP genes have been shown to affect the course of NAFLD, but these effects require further study. Therefore, the aim of this work was to analyze and systematize the available data from foreign articles over the past 10 years. In this study, 573 articles were analyzed, the most important 64 original research works were used here. Mutations in  the HSD17B13  gene are associated with a  milder course of  NAFLD, while GCKR gene polymorphisms, on the contrary, are associated with more severe histological manifestations of this disease, such as steatosis and fibrosis. The HFE and CP genes, although not directly related to macronutrient metabolism, nevertheless contribute to the development of more severe forms of NAFLD, which may be associated with the development of inflammation and oxidative stress caused by excessive accumulation of iron in hepatocytes.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>неалкогольная жировая болезнь печени</kwd><kwd>HSD17B13</kwd><kwd>GCKR</kwd><kwd>HFE</kwd><kwd>CP</kwd><kwd>обмен железа</kwd></kwd-group><kwd-group xml:lang="en"><kwd>nonalcoholic fatty liver disease</kwd><kwd>HSD17B13</kwd><kwd>GCKR</kwd><kwd>HFE</kwd><kwd>CP</kwd><kwd>iron metabolism</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Работа написана в рамках госзадания № 0287-2021-0005 «Исследование молекулярно-генетических и регуляторно-метаболических механизмов функциональной активности клеток иммунной системы в норме и при иммунопатологических состояниях».</funding-statement><funding-statement xml:lang="en">The work was written within the framework of the state task No. 0287-2021-0005 “Study of moleculargenetic and regulatory-metabolic mechanisms of the functional activity of cells of the immune system in normal and immunopathological conditions”.</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Vernon G., Baranova A., Younossi Z. 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