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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">ometendo</journal-id><journal-title-group><journal-title xml:lang="ru">Ожирение и метаболизм</journal-title><trans-title-group xml:lang="en"><trans-title>Obesity and metabolism</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2071-8713</issn><issn pub-type="epub">2306-5524</issn><publisher><publisher-name>Endocrinology Research Centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/omet12758</article-id><article-id custom-type="elpub" pub-id-type="custom">ometendo-12758</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>Научные обзоры</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Reviews</subject></subj-group></article-categories><title-group><article-title>Неалкогольная жировая болезнь печени и сахарный диабет 2 типа: проблема сопряженности и этапности развития</article-title><trans-title-group xml:lang="en"><trans-title>Non-alcoholic fatty liver disease and type 2 diabetes mellitus: the problem of conjunction and phasing</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-0217-9246</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Киселева</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Kiseleva</surname><given-names>E. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p> Киселева Елизавета Владимировна</p><p> Россия, 117997, Москва, ул. Островитянова, д. 1</p></bio><bio xml:lang="en"><p>Elizaveta V. Kiseleva</p><p>1 Ostrovityanova street, 117997 Moscow, Russia</p></bio><email xlink:type="simple">elizakiseleva10@gmail.com</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>Демидова</surname><given-names>Т. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>Demidova</surname><given-names>T. Y.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Демидова Татьяна Юльевна, д.м.н., профессор; eLibrary SPIN: 9600-9796; Scopus Author ID: 7003771623 </p><p>Москва</p></bio><bio xml:lang="en"><p>Tatiana Yu. Demidova, MD, PhD, Professor</p><p>Moscow</p></bio><email xlink:type="simple">t.y.demidova@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Российский национальный исследовательский медицинский университет имени Н.И. Пирогова</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Pirogov Russian National Research Medical University (RNRMU)</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2021</year></pub-date><pub-date pub-type="epub"><day>23</day><month>08</month><year>2021</year></pub-date><volume>18</volume><issue>3</issue><fpage>313</fpage><lpage>319</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Киселева Е.В., Демидова Т.Ю., 2021</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="ru">Киселева Е.В., Демидова Т.Ю.</copyright-holder><copyright-holder xml:lang="en">Kiseleva E.V., Demidova T.Y.</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.omet-endojournals.ru/jour/article/view/12758">https://www.omet-endojournals.ru/jour/article/view/12758</self-uri><abstract><p>Широкая распространенность неалкогольной жировой болезни печени (НАЖБП) и сахарного диабета 2 типа (СД2), а также их взаимосвязи определяет необходимость прицельного рассмотрения данной патологии с целью оптимизации подходов к диагностике и лечению пациентов с НАЖБП и СД2. Являясь компонентами метаболического синдрома, эти два заболевания во многом имеют схожие механизмы развития и прогрессирования, синергично повышая риск неблагоприятных исходов у коморбидных пациентов. Несмотря на общность патофизиологических механизмов, актуальным остается вопрос о последовательности развития НАЖБП и СД2.</p><p>По результатам анализа литературы выделено две основных теории: алиментарная и метаболическая. Согласно алиментарной теории, первичным звеном патогенеза выступают ожирение и сопряженное с ним избыточное накопление свободных жирных кислот и триглицеридов в печени, приводящее впоследствии к инсулинорезистентности и развитию СД2. В противоположность этому, в метаболической теории в качестве первичного удара рассматривается сопутствующая диабету инсулинорезистентность, которая независимо от ожирения создает предпосылки для повреждения печени. Помимо этого, в обзоре уделено особое внимание рассмотрению новой концепции — метаболически ассоциированной жировой болезни печени (МАЖБП), рассматриваемой в качестве печеночного компонента метаболического синдрома. В рамках данной концепции выделяют различные клинические фенотипы НАЖБП, определяющие путь, по которому развиваются рассматриваемые заболевания. В заключение в обзоре обсуждается патогенетически обоснованная терапия, акцент в которой сделан на преодоление инсулинорезистентности, коррекцию атерогенной дислипидемии и восстановление структуры и функции клеток печени.</p></abstract><trans-abstract xml:lang="en"><p>The widespread prevalence of non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM), as well as their combination, determines the need for a targeted analysis of this pathology in order to optimize approaches to the diagnosis and treatment of patients with NAFLD and T2DM. As components of the metabolic syndrome, these two diseases have largely similar mechanisms of development and progression, simultaneously increasing the risk of adverse outcomes in comorbid patients. Despite the common pathophysiological mechanisms, the question of the development of NAFLD and T2DM remains significant.</p><p>Upon conducting literature analysis, two main theories have been identified: alimentary and metabolic. According to the alimentary theory, the primary link in the pathogenesis is obesity and the associated excessive accumulation of free fatty acids and triglycerides in the liver, which subsequently leads to insulin resistance and the development of T2DM. In contrast, the metabolic theory considers diabetes-related insulin resistance as the first hit, which, regardless of obesity, creates preconditions for liver damage. In addition, the review focuses on the consideration of the new concept of Metabolic associated fatty liver disease (MAFLD) as a hepatic manifestation of the metabolic syndrome and considers the clinical phenotypes identified within this pathology. In conclusion, pathogenically based treatment goals in patients with NAFLD and T2DM are overcoming insulin resistance, correcting atherogenic dyslipidemia, and restoring the structures and functions of liver cells.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>неалкогольная жировая болезнь печени</kwd><kwd>сахарный диабет 2 типа</kwd><kwd>ожирение</kwd><kwd>инсулинорезистентность</kwd><kwd>метаболический синдром</kwd><kwd>МАЖБП</kwd></kwd-group><kwd-group xml:lang="en"><kwd>non-alcoholic fatty liver disease</kwd><kwd>type 2 diabetes mellitus</kwd><kwd>obesity</kwd><kwd>insulin resistance</kwd><kwd>metabolic syndrome</kwd><kwd>MAFLD</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">В Who.int [Internet]. The top 10 causes of death [cited 2020 9 Dec]. 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