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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">diaendo</journal-id><journal-title-group><journal-title xml:lang="ru">Сахарный диабет</journal-title><trans-title-group xml:lang="en"><trans-title>Diabetes mellitus</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2072-0351</issn><issn pub-type="epub">2072-0378</issn><publisher><publisher-name>Endocrinology research centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/DM12746</article-id><article-id custom-type="elpub" pub-id-type="custom">diaendo-12746</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>Обзоры</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Некоторые механизмы развития воспаления при сахарном диабете 2 типа</article-title><trans-title-group xml:lang="en"><trans-title>Some mechanisms of inflammation development in type 2 diabetes mellitus</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Бочкарева</surname><given-names>Л. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Bochkareva</surname><given-names>L. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Бочкарева Лейла Азимовна, аспирант </p><p>Москва</p></bio><bio xml:lang="en"><p>Leyla A. Bochkareva, MD, PhD student </p><p>Moscow</p></bio><email xlink:type="simple">lejlani@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/0000-0002-6823-2487</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Недосугова</surname><given-names>Л. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Nedosugova</surname><given-names>L. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Недосугова Людмила Викторовна, д.м.н., профессор </p><p>119991, Москва, ул. Трубецкая, д. 8, стр. 2 </p><p>eLibrary SPIN: 1853-0215; e-mail:  </p></bio><bio xml:lang="en"><p>Ludmila V. Nedosugova, MD, PhD, Professor</p><p>8/2 Trubetskaya, 119991 Moscow</p><p>eLibrary SPIN: 1853-0215 </p></bio><email xlink:type="simple">profmila@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/0000-0001-9390-1200</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Петунина</surname><given-names>Н. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Petunina</surname><given-names>N. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Петунина Нина Александровна, д.м.н., профессор, член-корр. РАН </p><p>eLibrary SPIN: 9784-3616 </p><p>Москва</p></bio><bio xml:lang="en"><p>Nina A. Petunina, MD, PhD, Professor</p><p>eLibrary SPIN: 9784-3616 </p><p>Moscow</p></bio><email xlink:type="simple">napetunina@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/0000-0001-8007-9721</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Тельнова</surname><given-names>М. Э.</given-names></name><name name-style="western" xml:lang="en"><surname>Теlnova</surname><given-names>M. Е.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Тельнова Милена Эдуардовна, к.м.н., доцент </p><p>eLibrary SPIN: 1007-4617 </p><p>Москва</p></bio><bio xml:lang="en"><p>Milena Е. Теlnova, MD, PhD, associate Professor</p><p>eLibrary SPIN: 1007-4617 </p><p>Moscow</p></bio><email xlink:type="simple">milena.telnova@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/0000-0001-7025-8427</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гончарова</surname><given-names>Е. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Goncharova</surname><given-names>E. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Гончарова Екатерина Валерьевна, к.м.н., доцент </p><p>eLibrary SPIN: 7148-4669 </p><p>Москва</p></bio><bio xml:lang="en"><p>Ekaterina V. Goncharova, MD, PhD, associate Professor</p><p>eLibrary SPIN: 7148-4669 </p><p>Moscow</p></bio><email xlink:type="simple">goncharova_ev@inbox.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Первый Московский государственный медицинский университет им. И.М. Сеченова (Сеченовский Университет)</institution><country>Россия</country></aff><aff xml:lang="en"><institution>I.M. Sechenov First Moscow State Medical University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2021</year></pub-date><pub-date pub-type="epub"><day>10</day><month>08</month><year>2021</year></pub-date><volume>24</volume><issue>4</issue><fpage>334</fpage><lpage>341</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Бочкарева Л.А., Недосугова Л.В., Петунина Н.А., Тельнова М.Э., Гончарова Е.В., 2021</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="ru">Бочкарева Л.А., Недосугова Л.В., Петунина Н.А., Тельнова М.Э., Гончарова Е.В.</copyright-holder><copyright-holder xml:lang="en">Bochkareva L.A., Nedosugova L.V., Petunina N.A., Теlnova M.Е., Goncharova E.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.dia-endojournals.ru/jour/article/view/12746">https://www.dia-endojournals.ru/jour/article/view/12746</self-uri><abstract><p>Воспаление играет ключевую роль в развитии и прогрессировании сахарного диабета 2 типа (СД2) — заболевания, характеризующегося периферической инсулинорезистентностью и системной глюколипотоксичностью. Основным источником воспаления на ранних стадиях заболевания является висцеральная жировая ткань (ЖT). Макрофаги — врожденные иммунные клетки, которые присутствуют во всех периферических тканях, включая ЖТ. Нарушение реакции макрофагов ЖT (МЖT) на изменения микросреды лежат в основе аберрантного воспаления и развития местной и системной инсулинорезистентности. Воспалительная активация макрофагов регулируется на нескольких уровнях: стимуляция рецепторов клеточной поверхности, внутриклеточная передача сигналов, транскрипция и метаболические уровни, которые активируются трансформацией макрофагов по провоспалительному либо по противовоспалительному пути. Такая поляризация макрофагов в современной иммунологии разделяется на классическую воспалительную М1 поляризацию и альтернативную противовоспалительную М2 поляризацию макрофагов. Соотношение М1/М2 макрофагов в процессе воспаления обеспечивает разрешение воспаления на разных стадиях его развития. В обзоре рассмотрены основные механизмы, участвующие в воспалении ЖT и развитии инсулинорезистентности при СД2, поддерживаемые с участием иммунокомпетентных клеток, М1/M2, а также выделяемых при этом факторов роста и гуморальных факторов иммунитета.</p></abstract><trans-abstract xml:lang="en"><p>Inflammation plays a key role in the development and progression of type 2 diabetes (T2DM), a disease characterized by peripheral insulin resistance and systemic glucolipotoxicity. The main source of inflammation in the early stages of the disease is visceral adipose tissue (VT). Macrophages are innate immune cells that are present in all peripheral tissues, including VT. Violation of the response of VT (MT) macrophages to changes in the microenvironment underlies aberrant inflammation and the development of local and systemic insulin resistance. The inflammatory activation of macrophages is regulated at several levels: stimulation of cell surface receptors, intracellular signaling, transcription, and metabolic levels. Which are activated by the transformation of macrophages along the pro-inflammatory or anti-inflammatory pathways. Such polarization of macrophages in modern immunology is divided into classical anti-inflammatory M1 polarization and alternative anti-inflammatory M2 polarization of macrophages. The M1 / M2 ratio of macrophages in the process of inflammation ensures the resolution of inflammation at different stages of its development. The review considers the main mechanisms involved in VT inflammation and the development of insulin resistance in T2DM, supported with the participation of immunocompetent cells, M1 / M2, as well as growth factors and humoral immunity factors secreted during this process.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>воспаление</kwd><kwd>сахарный диабет 2 типа</kwd><kwd>инсулинорезистентность</kwd><kwd>жировая ткань</kwd><kwd>макрофаги</kwd></kwd-group><kwd-group xml:lang="en"><kwd>inflammation</kwd><kwd>type 2 diabetes mellitus</kwd><kwd>insulin resistance</kwd><kwd>adipose tissue</kwd><kwd>macrophages</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">Shimobayashi M, Albert V, Woelnerhanssen B, et al. Insulin resistance causes inflammation in adipose tissue. 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