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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/omet12754</article-id><article-id custom-type="elpub" pub-id-type="custom">ometendo-12754</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>Влияние адипонектина на обмен углеводов, липидов и липопротеинов: анализ сигнальных механизмов</article-title><trans-title-group xml:lang="en"><trans-title>The influence of adiponectin on carbohydrates, lipids, and lipoproteins metabolism: analysis of signaling mechanisms</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-5321-8834</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Танянский</surname><given-names>Д. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Tanyanskiy</surname><given-names>D. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Танянский Дмитрий Андреевич - кандидат медицинских наук; Researcher ID: G-3307-2015; Scopus Author ID: 53878682400; eLibrary SPIN: 9303-9445.</p><p>197376, Санкт-Петербург, ул. акад. Павлова, д. 12</p></bio><bio xml:lang="en"><p>Dmitry A. Tanyanskiy, MD, PhD; Researcher ID: G-3307-2015; Scopus Author ID: 53878682400; eLibrary SPIN: 9303-9445;</p><p>12 acad. Pavlov street, 197376 Saint-Petersburg</p></bio><email xlink:type="simple">dmitry.athero@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-1613-0654</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Денисенко</surname><given-names>А. Д.</given-names></name><name name-style="western" xml:lang="en"><surname>Denisenko</surname><given-names>A. D.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Денисенко Александр Дорофеевич - доктор медицинских наук, профессор; Researcher ID: G-4774-2015; Scopus Author ID: 7005191805; eLibrary SPIN: 7496-1449.</p><p>Санкт-Петербург</p></bio><bio xml:lang="en"><p>Alexander D. Denisenko, MD, PhD, Professor; Researcher ID: G-4774-2015; Scopus Author ID: 7005191805; eLibrary SPIN: 7496-1449.</p><p>Saint-Petersburg</p></bio><email xlink:type="simple">add@iem.sp.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Институт экспериментальной медицины</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Institute of Experimental Medicine</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>07</month><year>2021</year></pub-date><volume>18</volume><issue>2</issue><fpage>103</fpage><lpage>111</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Танянский Д.А., Денисенко А.Д., 2021</copyright-statement><copyright-year>2021</copyright-year><copyright-holder xml:lang="ru">Танянский Д.А., Денисенко А.Д.</copyright-holder><copyright-holder xml:lang="en">Tanyanskiy D.A., Denisenko A.D.</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/12754">https://www.omet-endojournals.ru/jour/article/view/12754</self-uri><abstract><p>Диcрегуляция функций жировой ткани вносит существенный вклад в патогенез метаболического синдрома, одного из наиболее распространенных в последние годы заболеваний. Жировая ткань представляет собой орган, секретирующий по меньшей мере несколько десятков сигнальных молекул, адипокинов. Одним из наиболее изученных и при этом загадочных адипокинов является адипонектин. Последнее обусловлено отсутствием четких представлений о биологической роли данного адипокина, наличием у него нескольких молекулярных форм с отличающейся активностью и нескольких типов рецепторов, локализованных практически во всех клетках организма. Цель данного обзора — обобщение и анализ имеющихся сведений о молекулярных механизмах влияния адипонектина на обмен углеводов, липидов и липопротеинов. Поиск литературы проводился по ключевым словам «адипонектин» и «метаболический синдром» в базах Pubmed и Elibrary.ru за период с 1995 по 2021 гг.</p><p>По результатам анализа литературы сделано предположение об участии адипонектина в энергетическом обмене как гормона «сытости», способствующего утилизации и запасанию богатых энергией субстратов, жирных кислот и глюкозы, что предупреждает развитие или смягчает уже развившуюся инсулинорезистентность. Это способствует уменьшению количества триглицеридов и повышению уровня липопротеинов высокой плотности в плазме. Адипонектин оказывает влияние на метаболические процессы, активируя каскады AdipoR1-APPL1-LKB1-AMPK, AdipoR1-APPL1-p38, AdipoR2-PPARα, а также, возможно, посредством активации церамидазного и фосфоинозитидного путей и инсулинового сигналинга. Помимо рецепторов AdipoR1/2, в эндотелиальных и мышечных клетках в передаче адипонектинового сигнала, возможно, участвует молекула адгезии Т-кадгерин. Механизмы передачи сигнала от Т-кадгерина, а также от AdipoR2 остаются невыясненными. Исследования, посвященные изучению механизмов действия отдельных молекулярных форм адипонектина, встречаются крайне редко. Проведенный анализ свидетельствует о сложном характере сигналинга адипонектина, многие механизмы которого остаются нераскрытыми, и, возможно, уже ближайшее будущее принесет нам существенный прогресс в этой области.</p></abstract><trans-abstract xml:lang="en"><p>Dysregulation of adipose tissue functions makes a significant contribution to the pathogenesis of metabolic syndrome, one of the most common diseases in recent years. Adipose tissue is an organ that secretes at least several dozen signaling molecules, adipokines. One of the most studied and at the same time mysterious adipokines is adiponectin. The latter is due to the lack of clear ideas about the biological role of this adipokine, the presence of its several molecular forms with different activity and several types of receptors to this adipokine localized in almost all cells of the body. The purpose of this review is to summarize and analyze the available information about the molecular mechanisms of the effect of adiponectin on metabolism of carbohydrates, lipids and lipoproteins. The literature search was conducted by the keywords "adiponectin" and "metabolic syndrome" in the Pubmed and Elibrary.ru databases for the period from 1995 to 2021.</p><p>According to the results of the literature analysis, it is assumed that adiponectin is involved in energy metabolism as a «satiety» hormone that promotes the utilization and storage of energy-rich substrates, fatty acids and glucose, which prevents the development or mitigates the already developed insulin resistance. This reduces the amount of plasma triglycerides and increases the level of high-density lipoproteins in the plasma. Adiponectin affects metabolic processes by activating the AdipoR1-APPL1-LKB1-AMPK, AdipoR1-APPL1-p38, AdipoR2-PPARa cascades, and possibly by activating the ceramidase and phosphoinositide pathways and insulin signaling. In addition to the AdipoR1/2 receptors, the adhesion molecule T-cadherin may be involved in the transduction of the adiponectin signal in endothelial and muscle cells. The mechanisms of signal transduction from T-cadherin, as well as from AdipoR2, remain unclear. Studies on the mechanisms of the action of individual molecular forms of adiponectin are extremely rare. The analysis shows the complex nature of adiponectin signaling, many of the mechanisms of  which remain undiscovered, and it is possible that the near future will bring us significant progress in this area.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>адипонектин</kwd><kwd>ожирение</kwd><kwd>инсулинорезистентность</kwd><kwd>липопротеины</kwd><kwd>адипонектиновые рецепторы</kwd><kwd>АМФ-активируемая протеинкиназа</kwd><kwd>PPAR alpha</kwd></kwd-group><kwd-group xml:lang="en"><kwd>adiponectin</kwd><kwd>obesity</kwd><kwd>insulin resistance</kwd><kwd>lipoproteins</kwd><kwd>adiponectin receptors</kwd><kwd>AMP-activated protein kinase</kwd><kwd>PPAR alpha</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Работа выполнена по госзаданию, шифр НИР 0557-2019-0011</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">Sethi J K, Vidal-Puig AJ. 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