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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">cardio</journal-id><journal-title-group><journal-title xml:lang="ru">Кардиология</journal-title><trans-title-group xml:lang="en"><trans-title>Kardiologiia</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">0022-9040</issn><issn pub-type="epub">2412-5660</issn><publisher><publisher-name>Kardiomag</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18087/cardio.2026.2.n3116</article-id><article-id custom-type="elpub" pub-id-type="custom">cardio-3116</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>ОРИГИНАЛЬНЫЕ СТАТЬИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>RESEARCH ARTICLES</subject></subj-group></article-categories><title-group><article-title>Влияние семаглутида на массу тела, липидный состав крови и адипокиновый статус у пациентов с ожирением</article-title><trans-title-group xml:lang="en"><trans-title>Effect of Semaglutide on Body Weight, Blood Lipid Profile, and Adipokine Status in Obese Patients</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3505-2487</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Тюрина</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Tyurina</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н. младший научный сотрудник лаборатории нарушений липидного обмена</p><p> </p></bio><bio xml:lang="en"><p>Junior Researcher, Laboratory of Lipid Metabolism Disorders</p><p> </p></bio><email xlink:type="simple">alex.tyurina.cardio@yandex.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/0000-0001-8126-1330</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Курочкина</surname><given-names>Н. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Kurochkina</surname><given-names>N. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н. научный сотрудник лаборатории фенотипов атеросклероза</p><p> </p><p> </p></bio><bio xml:lang="en"><p>PhD, Researcher, Laboratory of Atherosclerosis Phenotypes</p><p> </p><p> </p></bio><email xlink:type="simple">nataly91@me.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/0000-0002-1518-6552</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ежов</surname><given-names>М. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Yezhov</surname><given-names>M. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., главный научный сотрудник, руководитель Лаборатории нарушений липидного обмена</p></bio><bio xml:lang="en"><p>MD, Chief Researcher, Head of the Laboratory of Lipid Metabolism Disorders</p></bio><email xlink:type="simple">marat_ezhov@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">ФГБУ «Национальный медицинский исследовательский центр кардиологии им. акад. Е. И. Чазова» Минздрава РФ, Москва<country>Россия</country></aff><aff xml:lang="en">Chazov National Medical Research Center of Cardiology, Moscow<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2026</year></pub-date><pub-date pub-type="epub"><day>02</day><month>04</month><year>2026</year></pub-date><volume>66</volume><issue>2</issue><fpage>31</fpage><lpage>40</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Тюрина А.В., Курочкина Н.С., Ежов М.В., 2026</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="ru">Тюрина А.В., Курочкина Н.С., Ежов М.В.</copyright-holder><copyright-holder xml:lang="en">Tyurina A.V., Kurochkina N.S., Yezhov M.V.</copyright-holder><license 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://cardio.elpub.ru/jour/article/view/3116">https://cardio.elpub.ru/jour/article/view/3116</self-uri><abstract><p>Цель     Оценка влияния терапии агонистом рецепторов глюкагоноподобного пептида-1 (арГПП-1) семаглутидом в динамике в течение 8 мес на антропометрические показатели, липидный состав крови и адипокиновый статус у пациентов с ожирением в зависимости от наличия или отсутствия сахарного диабета (СД) 2‑го типа.</p><p>Материал и методы   В исследование включены 65 пациентов с ожирением, у 26 из них был СД 2‑го типа. Всем участникам назначался семаглутид с титрацией дозы до 1 мг раз в неделю в течение 8 мес. До начала терапии и после ее окончания проводилась оценка антропометрических данных (масса тела, индекс массы тела, окружность талии), биохимических параметров (липидный состав крови, глюкоза, аспартатаминотрансфераза, аланинаминотрансфераза, креатинин) и уровней адипокинов (лептин, адипонектин, резистин) методом иммунофлуоресцентного анализа.</p><p>Результаты    На фоне терапии семаглутидом зафиксировано статистически значимое снижение массы тела (p&lt;0,001), индекса массы тела (p&lt;0,001) и уменьшение окружности талии (p&lt;0,001). В динамике отмечено улучшение липидного состава крови: снижение уровня холестерина липопротеидов низкой плотности (p=0,001), триглицеридов (p&lt;0,001) и общего холестерина (p=0,001), а также повышение уровня холестерина липопротеидов высокой плотности (p&lt;0,01). Терапия оказала существенное влияние на адипокиновый статус: зафиксировано статистически значимое повышение концентрации антиатерогенного адипонектина (p&lt;0,001) и снижение уровня лептина (p&lt;0,001), что свидетельствует об улучшении метаболической функции жировой ткани. При этом достоверных изменений в уровне резистина не выявлено. Наряду с этим отмечено положительное влияние на маркеры функции печени и почек, проявившееся в снижении активности аспартатаминотрансферазы, аланинаминотрансферазы и уровня креатинина. В подгруппе пациентов с СД 2‑го типа выявлено статистически значимое улучшение гликемии.</p><p>Заключение      Терапия семаглутидом в течение 8 мес у пациентов с ожирением продемонстрировала комплексный кардиометаболический эффект, включающий статистически значимое снижение массы тела, улучшение липидного состава крови, показателей функции печени и почек, а также благоприятную перестройку адипокинового статуса. Полученные данные подтверждают целесообразность применения арГПП-1 не только для контроля гликемии и массы тела, но и в качестве многофакторной кардиопротективной терапии у пациентов с ожирением.</p><p> </p></abstract><trans-abstract xml:lang="en"><p>Aim        To evaluate the dynamic impact of an 8-month glucagon-like peptide-1 receptor agonist (GLP-1 RA) therapy with semaglutide on anthropometric metrics, blood lipid profiles, and adipokine status in obese patients, with and without type 2 diabetes mellitus (T2DM).</p><p>Material and methods    The study included 65 patients with obesity, 26 of whom had T2DM. All participants were prescribed semaglutide, with dose titration up to 1 mg once weekly over 8 months. Before and after the treatment period, the following variables were assessed: anthropometric data (body weight, body weight index, waist circumference), biochemical parameters (lipid profile, glucose, aspartate aminotransferase, alanine aminotransferase, creatinine), and adipokine concentrations (leptin, adiponectin, resistin) via immunofluorescence assay.</p><p>Results  Semaglutide therapy was associated with a statistically significant reduction in body weight (p&lt;0.001), body mass index (p&lt;0.001), and waist circumference (p&lt;0.001). Improvements in the lipid profile were observed over time, including decreased concentrations of low-density lipoprotein cholesterol (p=0.001), triglycerides (p&lt;0.001), and total cholesterol (p=0.001), alongside an increase in high-density lipoprotein cholesterol (p&lt;0.01). Therapy significantly impacted adipokine status: a statistically significant increase in anti-atherogenic adiponectin (p&lt;0.001) and a decrease in leptin levels (p&lt;0.001) were recorded, indicating improved adipose tissue metabolic function. However, no significant changes in resistin concentrations were found. Additionally, positive effects on liver and kidney function markers were noted, manifested by reductions in aspartate aminotransferase and alanine aminotransferase activity, as well as creatinine levels. In the subgroup of patients with T2DM, a statistically significant improvement in glycemic control was observed.</p><p>Conclusion         Semaglutide therapy for 8 months in obese patients yielded a robust cardiometabolic impact, characterized by significant weight reduction, optimized lipid profiles, and improved liver and kidney function markers, alongside a favorable restructuring of adipokine status. These results support the use of GLP-1 RAs not only for glycemic and weight control but also as a multifaceted cardioprotective therapy for obese patients.</p><p> </p></trans-abstract><kwd-group xml:lang="ru"><kwd>Агонисты рецепторов глюкагоноподобного пептида-1</kwd><kwd>ожирение</kwd><kwd>сахарный диабет 2 го типа</kwd><kwd>адипокины</kwd></kwd-group><kwd-group xml:lang="en"><kwd>Glucagon-like peptide-1 receptor agonists</kwd><kwd>obesity</kwd><kwd>type 2 diabetes mellitus</kwd><kwd>adipokines</kwd></kwd-group><funding-group xml:lang="ru"><funding-statement>Финансирование Исследование проведено при поддержке компании ООО «Герофарм» (Россия). Данное обстоятельство не повлияло на результаты работы и позицию авторов.  Конфликт интересов отсутствует.</funding-statement></funding-group><funding-group xml:lang="en"><funding-statement>Funding This study was supported by Geropharm LLC (Russia). The funder had no influence on the results of the work or the position of the authors.   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