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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/DM9623</article-id><article-id custom-type="elpub" pub-id-type="custom">diaendo-9623</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>Сахарный диабет и ожирение. Роль агонистов рецепторов глюкагоноподобного пептида-1 в лечении сахарного диабета 2 типа</article-title><trans-title-group xml:lang="en"><trans-title>Diabetes and obesity. The role of agonists glucagon-like peptide-1 of in the treatment of type 2 diabetes</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9390-1200</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Петунина</surname><given-names>Нина Александровна</given-names></name><name name-style="western" xml:lang="en"><surname>Petunina</surname><given-names>Nina A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор</p></bio><bio xml:lang="en"><p>MD, PhD, Professor</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>Милена Эдуардовна</given-names></name><name name-style="western" xml:lang="en"><surname>Telnova</surname><given-names>Milena Е.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., доцент</p></bio><bio xml:lang="en"><p>MD, PhD, assistant lecturer</p></bio><email xlink:type="simple">milena.telnova@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>&lt;p&gt;Первый Московский государственный медицинский университет им. И.М. Сеченова (Сеченовский Университет)&lt;/p&gt;</institution><country>Россия</country></aff><aff xml:lang="en"><institution>&lt;p&gt;I.M. Sechenov First Moscow State Medical University&lt;/p&gt;</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2018</year></pub-date><pub-date pub-type="epub"><day>10</day><month>10</month><year>2018</year></pub-date><volume>21</volume><issue>4</issue><fpage>293</fpage><lpage>300</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Петунина Н.А., Тельнова М.Э., 2018</copyright-statement><copyright-year>2018</copyright-year><copyright-holder xml:lang="ru">Петунина Н.А., Тельнова М.Э.</copyright-holder><copyright-holder xml:lang="en">Petunina N.A., Telnova M.Е.</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/9623">https://www.dia-endojournals.ru/jour/article/view/9623</self-uri><abstract><p>Среди пациентов с сахарным диабетом 2 типа (СД2) значительное количество (80%) страдают ожирением. Известно, что даже нарушение толерантности к глюкозе, так же как и СД, может привести к развитию сосудистых осложнений. В то же время снижение массы тела может снизить риск СД2 у пациентов с ожирением и предиабетом. По имеющимся данным, у пациентов с СД2 и лиц с ожирением отмечается существенное снижение инкретинового эффекта. Так, снижение инкретинового эффекта ведет за собой нарушение инсулинового ответа на прием углеводов и, следовательно, увеличение уровня глюкозы в крови. Также установлено, что снижение инкретинового эффекта у пациентов с СД2 может быть связано с более низкой секрецией глюкагоноподобного пептида-1.</p><p>Следовательно, интерес представляют группы антидиабетических препаратов, способных регулировать гликемию путем влияния на секрецию инсулина и глюкагона в зависимости от ее уровня. К числу таких препаратов относятся агонисты рецептора глюкагоноподобного пептида-1 (АР ГПП-1). В статье показано преимущество использования у пациентов с СД2 и ожирением АР ГПП-1 длительного действия (албиглутида, дулаглутида, эксенатида с медленным высвобождением) в режиме дозирования 1 раз в неделю.</p></abstract><trans-abstract xml:lang="en"><p>Significant number of patients with type 2 diabetes mellitus are obese. It is known that even glucose intolerance, as well as diabetes, can lead to vascular complications. At the same time, weight loss can reduce the risk of type 2 diabetes in obese and pre-diabetic patients. According to available data, a significant decrease in the incretin effect is observed in patients with type 2 diabetes and obese individuals. Thus, a decrease in the incretin effect leads to a violation of the insulin response to the intake of carbohydrates, and, consequently, an increase in the level of glucose in the blood. It was also found that the decrease in the incretin effect in patients with type 2 diabetes can be associated with a lower secretion of glucagon-like peptide-1. The interest is represented by groups of antidiabetic drugs capable of regulating glycemia by affecting the secretion of insulin and glucagon, depending on its level. Such drugs include glucagon-like peptide-1 receptor agonists.</p><p>The article shows the advantage of prolonged action in patients with type 2 diabetes and obesity of the glucagon-like peptide 1 receptor agonists (albiglutide, dulaglutide, exenatide with slow release) dosing 1 time a week.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>сахарный диабет 2 типа</kwd><kwd>ожирение</kwd><kwd>инкретины</kwd><kwd>глюкагоноподобный пептид-1</kwd></kwd-group><kwd-group xml:lang="en"><kwd>type 2 diabetes</kwd><kwd>obesity</kwd><kwd>incretins</kwd><kwd>glucagon-like peptide-1</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">Дедов И.И., Шестакова М.В., Майоров А.Ю., и др. Алгоритмы специализированной медицинской помощи больным сахарным диабетом. / Под ред. 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