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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">10.14341/2071-8713-5241</article-id><article-id custom-type="elpub" pub-id-type="custom">ometendo-5241</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>Статьи</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>Патогенетическое обоснование и эффективность применениявилдаглиптина у больных сахарным диабетом 2 типа</article-title><trans-title-group xml:lang="en"><trans-title>Pathogenetic substantiation and effectiveness of vildagliptin use inpatients with diabetes mellitus type 2</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>Romantsova</surname><given-names>T I</given-names></name></name-alternatives><email xlink:type="simple">romantsovatatiana@rambler. ru</email></contrib></contrib-group><pub-date pub-type="collection"><year>2009</year></pub-date><pub-date pub-type="epub"><day>15</day><month>09</month><year>2009</year></pub-date><volume>6</volume><issue>3</issue><issue-title>№3 (2009)</issue-title><fpage>16</fpage><lpage>26</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Romantsova T.I., 2009</copyright-statement><copyright-year>2009</copyright-year><copyright-holder xml:lang="ru">Romantsova T.I.</copyright-holder><copyright-holder xml:lang="en">Romantsova T.I.</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/5241">https://www.omet-endojournals.ru/jour/article/view/5241</self-uri><abstract><p>Инсулинорезистентность на уровне мышечной ткани и печени в сочетании с функциональной недостаточностью В-клеток поджелудочной железы представляет собой основу патогенеза сахарного диабета 2 типа (СД2). Как у становлено в настоящее время, нарушения функции β-клеток являются гораздо более ранними и выраженными, чем это предполагалось сравнительно недавно. Следовательно, для достижения более оптимального управления диабетом, профилактики либо замедления прогрессирующей функциональной недостаточности β-клеток, определяющейся уже на стадии нарушения толерантности к глюкозе, необходима новая, более ранняя и агрессивная тактика терапии. Одним из возможных подходов является терапия, основанная на воспроизведении эффектов инкретиномиметика глюкагоноподобного пептида-1 (ГПП-1). В условиях гипергликемии ГПП-1 усиливает секрецию инсулина, подавляет продукцию глюкагона, улучшает функцию β-кле-ток и замедляет перистальтику желудка. У больных СД2 содержание ГПП-1 снижено. Кроме того, ГПП-1 быстро распадается под воздействием фермента дипептидилпептидазы-4 (ДПП-4). Резуль таты исследований показали, что новый ингибитор ДПП-4 вилдаглиптин существенно снижает показатели НЬА1с, уровни глюкозы натощак и после еды при его использовании как в виде монотерапии, так и при комбинации с традиционными сахароснижающими препаратами. Преимуществами применения вилдаглиптина является небольшой спектр побочных эффектов, низкая частота гипогликемии, нейтральное влияние на массу тела, удобный способ применения в виде перорального однократного приема. Кроме того, вилдаглиптин способен предотвращать снижение функции β-клеток. Таким образом, может модифицировать естественное прогрессирующее течение диабета, что, тем не менее, необходимо подтвердить с помощью долгосрочных контролируемых исследований.</p></abstract><trans-abstract xml:lang="en"><p>Insulin resistance in muscle and liver and β-cell failure represent the core pathophysiologic defects in type 2 diabetes. Now it isrecognized that the β-cell failure occurs much earlier and is more severe than previously thought. As a result, earlier and more aggressive new therapy is needed to achiev e better control of diabetes and to prev ent/slow the progressive B-cell failure that already is w ell established in IGT subjects. One approach is to target the incretin mimetic hormone glucagon-like peptide-1 (GLP-1). When blood glucose levels are elevated, GrP-1 stimulates insulin secretion, decreases glucagon secretion, impro ves β-cell function, and slows gastric emptying. GrP-1 production is reduced in patients with type 2 diabetes. Furthermore, GrP-1 is rapidly degraded by the dipeptidyl peptidase 4 (DPP-4) enzyme. Trials have showed, that new inhibitor DPP-4 vildagliptin (Galvus) hav e been demonstrated to significantly reduce HbA lc, fasting and prandial glucose levels when used as monotherapy and in соmbination with traditional agents. Advantages of vildagliptin include few adverse events, low risk of hypoglycemia, neutral effect on body weight, and a once-daily oral dosing regimen. Inaddition, vildagliptin may preserve the decline in β-cell function. Hence, vildagliptin may modify the natural progressive course of diabetes; this however, must be confirmed with longer-term controlled studies</p></trans-abstract><kwd-group xml:lang="ru"><kwd>вилдаглиптин</kwd><kwd>инкретины</kwd><kwd>глюкагоноподобный пептид - 1</kwd><kwd>ингибитор дипептидилпептидазы - IV</kwd></kwd-group><kwd-group xml:lang="en"><kwd>vildagliptin</kwd><kwd>incretins</kwd><kwd>glucagon-like peptide-1</kwd><kwd>dipeptidyl peptidase IV inhibitor</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">Abdul-Ghani M., Tripathy D., DeFronzo R.A. 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