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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">10.14341/2071-8713-5240</article-id><article-id custom-type="elpub" pub-id-type="custom">ometendo-5240</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>Потенциальные возможности применения альфа-липоевойкислоты (Берлитион®300) в лечении метаболического синдрома</article-title><trans-title-group xml:lang="en"><trans-title>Potential opportunities for treatment of metabolic syndrome withalpha-lipoic acid (Berlithion®300)</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 contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Kuznetsov</surname><given-names>I S</given-names></name></name-alternatives><email xlink:type="simple">-</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>10</fpage><lpage>14</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Romantsova T.I., Kuznetsov I.S., 2009</copyright-statement><copyright-year>2009</copyright-year><copyright-holder xml:lang="ru">Romantsova T.I., Kuznetsov I.S.</copyright-holder><copyright-holder xml:lang="en">Romantsova T.I., Kuznetsov I.S.</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/5240">https://www.omet-endojournals.ru/jour/article/view/5240</self-uri><abstract><p>Существует много экспериментальных данных, подтверждающих влияние альфа-липоевой кислоты на активность
фермента АМПК, рецепторов PPARα/γ и белков-термогенинов, разобщающих окислительное фосфорилирование (UCP1).
АМПК представляет собой фермент, влияющий на потребление пищи и энергетический обмен как на уровне гипоталамуса,
так и в периферических тканях. PPARγ является ключевым модулятором липидного гомеостаза и дифференциации адипоцитов. Белок UCP1 содержится в бурой жировой ткани и отвечает за термогенез. Посредством регуляции перечисленных биологических субстратов альфа-липоевая кислота (препарат Берлитион ®300) нормализует инсулинорезистентность, что способствует снижению массы тела и улучшению липидного профиля крови</p></abstract><trans-abstract xml:lang="en"><p>There are a lot of experi mental data confirmed the influence of alpha-lipoi с acid on activity of AMPK enzyme, receptors PPARα/γ and uncoupling proteins that prev ent oxidative phosphorylation (UCPl). AMPK is the enzyme responsible for food intake and energy expenditure in hypothalamus as w ell as in peripheral adipose tissue. PPARγ is the key modulator of lipid ho meostasis and adipocyte differentiation. UCPl is located in the brown adipose tissue and provides termogenesis. Via regulation of mentioned biological targets alpha-lipoic acid (Berlithion®300) lowers insulinresistance, favors weight losing process and improvement of blood lipid profile.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>метаболический синдром</kwd><kwd>аденозинмонофосфат-активированная протеинкиназа</kwd><kwd>рецептор</kwd><kwd>активирующий пролиферацию пероксисом</kwd><kwd>белок</kwd><kwd>разобщающий окислительное фосфорилирование</kwd></kwd-group><kwd-group xml:lang="en"><kwd>metabolic syndrome</kwd><kwd>adenosine monophosphate - activated protein kinase</kwd><kwd>peroxisome proliferator activated receptor</kwd><kwd>uncoupling protein</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">Eckel R.H., Grundy S.M., Zimmet P.Z. The metabolic syndrome. Lancet, 2005, 365:1415-28.</mixed-citation><mixed-citation xml:lang="en">Eckel R.H., Grundy S.M., Zimmet P.Z. 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