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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">pediatricjournal</journal-id><journal-title-group><journal-title xml:lang="ru">Архив педиатрии и детской хирургии</journal-title><trans-title-group xml:lang="en"><trans-title>Archives of Pediatrics and Pediatric Surgery</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2949-4664</issn><issn pub-type="epub">3033-6783</issn><publisher><publisher-name>НИКИ детства Минздрава Московской области</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.31146/2949-4664-apps-2-4-46-50</article-id><article-id custom-type="elpub" pub-id-type="custom">pediatricjournal-122</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>REVIEWS</subject></subj-group></article-categories><title-group><article-title>Роль мелатонина в регуляции метаболизма</article-title><trans-title-group xml:lang="en"><trans-title>Role of melatonin in metabolic regulation</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-4461-4322</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Трапезникова</surname><given-names>А. Ю.</given-names></name><name name-style="western" xml:lang="en"><surname>Trapeznikova</surname><given-names>A. Yu.</given-names></name></name-alternatives><email xlink:type="simple">ay.trapeznikova@yandex.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Гречкина</surname><given-names>А. Е.</given-names></name><name name-style="western" xml:lang="en"><surname>Grechkina</surname><given-names>A. E.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.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/0000-0003-2321-6843</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шальнева</surname><given-names>Т. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Shalneva</surname><given-names>T. V.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Крючкова</surname><given-names>Т. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Kruchkova</surname><given-names>T. A.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0009-0004-6162-1190</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Балакирева</surname><given-names>А. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Balakireva</surname><given-names>A. I.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-7308-7280</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Хавкин</surname><given-names>А. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Khavkin</surname><given-names>A. I.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-3"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное образовательное учреждение высшего образования «Санкт-Петербургский государственный педиатрический медицинский университет» Министерства здравоохранения Российской Федерации</institution></aff><aff xml:lang="en"><institution>Saint Petersburg State Pediatric Medical University of the Russian Ministry of Health</institution></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГАОУ ВО «Белгородский государственный национальный исследовательский университет»</institution></aff><aff xml:lang="en"><institution>Belgorod National Research University</institution></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru"><institution>ФГАОУ ВО «Белгородский государственный национальный исследовательский университет»; ГБУЗ МО Научно-исследовательский клинический института детства Министерства здравоохранения Московской области</institution></aff><aff xml:lang="en"><institution>Belgorod National Research University; Childhood Research Clinical Institute of the Moscow Region Ministry of Health</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>18</day><month>12</month><year>2024</year></pub-date><volume>2</volume><issue>4</issue><fpage>46</fpage><lpage>50</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Трапезникова А.Ю., Гречкина А.Е., Шальнева Т.В., Крючкова Т.А., Балакирева А.И., Хавкин А.И., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Трапезникова А.Ю., Гречкина А.Е., Шальнева Т.В., Крючкова Т.А., Балакирева А.И., Хавкин А.И.</copyright-holder><copyright-holder xml:lang="en">Trapeznikova A.Y., Grechkina A.E., Shalneva T.V., Kruchkova T.A., Balakireva A.I., Khavkin A.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://journal.nikid.ru/jour/article/view/122">https://journal.nikid.ru/jour/article/view/122</self-uri><abstract><p>Мелатонин представляет собой гормон белковой природы, вырабатывающийся в эпифизе и секретирующийся в кровь и спинномозговую жидкость. Довольно давно в научном мире известно о значении гормона шишковидной железы на циркадные ритмы. Однако мелатонин способен оказывать большое число плейотропных эффектов: антиоксидантный и противовоспалительный эффекты, иммунорегуляторные свойства, антигипертензивное и нейропротективное действия, влияние на развитие плаценты и плода, беременность, а также углеводный и липидный обмены. Нельзя забывать и про огромное влияние гормона на систему мать - плацента - плод. Растет интерес в изучении действия мелатонина на системные и тканевые воспалительные реакции, являющиеся одной из причин развития гипертонической болезни и ожирения. Прогрессирующее поражение органов-мишеней, включающее избыточную выработку медиаторов воспаления, делает противовоспалительные стратегии терапии неэффективными. Доказано, что мелатонин способствует снижению артериального давления, массы тела и воспаления. Механизмы действия этой древней молекулы защиты включают несколько уровней, от субклеточного до межклеточного. Митохондрии клетки являются ключевым элементом, способствующим развитию воспалительной реакции в сосудистой и жировой ткани и, соответственно, потенциальной фармакологической мишенью. Мелатонин, в свою очередь, защищает от митохондриальной дисфункции. В данной статье будут рассмотрены основные механизмы влияния гормона на метаболизм, его роль в предотвращении развития системного воспаления.</p></abstract><trans-abstract xml:lang="en"><p>Melatonin is a protein hormone produced in the epiphysis and secreted into the blood and cerebrospinal fluid. For quite a long time in the scientific world it has been known about the importance of the hormone of the pineal gland on circadian rhythms. However, melatonin can have a large number of pleiotropic effects: antioxidant and anti-inflammatory effects, immunoregulatory properties, antihypertensive and neuroprotective effects, effects on the development of the placenta and fetus, pregnancy, as well as carbohydrate and lipid metabolism. We must not forget about the huge influence of the hormone on the mother - placenta - fetus system. There is growing interest in studying the effect of melatonin on systemic and tissue inflammatory reactions, which are one of the causes of hypertension and obesity. Progressive target organ damage involving excessive production of inflammatory mediators renders anti-inflammatory therapy strategies ineffective. Melatonin has been proven to help lower blood pressure, body weight and inflammation. The mechanisms of action of this ancient defense molecule involve several levels, from subcellular to intercellular. Cell mitochondria are a key element contributing to the development of an inflammatory response in vascular and adipose tissue and, accordingly, a potential pharmacological target. Melatonin, in turn, protects against mitochondrial dysfunction. This article will consider the main mechanisms of the influence of the hormone on metabolism, its role in preventing the development of systemic inflammation.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>мелатонин</kwd><kwd>метаболизм</kwd><kwd>ожирение</kwd><kwd>дети</kwd></kwd-group><kwd-group xml:lang="en"><kwd>melatonin</kwd><kwd>metabolism</kwd><kwd>obesity</kwd><kwd>children</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">Owino S., Sánchez-Bretaño A., Tchio C. et al. Nocturnal activation of melatonin receptor type 1 signaling modulates diurnal insulin sensitivity via regulation of PI3K activity. 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