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<article article-type="review-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">problendo</journal-id><journal-title-group><journal-title xml:lang="ru">Проблемы Эндокринологии</journal-title><trans-title-group xml:lang="en"><trans-title>Problems of Endocrinology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">0375-9660</issn><issn pub-type="epub">2308-1430</issn><publisher><publisher-name>Endocrinology Research Centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/probl13624</article-id><article-id custom-type="elpub" pub-id-type="custom">problendo-13624</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>Клиническая эндокринология</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Clinical endocrinology</subject></subj-group></article-categories><title-group><article-title>Связь болезни Паркинсона с метаболическими нарушениями: влияние системных дисфункций на нейродегенерацию</article-title><trans-title-group xml:lang="en"><trans-title>The relationship between Parkinson’s disease and metabolic disorders: the impact of systemic dysfunctions on neurodegeneration</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-0632-6653</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Юсупов</surname><given-names>Ф. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Yusupov</surname><given-names>F. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Юсупов Фуркат Абдулахатович - д.м.н., профессор,</p><p>Ош</p></bio><bio xml:lang="en"><p>Furkat A. Yusupov - MD, Professor,</p><p>Osh</p></bio><email xlink:type="simple">furcat_y@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/0000-0001-5549-3832</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Абдыкадыров</surname><given-names>М. Ш.</given-names></name><name name-style="western" xml:lang="en"><surname>Abdykadyrov</surname><given-names>M. Sh.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Абдыкадыров Мухаммадюсуф Шкуратович - аспирант,</p><p>Ош</p></bio><bio xml:lang="en"><p>Mukhammadiusuf Sh. Abdykadyrov,</p><p>Osh</p></bio><email xlink:type="simple">aratingo@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">Ошский государственный университет (ОшГУ)<country>Кыргызстан</country></aff><aff xml:lang="en">Osh State University (OshSU)<country>Kyrgyzstan</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2026</year></pub-date><pub-date pub-type="epub"><day>07</day><month>03</month><year>2026</year></pub-date><volume>72</volume><issue>1</issue><fpage>48</fpage><lpage>55</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Юсупов Ф.А., Абдыкадыров М.Ш., 2026</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="ru">Юсупов Ф.А., Абдыкадыров М.Ш.</copyright-holder><copyright-holder xml:lang="en">Yusupov F.A., Abdykadyrov M.S.</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://www.probl-endojournals.ru/jour/article/view/13624">https://www.probl-endojournals.ru/jour/article/view/13624</self-uri><abstract><p>Данный обзор посвящен анализу взаимосвязи между болезнью Паркинсона и сахарным диабетом - двумя глобальными эпидемиями, тесно связанными со старением. Обзор опирается на новейшие эпидемиологические данные, согласно которым наличие сахарного диабета не только значительно повышает риск развития болезни Паркинсона, но и усиливает ее прогрессирование, ухудшая как моторные, так и когнитивные функции. В работе подробно рассматриваются общие патофизиологические механизмы, включающие нарушение сигнализации инсулина, развитие инсулинорезистентности, окислительный стресс, митохондриальную дисфункцию, хроническое воспаление и нейровоспаление, а также дисрегуляцию глюкозного обмена и дисбиоз кишечной микробиоты. Эти взаимосвязанные процессы формируют порочный круг, при котором каждое патологическое изменение способствует нейродегенерации, особенно в уязвимых дофаминергических нейронах черной субстанции. Особенность данного обзора заключается в интеграции современных исследований, что позволяет взглянуть на проблему двойственной природы данной коморбидности с позиции как нейродегенеративных, так и метаболических нарушений. Понимание совместных патофизиологических путей открывает перспективы для разработки многоцелевых терапевтических стратегий, включая диетические вмешательства, модификацию образа жизни и модуляцию кишечной микробиоты. Такой подход отличает данный обзор от аналогичных работ, предоставляя целостное видение проблемы и указывая на необходимость дальнейших исследований для выявления точных биомаркеров и разработки эффективных методов лечения, способных изменить течение заболевания.</p></abstract><trans-abstract xml:lang="en"><p>This review examines the association between Parkinson’s disease (PD) and diabetes, two global epidemics closely linked to aging. The analysis is based on recent epidemiological data indicating that diabetes significantly increases the risk of developing PD and exacerbates its progression, affecting both motor and cognitive functions. The paper explores shared pathophysiological mechanisms, including impaired insulin signaling, insulin resistance, oxidative stress, mitochondrial dysfunction, chronic inflammation and neuroinflammation, dysregulated glucose metabolism, and gut microbiota dysbiosis. These interconnected processes create a vicious cycle in which each pathology reinforces the others, driving neurodegeneration, particularly in vulnerable dopaminergic neurons of the substantia nigra. The uniqueness of this review lies in the integration of current research, providing a dual-perspective approach to comorbidity — addressing both neurodegenerative and metabolic dysfunctions. Understanding these shared mechanisms opens avenues for developing multi-targeted therapeutic strategies, including dietary interventions, lifestyle modifications, and gut microbiota modulation. This approach distinguishes the present review from similar works by offering a comprehensive perspective on the issue and emphasizing the need for further studies to identify precise biomarkers and develop effective disease-modifying treatments.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>болезнь Паркинсона</kwd><kwd>сахарный диабет</kwd><kwd>инсулинорезистентность</kwd><kwd>диета</kwd><kwd>микробиота</kwd><kwd>митохондриальная дисфункция</kwd><kwd>окислительный стресс</kwd></kwd-group><kwd-group xml:lang="en"><kwd>Parkinson’s disease</kwd><kwd>diabetes</kwd><kwd>insulin resistance</kwd><kwd>diet</kwd><kwd>microbiota</kwd><kwd>mitochondrial dysfunction</kwd><kwd>oxidative stress</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">Labandeira CM, Fraga-Bau A, Arias Ron D, Alvarez-Rodriguez E, Vicente-Alba P, Lago-Garma J, Rodriguez-Perez AI. 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