mrjСовременная ревматологияModern Rheumatology Journal1996-70122310-158XIMA-PRESS, LLC10.14412/1996-7012-2023-5-118-122mrj-1487Research ArticleОБЗОРЫREVIEWSСистематический обзор молекулярных механизмов регуляции метаболизма мочевой кислоты в кишечнике человекаMolecular mechanisms regulating uric acid metabolism in the human intestine, systematic literature reviewhttps://orcid.org/0000-0002-6547-9425КонышкоН. А.KonyshkoN. A.

Наталья Александровна Конышко

119991

ул. Трубецкая, 8, стр. 2

Москва

Natalya Aleksandrovna Konyshko

119991

8, Trubetskaya Street, Build. 2

Moscow

nkonyshko@yandex.ruhttps://orcid.org/0009-0002-1915-1127КонышкоГ. С.KonyshkoG. S.

214019

ул. Крупской, 28

Смоленск

214019

28, Krupskaya Street

Smolensk

ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет)РоссияI.M. Sechenov First Moscow State Medical University, Ministry of Health of Russia (Sechenov University)Russian FederationФГБОУ ВО «Смоленский государственный медицинский университет» Минздрава РоссииРоссияSmolensk State Medical UniversityRussian Federation202318102023175118122Copyright © Конышко Н.А., Конышко Г.С., 20232023Конышко Н.А., Конышко Г.С.Konyshko N.A., Konyshko G.S.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://mrj.ima-press.net/mrj/article/view/1487

   В обзоре представлены современные данные о прямых и опосредованных патогенетических взаимосвязях метаболизма пуриновых соединений с биохимическими процессами в клетках пищеварительной системы. Проведен комплексный анализ доступных современных публикаций за период с 2000 по 2022 гг. в базах Scopus, PubMed, eLIIBRARY, Google Scholar. Гипотеза, которая связывает патогенез гиперурикемии с «перегрузкой почек», предполагает, что заболевание может развиваться вследствие нарушения почечной экскреции при недостаточной элиминации мочевой кислоты (МК) через кишечник. Часть транспортных систем МК активно работает в гепато- и энтероцитах, что определяет ее образование и клиренс. Белки-переносчики МК подразделяют на две категории: транспортеры реабсорбции уратов и транспортеры экскреции уратов, их экспрессия регулируется факторами транскрипции, гормонами и метаболитами кишечной микрофлоры. Влияние микробиоты кишечника на метаболизм МК связано с ее участием в пуриновом обмене, разложении и элиминации МК с метаболитами кишечной флоры и подавлением подагрического воспаления и оценивается как новый терапевтический потенциал при подагре и гиперурикемии, позволяющий избежать повреждения почек и уролитиаза.

   This review presents recent data on direct and indirect pathogenetic relationships between metabolism of purine compounds and biochemical processes in cells of the digestive system. A comprehensive analysis of available modern publications for the period from 2000 to 2022 in the Scopus, PubMed, eLIIBRARY, and Google Scholar databases was performed. The hypothesis linking the pathogenesis of hyperuricemia to “renal overload” suggests that the disease may develop due to impaired renal excretion with insufficient excretion of uric acid (UA) via the intestine. Some of the UA transport systems work actively in hepatocytes and enterocytes, which determines their formation and excretion. UA transporter proteins are divided into two categories: urate reabsorption transporters and urate excretion transporters; their expression is regulated by transcription factors, hormones, and metabolites of the intestinal microflora. The influence of intestinal microbiota on UA metabolism is associated with its involvement in purine metabolism, degradation and excretion of UA together with metabolites of intestinal flora, and suppression of gout inflammation, and is evaluated as a new therapeutic potential for gout and hyperuricemia to prevent renal damage and urolithiasis.

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The authors declare that there are no conflicts of interest present.