endofocusFOCUS ЭндокринологияFOCUS. Endocrinology2713-01772713-0185ООО "Издательство "Перо"10.62751/2713-0177-2026-7-1-06endofocus-213Research ArticleОБЗОРЫ ЛИТЕРАТУРЫLITERATURE REVIEWSФенотипические и генетические кластеры сахарного диабета 2 типа: ассоциации с риском осложнений и терапевтические стратегииPhenotypic and genetic clusters of type 2 diabetes mellitus: Associations with complication risk and therapeutic strategieshttps://orcid.org/0000-0001-6385-540XДемидоваТ. Ю.DemidovaT. Yu.

Татьяна Юльевна Демидова, д. м. н., профессор, заведующая кафедрой, заслуженный врач РФ

Москва

Tatyana Yu. Demidova, Dr. Sci (Med.), professor. Honored Doctor of the Russian Federation

Moscow

t.y.demidova@gmail.comhttps://orcid.org/0000-0002-8684-6095ТитоваВ. В.TitovaV. V.

Виктория Викторовна Титова, ассистент

Институт клинической медицины; кафедра эндокринологии

117513; ул. Островитянова, д. 1; Москва

Victoria V. Titova, assistant

Institute of clinical medicine; Department of endocrinology

117513; 1 Ostrovityanova St.; Moscow

meteora-vica@mail.ruРоссийский национальный исследовательский медицинский университет имени Н.И. Пирогова (Пироговский университет)Pirogov Russian National Research Medical University202603052026714857Copyright © Демидова Т.Ю., Титова В.В., 20262026Демидова Т.Ю., Титова В.В.Demidova T.Y., Titova V.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://endofocus.elpub.ru/jour/article/view/213

   Сахарный диабет 2 типа (СД2) представляет собой одно из наиболее распространенных неинфекционных заболеваний, достигших масштабов глобальной пандемии. Несмотря на значительный прогресс в понимании его патогенеза и появление новых классов сахароснижающих препаратов, эффективность профилактики и лечения СД2 остается ограниченной, что проявляется высокими показателями инвалидизации и смертности вследствие микро- и макрососудистых осложнений.

   Ключевая проблема, препятствующая разработке оптимальных терапевтических стратегий, заключается в выраженной гетерогенности СД2.

   Заболевание представляет собой не единую нозологическую форму, а, скорее, синдром, объединяющий множество различных патологических состояний, которые характеризуются хронической гипергликемией, но различаются по этиологии, патофизиологическим механизмам, клинической картине, темпам прогрессирования и спектру развивающихся осложнений. В последние годы активно разрабатываются методы стратификации СД2 на основе кластерного анализа клинических и генетических данных. Фундаментальное исследование Ahlqvist E. et al. позволило выделить 5 подтипов СД2, различающихся по патогенезу, прогрессированию и риску осложнений. Параллельно развитие полногеномного поиска ассоциаций (GWAS) и методов машинного обучения (байесовская неотрицательная матричная факторизация, мягкая кластеризация) дало возможность сгруппировать сотни генетических локусов в физиологические кластеры, соответствующие дисфункции β-клеток, ожирению, липодистрофии и нарушениям липидного обмена. Установлены устойчивые ассоциации между выделенными подтипами диабета и исходами – риском ретинопатии, нефропатии и сердечно-сосудистых событий. Интеграция фенотипической и генетической кластеризации открывает перспективы для разработки патогенетически обоснованных терапевтических стратегий: раннего назначения инсулина в кластерах с дефицитом инсулина, приоритетного использования ингибиторов натрий-глюкозного котранспортера-2 и агонистов рецепторов глюкагоноподобного пептида-1 в инсулинорезистентном кластере, фокуса на снижение массы тела в кластерах ожирения и минимизации риска гипогликемий при возрастном диабете.

   Type 2 diabetes mellitus (T2DM) is one of the most common noncommunicable diseases of our time, reaching global pandemic proportions. Despite significant advances in understanding the pathogenesis of the disease and the emergence of new classes of hypoglycemic medications, the effectiveness of T2DM prevention and treatment remains limited, resulting in high rates of disability and mortality due to micro- and macrovascular complications.

   A key challenge hindering the development of optimal therapeutic strategies is the marked heterogeneity of T2DM.

   The disease is not a single nosological entity, but rather a syndrome encompassing a multitude of different pathological conditions characterized by chronic hyperglycemia but differing in etiology, pathophysiological mechanisms, clinical presentation, rate of progression, and spectrum of complications. In recent years, methods for stratifying T2DM based on cluster analysis of clinical and genetic data have been actively developed. A fundamental study by Ahlqvist E. et al. identified five T2DM subtypes that differ in pathogenesis, progression, and risk of complications. Concurrently, the development of genome-wide association studies (GWAS) and machine learning methods (Bayesian nonnegative matrix factorization, soft clustering) has enabled the grouping of hundreds of genetic loci into physiological clusters corresponding to β-cell dysfunction, obesity, lipodystrophy, and lipid metabolism disorders. Stable associations have been established between the identified subtypes and outcomes, including the risk of retinopathy, nephropathy, and cardiovascular events. The integration of phenotypic and genetic clustering opens up prospects for the development of pathogenetically based therapeutic strategies: early insulin administration in insulin-deficient clusters, prioritization of SGLT2 inhibitors and GLP-1 receptor agonists in the insulin-resistant cluster, a focus on weight loss in obesity clusters, and minimization of the risk of hypoglycemia in age-related diabetes.

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