diaendoСахарный диабетDiabetes mellitus2072-03512072-0378Endocrinology research centre10.14341/DM13416diaendo-13506Research ArticleОБЗОРЫREVIEWSИзменения энергетического обмена костной ткани при сахарном диабете и старении как причина повышенной хрупкости скелетаChanges in bone tissue energy metabolism in diabetes mellitus and aging as a cause of increased skeletal fragilityhttps://orcid.org/0000-0002-2948-5019ЖдановаА. С.ZhdanovaA. S.

Жданова Анастасия Станиславовна – аспирант.

117292, Москва, ул. Дмитрия Ульянова, д. 11

Anastasiia S. Zhdanova - MD, PhD student.

11 Dmitria Uljanova street, 117292 Moscow

zhdanova.a.doc@mail.ruhttps://orcid.org/0000-0002-6674-6441БелаяЖ. Е.BelayaZh. E.

Белая Жанна Евгеньевна - д.м.н.

Москва

Zhanna E. Belaya - MD, PhD.

Moscow

jannabelaya@gmail.comhttps://orcid.org/0009-0006-2170-4957КатаеваД. А.KataevaD. A.

Катаева Дарья Альбертовна - клинический ординатор.

Москва

Dariia A. Kataeva - MD, clinical resident.

Moscow

dashakataeva27@yandex.ruhttps://orcid.org/0009-0006-1702-924XОмельченкоК. А.OmelchenkoK. A.

Омельченко Константин Анатольевич - к.м.н.

Москва

Konstantin A. Omelchenko - MD, PhD.

Moscow

panerio77@gmail.comГНЦ РФ ФГБУ «Национальный медицинский исследовательский центр эндокринологии им. академика И.И. Дедова»РоссияEndocrinology Research CentreRussian FederationГородская клиническая больница №31 имени академика Г.М. СавельевойРоссияCity Clinical Hospital № 31 named after academician G.M. SavelievaRussian Federation202618052026292191202Copyright © Жданова А.С., Белая Ж.Е., Катаева Д.А., Омельченко К.А., 20262026Жданова А.С., Белая Ж.Е., Катаева Д.А., Омельченко К.А.Zhdanova A.S., Belaya Z.E., Kataeva D.A., Omelchenko K.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.dia-endojournals.ru/jour/article/view/13506

Интерес к изучению продуктов промежуточного метаболизма и клеточной биоэнергетики связан с глобальным ростом распространенности метаболических заболеваний. Структурные особенности костной ткани с повышенным риском низкоэнергетических переломов при сахарном диабете связаны с комплексными нарушениями костного метаболизма, включая накопление конечных продуктов гликирования, подавление остеобластогенеза, усиление экспрессии склеростина, развитие окислительного стресса и усиление катаболических процессов в клетках под влиянием гипергликемии. Патогенетические изменения при остеопорозе в свою очередь связаны со сложными изменениями клеточного энергообмена, митохондриальной функции, а также нарушениями синтеза и распада пуринов, которые способствуют прогрессирующему дисбалансу костного ремоделирования и снижению биомеханических свойств костной ткани. В настоящем обзоре литературы собрана информация об основных источниках и путях синтеза аденозинтрифосфата в костных клетках, механизмах регуляции энергообмена в норме, а также в условиях гипергликемии при сахарном диабете и в условиях возрастных изменений организма с развитием остеопороза. Представленные данные открывают новые перспективы для разработки таргетной терапии описанных метаболических нарушений как потенциального подхода к профилактике и лечению патологии костной ткани.

Interest in studying intermediary metabolic products and cellular bioenergetics is driven by the global increase in the prevalence of metabolic diseases. Structural features of bone tissue associated with an increased risk of fragility fractures in diabetes mellitus are associated with complex disorders of bone metabolism, including the accumulation of advanced glycation end products, suppression of osteoblastogenesis, increased sclerostin expression, development of oxidative stress and enhancement of catabolic processes under the influence of hyperglycemia. Pathogenetic changes in osteoporosis, in turn, are associated with complex alterations in cellular energy metabolism, mitochondrial function, and purine homeostasis, which contribute to a progressive imbalance in bone remodeling and a decrease in the biomechanical properties of bone tissue. This literature review provides information on the main sources and pathways of adenosine triphosphate synthesis in bone cells, the mechanisms of energy metabolism regulation under normal conditions, as well as under conditions of hyperglycemia in diabetes mellitus and under conditions of age-related changes in the body with the development of osteoporosis. The presented data reveal promising prospects for the development of targeted therapies aimed at the described metabolic alterations, offering a potential approach for the prevention and management of bone disorders.

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