References

porozendo

Остеопороз и остеопатии

Osteoporosis and Bone Diseases

2072-26802311-0716

Endocrinology Research Centre

10.14341/osteo2017382-89

porozendo-9525

Research Article

Научный обзор

Review

Особенности костного метаболизма при сахарном диабете

Features of bone metabolism in diabetes mellitus

https://orcid.org/0000-0002-4394-8446

Нуруллина

Гузель Михайловна

Nurullina

Guzel M.

очный аспирант кафедры факультетской терапии с курсами эндокринологии и гематологии

MD, PhD-student

dalllila@mail.ru

https://orcid.org/0000-0003-1876-2516

Ахмадуллина

Гузяль Илгисовна

Akhmadullina

Guzyal I.

кандидат медицинских наук, доцент кафедры факультетской терапии с курсами эндокринологии и гематологии

MD, PhD, assistant professor

guzal-work@mail.ru

<p>ФГБОУ ВО "Ижевская государственная медицинская академия" Минздрава России</p>Россия<p>Izhevsk State Medical Academy</p>Russian Federation

2017

24042018

2038289

2017

Нуруллина Г.М., Ахмадуллина Г.И.

Nurullina G.M., Akhmadullina G.I.

This work is licensed under a Creative Commons Attribution 4.0 License.

https://www.osteo-endojournals.ru/jour/article/view/9525

Пациенты с сахарным диабетом (СД) имеют повышенный риск развития остеопоротических переломов, что связано со снижением прочности кости.

Накопление конечных продуктов гликирования, гипергомоцистеинемия увеличивают апоптоз остеоцитов, уменьшают костеобразование и замедляют костное ремоделирование, при СД. Адипонектин стимулирует экспрессию остеокальцина и дифференцировку остеобластов посредством активации 5'АМФ-активируемой протеинкиназы (AMФK). AMФK-активация стимулирует дифференцировку и минерализацию остеобластов. Гипоадипонектинемия, которая часто наблюдается при ожирении и диабете, может участвовать в снижении прочности кости при СД.

Замедленный костный метаболизм у пациентов сахарным диабетом подтверждается при изучении уровня маркеров костного ремоделирования. Об этом свидетельствует снижение уровня маркеров костного образования (остеокальцин, P1NP), маркеров костной резорбции (CTX, TRAP), повышение маркеров-регуляторов костного обмена (OPG, склеростин).

Таким образом, изучение патофизиологии костного метаболизма, уровня маркеров костного обмена у пациентов с сахарным диабетом дает широкие перспективы в понимании механизмов развития остеопороза как осложнения сахарного диабета, подбора таргетной терапии и улучшения ранней диагностики заболевания.

Patients with diabetes mellitus (DM) have an increased risk of osteoporotic fractures, which is associated with a bone fragility.

Accumulation of advanced glycation end products, hyperhomocysteinemia causes increased apoptosis of osteocytes, decreased bone formation and bone remodeling in DM. Adiponectin stimulates osteocalcin expression and osteoblast differentiation through the activation of AMPK. AMPK-activation stimulates differentiation and mineralization of osteoblasts. Hypoadiponectinemia, which is often observed in obesity and diabetes, can causes bone fragility.

Diabetes mellitus is a state of low bone turnover, which is confirmed by decreased markers of bone formation (osteocalcin, P1NP), decreased markers of bone resorption (CTX, TRAP), increased regulatory markers of bone remodeling (OPG, sclerostin).

Thus, the study of the pathophysiology of bone metabolism, the level of bone metabolism markers in patients with diabetes mellitus gives broad prospects in understanding the mechanisms of osteoporosis as complication of diabetes mellitus, the selection of targeted therapy and the improvement of early diagnosis of the disease.

Сахарный диабет 2 типаостеопорозособенности костного метаболизма

Diabetes mellitusosteoporosisbone turnover

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