Features of bone metabolism in diabetes mellitus
Abstract
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.
About the Authors
Guzel M. NurullinaIzhevsk State Medical Academy
Russian Federation
MD, PhD-student
Guzyal I. Akhmadullina
Izhevsk State Medical Academy
Russian Federation
MD, PhD, assistant professor
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Supplementary files
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1. Fig. 1. The receptor for AGE (RAGE) is expressed on osteoblasts. Hyperglycemia increases expression (RAGE). KPG induces osteoplastic apoptosis and suppresses the growth of osteoblasts. KPG inhibits the differentiation and mineralization of osteoblasts through endoplasmic reticulum dysfunction and the expression of transforming growth factor β (TGFβ), leading to a decrease in bone formation. IRE1α - inositol regulating enzyme 1α. ATF6 - Activating Transcription Factor 6 | |
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2. Fig. 2. Hcy (homocysteine) increases intracellular oxidative stress in osteoblasts and induces apoptosis. Hcy inhibits the expression of lysyloxidase, which is the most important enzyme for the formation of collagen cross-links and increases the extracellular accumulation of pentosidine | |
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3. Fig. 3. Slowed bone metabolism in diabetes mellitus | |
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For citations:
Nurullina G.M., Akhmadullina G.I. Features of bone metabolism in diabetes mellitus. Osteoporosis and Bone Diseases. 2017;20(3):82-89. (In Russ.)
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