Open AccessFeatures of bone metabolism in diabetes mellitus
Author(s) -
Guzel M. Nurullina,
Нуруллина Гузель Михайловна,
Г. И. Ахмадуллина,
Г. И. Ахмадуллина
Publication year - 2018
Publication title -
osteoporoz i osteopatii
Language(s) - English
Resource type - Journals
eISSN - 2311-0716
pISSN - 2072-2680
DOI - 10.14341/osteo2017382-89
Subject(s) - bone remodeling , endocrinology , osteocalcin , medicine , diabetes mellitus , osteoporosis , adiponectin , osteoblast , bone resorption , sclerostin , leptin , advanced glycation end product , glycation , chemistry , obesity , insulin resistance , signal transduction , wnt signaling pathway , biochemistry , alkaline phosphatase , in vitro , enzyme
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.