骨量减少
内分泌学
内科学
骨质疏松症
骨矿物
骨钙素
成骨细胞
破骨细胞
链脲佐菌素
骨重建
医学
兰克尔
化学
糖尿病
体外
碱性磷酸酶
受体
激活剂(遗传学)
酶
生物化学
作者
Hao Zhang,Lu Gan,Xiaoquan Zhu,Jun Wang,Han Li-cun,Cheng Peng,Da Jing,Xiaodong Zhang,Qingshun Shan
出处
期刊:Bone
[Elsevier BV]
日期:2017-10-27
卷期号:107: 36-44
被引量:44
标识
DOI:10.1016/j.bone.2017.10.024
摘要
Type 1 diabetes mellitus (T1DM) has been associated with deterioration of bone microarchitecture and strength, resulting in increased fracture risk. Substantial studies have revealed the capacity of moderate-intensity static magnetic fields (SMF) on promoting osteoblastogenesis in vitro and stimulating bone growth and bone regeneration in vivo, whereas it is unknown whether SMF can resist T1DM-associated osteopenia/osteoporosis. We herein investigated the potential effects of whole-body SMF exposure with 4mT on bone loss in streptozotocin-induced T1DM rats. We found that SMF exposure for 16weeks inhibited architectural deterioration of trabecular bone and cortical bone and mechanical strength reduction in T1DM rats, as evidenced by the MicroCT and 3-point bending findings. Our serum biochemical, bone histomorphometric and PCR results revealed that SMF induced higher serum osteocalcin, mineral apposition rate and osteoblast number of trabecular bone, and higher skeletal osteocalcin, BMP2 and Runx2 gene expression in T1DM rats, whereas SMF showed no significant alteration in serum CTX, skeletal osteoclast number, or osteoclastogenesis-related RANKL-RANK signaling gene expression. Together, our findings suggest that moderate SMF prevented bone architectural deterioration and strength reduction by inhibiting the reduction of bone formation in T1DM rats, and indicate that SMF might become a promising biophysical countermeasure for T1DM-related osteopenia/osteoporosis.
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