Vitamin D Research Institute, College of Biological Science and Engineering, Shaanxi University of Technology, Hanzhong, 723000, Shaanxi, China.
Chinese-German Joint Laboratory for Natural Product Research, College of Biological Science and Engineering, Shaanxi University of Technology, Hanzhong, 723000, China.
Biol Trace Elem Res. 2020 Apr;194(2):493-501. doi: 10.1007/s12011-019-01810-7. Epub 2019 Jul 30.
Diabetic osteoporosis (DOP) is a complication of diabetes, with the characteristics of bone mineral density (BMD) reduction and bone structure destruction. Zinc was reported has a benefit effect on postmenopausal osteoporosise, it was also has hypoglycemic effect, whether zinc was beneficial on diabetes-induced osteoporosis has not been reported. So in the present study, we established a diabetic rat model by streptozotocin injection (60 mg/kg), and administered zinc sulfate by oral gavage to investigate the protective effects of zinc on DOP and the underline possible mechanism. Thirty six Sprague Dawley rats were divided into T1DM group (diabetic rats), control group (vehicle treatment), and T1DM-Zinc group (diabetic rats administered zinc sulfate 0.25 mg/kg by oral gavage). The bone histomorphological parameters, serum bone metabolism markers (including ALP, OPG, RUNX 2, and RANKL), BMD, and bone marrow adipocyte numbers were detected after eight weeks of zinc sulfate treatment. The results showed zinc sulfate administration (0.25 mg/kg/d) decreased blood glucose, increased the BMD, decreased serum ALP, and RANKL, increased serum OPG and RUNX 2 levels, as well as OPG/RANKL ratio of T1DM rats. Meanwhile, the bone histomorphological parameters, bone marrow adipocytes numbers were returned to be normal. The RUNX 2, and OPG mRNA expression levels in bone tissues of T1DM-Zinc group rats were increased after zinc sulfate treatment compared with the diabetic rats (P < 0.05). Those indicating that zinc sulfate can prevent DOP, the protective mechanism were mainly related to its hypoglycemic effect, bone marrow lipogenesis inhibition effect, OPG/RANKL ratio and RUNX 2 up-regulation effect.
糖尿病性骨质疏松症（DOP）是糖尿病的一种并发症，其特征是骨密度（BMD）降低和骨结构破坏。锌被报道对绝经后骨质疏松症有有益的作用，它也有降血糖作用，锌是否对糖尿病性骨质疏松症有益尚未有报道。因此，在本研究中，我们通过链脲佐菌素（60mg/kg）注射建立了糖尿病大鼠模型，并通过口服灌胃给予硫酸锌，以研究锌对 DOP 的保护作用及其潜在的可能机制。36 只 Sprague Dawley 大鼠分为 T1DM 组（糖尿病大鼠）、对照组（载体处理）和 T1DM-Zinc 组（糖尿病大鼠给予硫酸锌 0.25mg/kg 口服灌胃）。在硫酸锌治疗 8 周后，检测骨组织形态学参数、血清骨代谢标志物（包括 ALP、OPG、RUNX2 和 RANKL）、BMD 和骨髓脂肪细胞数量。结果表明，硫酸锌（0.25mg/kg/d）给药降低了血糖，增加了 BMD，降低了血清 ALP 和 RANKL，增加了血清 OPG 和 RUNX2 水平，以及 OPG/RANKL 比值。同时，骨组织形态学参数和骨髓脂肪细胞数量也恢复正常。与糖尿病大鼠相比，T1DM-Zinc 组大鼠骨组织中 RUNX2 和 OPG mRNA 表达水平在硫酸锌治疗后增加（P<0.05）。这些表明硫酸锌可以预防 DOP，其保护机制主要与其降血糖作用、骨髓脂生成抑制作用、OPG/RANKL 比值和 RUNX2 上调作用有关。
