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  • Title: Zinc Supplementation Increased Bone Mineral Density, Improves Bone Histomorphology, and Prevents Bone Loss in Diabetic Rat.
    Author: Qi S, He J, Zheng H, Chen C, Jiang H, Lan S.
    Journal: Biol Trace Elem Res; 2020 Apr; 194(2):493-501. PubMed ID: 31363990.
    Abstract:
    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.
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