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首页> 外文期刊>Biological trace element research >Zinc Supplementation Increased Bone Mineral Density, Improves Bone Histomorphology, and Prevents Bone Loss in Diabetic Rat
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Zinc Supplementation Increased Bone Mineral Density, Improves Bone Histomorphology, and Prevents Bone Loss in Diabetic Rat

机译:锌补充增加骨密度,改善骨组织骨髓,并防止糖尿病大鼠骨质损失

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摘要

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.
机译:糖尿病骨质疏松症(DOP)是糖尿病的并发症,具有骨矿物密度(BMD)的特点和骨结构破坏。锌报道锌对绝经后骨质疏松症有益效果,也有降血糖作用,锌是否对糖尿病诱导的骨质疏松症有益。因此,在本研究中,我们通过链脲佐菌素注射(60mg / kg)建立了一种糖尿病大鼠模型,并通过口服饲喂硫酸锌来研究锌对DOP的保护作用和下划线可能的机制。将三十六只Sprague Dawley大鼠分为T1DM组(糖尿病大鼠),对照组(载体处理)和T1DM-ZINC组(糖尿病大鼠通过口服饲养给予硫酸锌0.25mg / kg)。在硫酸锌处理八周后,检测骨组织骨髓标记,血清骨代谢标记物(包括ALP,OPG,RUNX 2和RANKL),BMD和骨髓脂肪细胞数。结果显示硫酸锌给药(0.25mg / kg / d)降低血糖,增加了BMD,血清ALP和RANKL,血清OPG和RUNX 2水平,以及T1DM大鼠的OPG / RANKL比率。同时,骨组织形态学参数,骨髓脂肪细胞数恢复正常。在硫酸锌处理与糖尿病大鼠相比(P <0.05)相比,在硫酸锌治疗后,润滑2和OPG mRNA表达水平增加(P <0.05)。表明硫酸锌可以预防DOP的那些,保护机制主要与其降血糖效应,骨髓脂肪生成抑制作用,OPG / RANKL比和RUNX 2上调效应有关。

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  • 来源
    《Biological trace element research》 |2020年第2期|共9页
  • 作者单位

    Shaanxi Univ Technol Coll Biol Sci &

    Engn Vitamin D Res Inst Hanzhong 723000 Shaanxi Peoples R;

    Shaanxi Univ Technol Coll Biol Sci &

    Engn Vitamin D Res Inst Hanzhong 723000 Shaanxi Peoples R;

    Shaanxi Univ Technol Coll Biol Sci &

    Engn Chinese German Joint Lab Nat Prod Res Hanzhong 723000;

    Shaanxi Univ Technol Coll Biol Sci &

    Engn Chinese German Joint Lab Nat Prod Res Hanzhong 723000;

    Shaanxi Univ Technol Coll Biol Sci &

    Engn Chinese German Joint Lab Nat Prod Res Hanzhong 723000;

    Shaanxi Univ Technol Coll Biol Sci &

    Engn Vitamin D Res Inst Hanzhong 723000 Shaanxi Peoples R;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物化学;
  • 关键词

    Zinc; Diabetic osteoporosis; Bone metabolism; BMD; Rats;

    机译:锌;糖尿病骨质疏松症;骨代谢;BMD;老鼠;

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