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Skeletal effects of zinc deficiency in growing rats.

机译:锌缺乏对成年大鼠的骨骼影响。

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There is ample evidence that zinc plays an important role in bone metabolism and zinc deficiency has been implicated as a risk factor in the development of osteoporosis. It was the aim of the present study to investigate the skeletal effects of alimentary zinc deficiency in growing rats using quantitative bone histomorphometry. Twenty-four male Sprague Dawley rats with a mean initial body weight of 101 +/- 2 g were allocated in two groups of 12 rats each and had free access to a semi-synthetic, casein-based, zinc-deficient diet (0.76 mg zinc/kg) or to the same diet supplemented with 60 mg zinc per kg. All rats were sacrificed 42 days after the start of the experiment and the right distal femur was removed for bone histomorphometry. Relative to controls (+Zn), the zinc-deficient rats (-Zn) had a significantly lower body weight and about an 80% reduction in plasma and femur zinc concentration. The histomorphometric evaluation of the distal femoral metaphysis showed that zinc deficiency led to a 45% reduction (p < 0.01) in cancellous bone mass and to a deterioration of trabecular bone architecture, with fewer and thinner trabeculae. The osteopenia in -Zn rats was accompanied by significant reductions in osteoid perimeter (-31%, p < 0.05), osteoblast perimeter (-30%, p < 0.05), and osteoclast number (-38%, p < 0.01) relative to +Zn controls. We conclude that zinc deficiency induced low turnover osteopenia in femoral cancellous bone of growing rats. These results support the hypothesis that zinc deficiency during growth may impair the accumulation of maximal bone mass in humans; additionally, they suggest that zinc deficiency may play a role as a risk factor in the pathogenesis of osteoporosis.
机译:有充分的证据表明锌在骨代谢中起重要作用,而锌缺乏已被认为是骨质疏松症发展的危险因素。本研究的目的是使用定量骨组织形态计量学研究生长中的大鼠饮食中锌缺乏的骨骼作用。将平均初始体重为101 +/- 2 g的二十四只雄性Sprague Dawley大鼠分为两组,每组12只,每只大鼠均可免费使用半合成的,基于酪蛋白的锌缺乏饮食(0.76 mg锌/千克)或在相同饮食中每千克补充60毫克锌。在实验开始42天后处死所有大鼠,并取出右股骨远端用于骨组织形态测定。相对于对照组(+ Zn),缺锌大鼠(-Zn)的体重明显降低,血浆和股骨锌的浓度降低了约80%。股骨远端干physi端的组织形态计量学评估表明,锌缺乏导致松质骨质量减少了45%(p <0.01),并使小梁骨结构恶化,小梁越来越少和变薄。与-Zn大鼠相比,骨质减少伴随着类固醇周长(-31%,p <0.05),成骨细胞周长(-30%,p <0.05)和破骨细胞数目(-38%,p <0.01)显着减少+ Zn对照。我们得出的结论是,锌缺乏症在成年大鼠的股骨松质骨中引起低周转性骨质减少。这些结果支持以下假设:生长过程中锌缺乏会损害人类最大骨量的积累;此外,他们认为锌缺乏可能是骨质疏松症发病机制中的危险因素。

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