Hosea Heather J, Taylor Carla G, Wood Trisha, Mollard Rebecca, Weiler Hope A
Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, MB, R3T 2N2, Canada.
Exp Biol Med (Maywood). 2004 Apr;229(4):303-11. doi: 10.1177/153537020422900404.
The objective of this study was to investigate the effects of dietary zinc deficiency and diet restriction on bone development in growing rats, and to determine whether any adverse effects could be reversed by dietary repletion. Weanling rats were fed either a zinc-deficient diet ad libitum (ZD; <1 mg zinc/kg) or nutritionally complete diet (30 mg zinc/kg) either ad libitum (CTL) or pair-fed to the intake of the ZD group (DR; diet-restricted) for 3 weeks (deficiency phase) and then all groups were fed the zinc-adequate diet ad libitum for 3, 7, or 23 days (repletion phase). Excised femurs were analyzed for bone mineral density (BMD) using dual-energy x-ray absorptiometry, and plasma was analyzed for markers of bone formation (osteocalcin) and resorption (Ratlaps). After the deficiency phase, ZD had lower body weight and reduced femur BMD, zinc, and phosphorus concentrations compared with DR; and these parameters were lower in DR compared with CTL. Femur calcium concentrations were unchanged among the groups. Reduced plasma osteocalcin in ZD and elevated plasma Ratlaps in DR suggested that zinc deficiency limits bone formation while diet restriction accelerates bone resorption activity. After 23 days of repletion, femur size, BMD, and zinc concentrations remained lower in ZD compared with DR and CTL. Body weight and femur phosphorus concentrations remained lower in both ZD and DR compared with CTL after repletion. There were no differences in plasma osteocalcin concentrations after the repletion phase, but the plasma Ratlaps concentrations remained elevated in DR compared with CTL. In summary, both ZD and DR lead to osteopenia during rapid growth, but the mechanisms appear to be due to reduced modeling in ZD and higher turnover in DR. Zinc deficiency was associated with a greater impairment in bone development than diet restriction, and both deficiencies limited bone recovery during repletion in growing rats.
本研究的目的是调查膳食锌缺乏和饮食限制对生长中大鼠骨骼发育的影响,并确定膳食补充是否可以逆转任何不良影响。将断奶大鼠随意喂食缺锌饮食(ZD;锌含量<1 mg/kg)或营养完全的饮食(锌含量30 mg/kg),随意进食组(CTL)或与ZD组摄入量配对喂食(DR;饮食限制)3周(缺乏阶段),然后所有组随意喂食锌充足的饮食3、7或23天(补充阶段)。使用双能X线吸收法分析切除的股骨的骨矿物质密度(BMD),并分析血浆中的骨形成标志物(骨钙素)和骨吸收标志物(Ratlaps)。在缺乏阶段后,与DR相比,ZD的体重较低,股骨BMD、锌和磷浓度降低;与CTL相比,DR中的这些参数更低。各组之间股骨钙浓度没有变化。ZD中血浆骨钙素降低和DR中血浆Ratlaps升高表明锌缺乏限制骨形成,而饮食限制加速骨吸收活性。补充23天后,与DR和CTL相比,ZD的股骨大小、BMD和锌浓度仍然较低。补充后,ZD和DR的体重和股骨磷浓度与CTL相比仍然较低。补充阶段后血浆骨钙素浓度没有差异,但与CTL相比,DR中的血浆Ratlaps浓度仍然升高。总之,ZD和DR在快速生长期间都会导致骨质减少,但机制似乎是由于ZD中骨建模减少和DR中骨转换增加。锌缺乏比饮食限制对骨骼发育的损害更大,并且两种缺乏都限制了生长中大鼠补充期间的骨骼恢复。