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镁和锌缺乏对骨骼肌和心脏生长及蛋白质合成的影响。

Effects of magnesium and zinc deficiencies on growth and protein synthesis in skeletal muscle and the heart.

作者信息

Dørup I, Clausen T

机构信息

Institute of Physiology, University of Aarhus, Denmark.

出版信息

Br J Nutr. 1991 Nov;66(3):493-504. doi: 10.1079/bjn19910050.

Abstract

The effects of magnesium or zinc deficiency on growth, tissue contents of Mg or Zn and protein synthesis have been compared in 4-13-week-old rats. When maintained on Mg-deficient fodder (1.6 mmol/kg) or Zn-deficient fodder (27 mumol/kg) rats showed a reduced weight gain, whereas repletion caused increased growth rates. Pair-feeding experiments showed that this could not be attributed to reduced energy intake only. In rats maintained on Mg-deficient fodder for 14 d [3H] leucine incorporation into skeletal muscle and the heart was reduced by 24-38% compared with pair-fed controls (P less than 0.001-0.002). The incorporation of [3H]phenylalanine was reduced by 19-31%. Tissue Mg contents, however, were only reduced by 6-7% (not significant). The pair-fed rats showed no reduction in the [3H]leucine incorporation compared with ad lib.-fed animals. In rats maintained on Zn-deficient fodder for 15 d [3H]leucine incorporation into skeletal and heart muscle was reduced by 57-64% compared with pair-fed controls. The pair-fed rats showed no reduction in the [3H]leucine incorporation compared with ad lib. fed animals. In the Zn-deficient animals the content of Zn was not reduced in the skeletal muscles, whereas there was a small (15%) but significant loss of Zn in the heart. In another experiment, Zn depletion for 17 d caused a reduction in [3H]leucine incorporation of 35-41%. After 5 d of Zn repletion this defect was restored, and the [3H]leucine incorporation was above control level in the skeletal muscles. It is concluded that the intact organism is very sensitive to dietary Mg or Zn deficiency, and that the reduced growth and protein synthesis cannot easily be attributed to the reduction of tissue Mg or Zn content per se. This points to the existence of other control mechanisms mediating down-regulation of growth and protein synthesis in response to reduced dietary supplies and the ensuing drop in the plasma concentrations of Mg and Zn.

摘要

在4至13周龄的大鼠中,比较了镁或锌缺乏对生长、组织中镁或锌含量以及蛋白质合成的影响。当大鼠食用缺镁饲料(1.6 mmol/kg)或缺锌饲料(27 μmol/kg)时,体重增加减少,而补充后生长速率增加。配对喂养实验表明,这不能仅归因于能量摄入减少。在食用缺镁饲料14天的大鼠中,与配对喂养的对照组相比,[3H]亮氨酸掺入骨骼肌和心脏的量减少了24%至38%(P<0.001 - 0.002)。[3H]苯丙氨酸的掺入减少了19%至31%。然而,组织中的镁含量仅减少了6%至7%(无显著性差异)。与自由采食的动物相比,配对喂养的大鼠[3H]亮氨酸掺入量没有减少。在食用缺锌饲料15天的大鼠中,与配对喂养的对照组相比,[3H]亮氨酸掺入骨骼肌和心肌的量减少了57%至64%。与自由采食的动物相比,配对喂养的大鼠[3H]亮氨酸掺入量没有减少。在缺锌动物中,骨骼肌中的锌含量没有降低,而心脏中的锌有少量(15%)但显著的损失。在另一项实验中,锌缺乏17天导致[3H]亮氨酸掺入量减少35%至41%。锌补充5天后,这一缺陷得到恢复,骨骼肌中[3H]亮氨酸掺入量高于对照水平。结论是,完整的生物体对饮食中镁或锌缺乏非常敏感,生长和蛋白质合成减少不能轻易归因于组织中镁或锌含量本身的降低。这表明存在其他控制机制,介导生长和蛋白质合成的下调,以应对饮食供应减少以及随之而来的血浆镁和锌浓度下降。

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