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营养不良时再生大鼠肝脏中的蛋白质合成

Protein synthesis in regenerating rat liver during malnutrition.

作者信息

Skullman S, Wirén M, Garlick P J, McNurlan M A, Larsson J

机构信息

Department of Medico-Surgical Gastroenterology, University Hospital, Linköping, Sweden.

出版信息

J Hepatol. 1994 Aug;21(2):174-81. doi: 10.1016/s0168-8278(05)80391-5.

Abstract

To examine the effect of malnutrition on liver protein metabolism and synthesis during liver regeneration, 104 rats were allocated to semi-starvation or ordinary food intake for 1 week. Half of each group was sham operated and the other half was partially hepatectomized. Specimens were taken from the liver at the time of liver resection and from animals killed 24, 48 and 72 h after the primary operation. Liver samples were analysed for DNA and protein, and in the 48-h groups RNA and protein synthesis were also analysed. Protein synthesis was measured by the flooding method using L[4-3H] phenylalanine. The liver weight during regeneration increased very rapidly in the well-nourished animals, but when expressed as percent of body weight or as proportional increases, the difference between well-nourished and malnourished animals disappeared. The fractional rate of protein synthesis was not changed in sham-operated malnourished or well-nourished animals. During regeneration, protein synthesis in well-nourished animals was elevated compared to sham-operated controls, but a lesser stimulation was seen in malnourished rats. It was concluded that the mechanism of liver regeneration depends on nutritional state, involving an increase in protein synthesis in well-nourished animals, but relying more on a decrease in protein degradation or cessation of secretory protein synthesis in malnourished animals.

摘要

为研究营养不良对肝脏再生过程中肝脏蛋白质代谢和合成的影响,将104只大鼠分为半饥饿组或正常饮食组,持续1周。每组一半大鼠接受假手术,另一半大鼠接受部分肝切除术。在肝切除时以及初次手术后24、48和72小时处死动物,采集肝脏标本。对肝脏样本进行DNA和蛋白质分析,对48小时组的样本还进行RNA和蛋白质合成分析。采用L-[4-³H]苯丙氨酸的灌流法测定蛋白质合成。在营养良好的动物中,再生期间肝脏重量增长非常迅速,但以体重百分比或比例增长表示时,营养良好和营养不良动物之间的差异消失。在接受假手术的营养不良或营养良好的动物中,蛋白质合成的分数率没有变化。在再生过程中,与接受假手术的对照组相比,营养良好的动物蛋白质合成增加,但营养不良的大鼠中蛋白质合成的刺激较小。得出的结论是,肝脏再生机制取决于营养状态,在营养良好的动物中涉及蛋白质合成增加,但在营养不良的动物中更多地依赖于蛋白质降解的减少或分泌性蛋白质合成的停止。

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