内脏和全身亮氨酸动力学对治疗水肿性蛋白质-能量营养不良伴感染患儿的反应。

M. Reid, A. Badaloo, T. Forrester, W. Heird, F. Jahoor
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引用次数: 20

摘要

背景:虽然蛋白质-能量营养不良(PEM)引起的全身蛋白质周转和净蛋白质损失的减少已经有了很好的文献记载,但目前尚不清楚由长期摄入不足的膳食蛋白质和能量引起的蛋白质节约机制是否受到感染的蛋白质分解代谢反应的影响。目的本研究的目的是确定感染的存在是否会改变pem诱导的全身蛋白质代谢的减少。设计:我们测定了4名6-15个月的男孩和3名女孩的全身亮氨酸动力学,这些男孩和3名女孩在入院后大约3天患有PEM水肿和感染(研究1),当时他们同时感染和营养不良;入院后大约11天(研究2),感染已经消退,但人体测量学上仍然营养不良;在恢复时(研究3),体重长度比至少是预期的90%。结果研究1和研究2的儿童亮氨酸通量明显低于研究3。在研究1和研究2中,从蛋白质分解中释放的亮氨酸或用于蛋白质合成的亮氨酸的数量没有显著差异。在3项研究中,亮氨酸平衡、内脏组织提取亮氨酸的量和百分比均无显著差异。结论:当受试者处于进食状态时,严重的PEM会导致全身蛋白质合成和分解率显著降低,而感染的存在不会改变这种适应,因此也不会改变整体蛋白质平衡。一个推论是,患有严重PEM的儿童不会对感染产生蛋白质分解代谢反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Response of splanchnic and whole-body leucine kinetics to treatment of children with edematous protein-energy malnutrition accompanied by infection.
BACKGROUND Although the reduction in whole-body protein turnover and net protein loss induced by protein-energy malnutrition (PEM) has been well documented, it is unclear whether the protein-sparing mechanisms elicited by chronically inadequate intakes of dietary protein and energy are affected by the protein catabolic response to infection. OBJECTIVE The objective of this study was to determine whether the presence of infection alters the PEM-induced reduction in whole-body protein metabolism. DESIGN We determined whole-body leucine kinetics in 4 boys and 3 girls aged 6-15 mo with edematous PEM and infection approximately 3 d after admission (study 1), when they were both infected and malnourished; approximately 11 d after admission (study 2), when infection had resolved but they were still anthropometrically malnourished; and at recovery (study 3), when weight-for-length was at least 90% of that expected. RESULTS The children had significantly less leucine flux in both study 1 and study 2 than they had in study 3. There were no significant differences in the amount of leucine released from protein breakdown or used for protein synthesis between study 1 and study 2. There were no significant differences in leucine balance or in either the amount or percentage of enteral leucine extracted by the splanchnic tissues among the 3 studies. CONCLUSIONS When subjects are in the fed state, severe PEM induces a marked reduction in whole-body protein synthesis and breakdown rates, and the presence of infection does not alter this adaptation and hence the overall protein balance. A corollary is that children with severe PEM do not mount a protein catabolic response to infection.
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