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大鼠体内细胞因子给药诱导宿主消瘦的机制。

Mechanisms of host wasting induced by administration of cytokines in rats.

作者信息

Ling P R, Schwartz J H, Bistrian B R

机构信息

Laboratory of Nutrition/Infection, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.

出版信息

Am J Physiol. 1997 Mar;272(3 Pt 1):E333-9. doi: 10.1152/ajpendo.1997.272.3.E333.

DOI:10.1152/ajpendo.1997.272.3.E333
PMID:9124536
Abstract

This study determined the effects of chronic administration of the two principal proximate cytokines, interleukin-1 (IL-1) and tumor necrosis factor (TNF), on host wasting in rats. The effects were compared with those observed in a matched pair-fed group to distinguish the contribution from anorexia. Both TNF and IL-1 produced weight loss, net nitrogen loss, and skeletal muscle catabolism and increased liver weight. Such effects were independent from and additive to those resulting from semistarvation. However, under equivalent nutritional conditions, TNF infusion led to a greater effect on muscle protein catabolism and liver weight and caused liver protein anabolism, whereas only the group receiving IL-1 had altered glucose metabolism in the postabsorptive state. Tachyphylaxis was seen in the response of food intake over time after administration of IL-1. These actions define the two principal mechanisms for the development of protein calorie malnutrition that occur because of cytokine action, anorexia producing semistarvation and an increased net protein catabolic rate reducing anabolic efficiency.

摘要

本研究确定了长期给予两种主要的近端细胞因子白细胞介素-1(IL-1)和肿瘤坏死因子(TNF)对大鼠宿主消瘦的影响。将这些影响与在配对喂食对照组中观察到的影响进行比较,以区分厌食症的作用。TNF和IL-1均导致体重减轻、净氮损失、骨骼肌分解代谢并增加肝脏重量。这些影响独立于半饥饿导致的影响且与之相加。然而,在同等营养条件下,输注TNF对肌肉蛋白质分解代谢和肝脏重量的影响更大,并导致肝脏蛋白质合成代谢,而只有接受IL-1的组在吸收后状态下葡萄糖代谢发生了改变。给予IL-1后,随着时间推移食物摄入量的反应出现了快速耐受现象。这些作用确定了由于细胞因子作用导致蛋白质热量营养不良发生的两种主要机制,厌食症导致半饥饿,而净蛋白质分解代谢率增加降低了合成代谢效率。

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