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全胃肠外营养所致肝脂肪变性:短肠综合征、再喂养及小肠移植的影响

Hepatic steatosis due to total parenteral nutrition: the influence of short-gut syndrome, refeeding, and small bowel transplantation.

作者信息

Langrehr J M, Reilly M J, Banner B, Warty V J, Lee K K, Schraut W H

机构信息

Department of Surgery, School of Medicine, University of Pittsburgh, Pennsylvania 15261.

出版信息

J Surg Res. 1991 Apr;50(4):335-43. doi: 10.1016/0022-4804(91)90200-6.

Abstract

This study was undertaken to determine whether refeeding through the native small intestine or through a small bowel transplant would reverse hepatic steatosis induced by total parenteral nutrition (TPN), and of what influence a coexisting short-gut syndrome is. Three short-gut syndromes of different severity were established in Lewis rats (short-gut I, mild; short-gut II, moderate; short-gut III, severe). TPN was administered for 10 days and the animals were refed for 20 days. A liver biopsy after the TPN period confirmed a mild to moderate fatty infiltration of the liver in all groups. After the refeeding period a second liver biopsy was obtained and no evidence of hepatic steatosis was observed in Groups 1, 2, 3, and 4 (normal Lewis rat, short-gut I, II, and III). The animals in group 5 (short-gut I) received a syngeneic small bowel transplant after discontinuation of TPN. After the refeeding period the liver biopsies showed no evidence of fatty infiltration. The intestinal graft also reversed the nutritional deficiencies which were observed in the animals with short-gut and showed normal body weight gain and nitrogen and fat uptake in comparison to the normal animals (Group 1). These data show that a small bowel graft is capable of reversing the deleterious sequelae of short-gut syndrome as well as the TPN-related hepatic steatosis.

摘要

本研究旨在确定通过天然小肠或小肠移植进行再喂养是否能逆转全肠外营养(TPN)诱导的肝脂肪变性,以及共存的短肠综合征会产生何种影响。在Lewis大鼠中建立了三种不同严重程度的短肠综合征(短肠I型,轻度;短肠II型,中度;短肠III型,重度)。给予TPN 10天,然后对动物进行20天的再喂养。TPN期结束后的肝活检证实所有组均有轻度至中度肝脂肪浸润。再喂养期结束后进行第二次肝活检,第1、2、3和4组(正常Lewis大鼠、短肠I型、II型和III型)未观察到肝脂肪变性的证据。第5组(短肠I型)的动物在停止TPN后接受了同基因小肠移植。再喂养期结束后的肝活检未显示脂肪浸润的证据。肠移植还逆转了短肠动物中观察到的营养缺乏,与正常动物(第1组)相比,体重增加正常,氮和脂肪摄取正常。这些数据表明,小肠移植能够逆转短肠综合征的有害后遗症以及与TPN相关的肝脂肪变性。

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