Mechanisms underlying intestinal adaptation after massive intestinal resection in the rat

被引:31
作者
Sigalet, DL [1 ]
Martin, GR [1 ]
机构
[1] Childrens Mercy Hosp, Dept Surg, Sect Transplant Surg, Kansas City, MO 64108 USA
关键词
sodium glucose cotransporter; nutrient transport; Ussing chamber; short bowel syndrome;
D O I
10.1016/S0022-3468(98)90667-4
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Background/Purpose: The regulatory events that control the adaptive response after massive intestinal resection are poorly understood. An improved understanding could lead to improved clinical therapies. This study tests the hypothesis that massive intestinal resection increases nutrient transport by upregulation of mRNA for the sodium glucose cotransporter (SGLT1). Method: Male Lewis rats (225 to 250 g) were studied. Control animals (Con, n = 6) underwent ileal transection 15 cm proximal to the cecum; resected animals (Res, n = 8) underwent resection of all bowel proximal to the terminal 15 cm of ileum. Animals were followed up for 14 days, pair fed, and weighed daily. At the time of death the terminal ileum was studied quantifying SGLT1 mRNA using reverse transcriptase-polymerase chain reaction (RT-PCR) normalized to B-actin, in vitro glucose transport in Ussing Chambers, and histology. Results: All animals survived; animals that were transected regained preoperative weight by day 10, and underwent resection by day 14. Significant adaptation occurred with increases in villus height, (control jejunum 934 +/- 79; control ileum, 811 +/- 64 v resected ileum, 949 +/- 83 [P < .05]). Nutrient flux (J mucosal --> serosa; Jms) was increased in resected ileum (3-0 Methyl-D-Glucose flux: 0.71 +/- 0.2 v 0.56 +/- 0.04 in Con ileum [P < .05; units, mu mol/cm(2)/hr of 3-0 Methyl-D-Glucose]). This was paralleled by an increase in expression of the SGLT1 gene in resected ileum, 104 +/- 14, versus Con ileum, 74 +/- 9 (P < .05; values normalized versus expression of B-actin). Conclusion: SGLT1 expression may be useful as a marker of the adaptive process after massive resection and potentially may be used as an endpoint of therapy after resection clinically, J Pediatr Surg 33:889-892. Copyright (C) 1998 by W.B. Saunders Company.
引用
收藏
页码:889 / 892
页数:4
相关论文
共 17 条
[1]   A BIOCHEMICAL PERSPECTIVE OF THE POLYMERASE CHAIN-REACTION [J].
BLOCH, W .
BIOCHEMISTRY, 1991, 30 (11) :2735-2747
[2]   INCREASED ACTIVITY OF DIGESTIVE ENZYMES IN ILEAL ENTEROCYTES ADAPTING TO PROXIMAL SMALL-BOWEL RESECTION [J].
CHAVES, M ;
SMITH, MW ;
WILLIAMSON, RCN .
GUT, 1987, 28 (08) :981-987
[3]  
Collins J B, 1995, Semin Pediatr Surg, V4, P60
[4]  
DOWLING RH, 1967, CLIN SCI, V32, P139
[5]   ALTERED GLUCOSE CARRIER EXPRESSION - MECHANISM OF INTESTINAL ADAPTATION DURING STREPTOZOCIN-INDUCED DIABETES IN RATS [J].
FEDORAK, RN ;
CHEESEMAN, CI ;
THOMSON, ABR ;
PORTER, VM .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 261 (04) :G585-G591
[6]   CRYPT-VILLUS SITE OF SUBSTRATE-DEPENDENT REGULATION OF MOUSE INTESTINAL GLUCOSE TRANSPORTERS [J].
FERRARIS, RP ;
DIAMOND, JM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (12) :5868-5872
[7]   EXPRESSION CLONING AND CDNA SEQUENCING OF THE NA+/GLUCOSE COTRANSPORTER [J].
HEDIGER, MA ;
COADY, MJ ;
IKEDA, TS ;
WRIGHT, EM .
NATURE, 1987, 330 (6146) :379-381
[8]   ADAPTATION OF THE NA+/GLUCOSE COTRANSPORTER FOLLOWING INTESTINAL RESECTION [J].
HINES, OJ ;
BILCHIK, AJ ;
ZINNER, MJ ;
SKOTZKO, MJ ;
MOSER, AJ ;
MCFADDEN, DW ;
ASHLEY, SW .
JOURNAL OF SURGICAL RESEARCH, 1994, 57 (01) :22-27
[9]   IGF-I AND THE TRUNCATED ANALOG DES-(1-3)IGF-I ENHANCE GROWTH IN RATS AFTER GUT RESECTION [J].
LEMMEY, AB ;
MARTIN, AA ;
READ, LC ;
TOMAS, FM ;
OWENS, PC ;
BALLARD, FJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 260 (02) :E213-E219
[10]   3-DIMENSIONAL STRUCTURE AND CELL-KINETICS AT DIFFERENT SITES OF RAT INTESTINAL REMNANTS DURING THE EARLY ADAPTIVE RESPONSE TO RESECTION [J].
MENGE, H ;
HOPERT, R ;
ALEXOPOULOS, T ;
RIECKEN, EO .
RESEARCH IN EXPERIMENTAL MEDICINE, 1982, 181 (02) :77-94