Mechanisms underlying intestinal adaptation after massive intestinal resection in the rat

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).

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.

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, micromol/cm2/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).

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.