Abstract

Background/Purpose: Short bowel syndrome results from small intestine loss but frequently is associated with survival of the colon. This study was designed to determine if colonic mucosa could be induced to absorb galactose by tranfection of the sodium glucose cotransporter, SGLT-1 into a colonic segment. Methods: Using 10 rats, a 7-cm segment of colon was infused for 1 hour with a solution containing 50 μg/mL of a plasmid with or without an SGLT-1 insert. An 80% small bowel resection was performed, and the segment was interposed into the small bowel. On the third day [14C] galactose absorption was measured. Mucosal RNA was extracted, and relative band intensities were measured using primers for SGLT-1. Statistical analysis was performed using the Student's t test and expressed as mean ± SEM. Results: Rats transfected with the SGLT-1 plasmid showed a significant increase (194%) in galactose absorption compared with controls. Transfected animals also showed high levels of of SGLT-1 transcription when compared with controls (792% increase). Conclusions: These data show that in vivo exposure of colon mucosa to a plasmid containing SGLT-1 allows transfer of that gene into enterocytes. Expression of SGLT-1 can create an absorptive segment that may in part alleviate the malabsorption associated with short bowel syndrome. J Pediatr Surg 37:1076-1080. Copyright 2002, Elsevier Science (USA). All rights reserved.

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