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Am J Physiol Regul Integr Comp Physiol (January 30, 2003). doi:10.1152/ajpregu.00721.2001
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Submitted on December 3, 2001
Accepted on January 17, 2003

NORMAL AND GLUCOCORTICOID INDUCED DEVELOPMENT OF THE HUMAN SMALL INTESTINAL XENOGRAFT

N. N Nanthakumar1*, Corrie E Klopcic2, and W. A Walker1

1 Pediatric Gastroenterology and Nutrition, Massachusetts General Hospital, Chalestown, MA, USA; Pediatrics, Harvard Medical School, Boston, MA, USA
2 Pediatric Gastroenterology and Nutrition, Massachusetts General Hospital, Chalestown, MA, USA

* To whom correspondence should be addressed. E-mail: nanthaku{at}helix.mgh.harvard.edu.

The aim was to determine whether intestinal xenografts could recapitulate human in utero development, using disaccharidases as markers. Twenty-week-old fetal intestine was transplanted into immunocompromised mice and was followed. At 20-weeks of gestation, the fetal human intestine is morphologically developed with high sucrase and trehalase but low lactase activities. By nine weeks post-transplantation, jejunal xenografts were morphologically and functionally developed and were then monitored for up to six months. Both sucrase and trehalase activities remained unchanged, but lactase activity increased in a manner similar to that described in in utero development. The changes in sucrase and lactase activities were paralleled by protein levels. Cortisone acetate (CA) treatment at 20 weeks post-transplantation accelerated the ontogeny of lactase but didn't alter sucrase and trehalase activities. Biopsies from 1-2 year old infant intestine showed that all activities, except trehalase in the proximal intestine, corresponded to the levels found in jejunal xenografts at 24 week post-transplantation. These studies suggest that 20 week old fetal intestine has the extrauterine developmental potential to follow normal intrauterine ontogeny as a xenograft.




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