Carbenoxolone accelerates maturation of rat intestine.

Abstract:

:The rat undergoes profound maturational changes in the intestinal structure and function during the third week of its life. To investigate the role of peripheral glucocorticoid metabolism in this process, we studied the postnatal maturation of intestinal structure and function. The peripheral metabolism of glucocorticoids depends on enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD), which is responsible for the interconversion of corticosterone to 11-dehydrocorticosterone and thus for the modulation of glucocorticoid access to corticosteroid receptors. The pups were treated with carbenoxolone (CBX), an inhibitor of 11betaHSD, for 10 d during the suckling (days 8-18) or weaning period (days 14-24 or days 20-30), and we determined the parameters of intestinal growth and activities of sucrase, alkaline phosphatase, and Na,K-ATPase. The CBX treatment increased plasma concentrations of corticosterone as a result of a significant reduction of peripheral degradation of corticosterone catalyzed by 11betaHSD. This also stimulated intestinal growth without changing somatic growth. The mucosal cell mass was significantly higher in CBX-treated suckling rats, whereas the effect of this treatment was less obvious in weanling animals. CBX increased the crypt depth and villus height in 18- and 24-d-old pups but not in 30-d-old animals. The small intestinal activities of sucrase, alkaline phosphatase, and Na,K-ATPase were not influenced by CBX. In contrast, colonic Na,K-ATPase was stimulated by CBX. We conclude that the administration of CBX results in acceleration of intestinal growth and structural maturation without any influence on the developmental pattern of brush-border hydrolases. The results indicate an important role of peripheral glucocorticoid metabolism in the regulation of intestinal growth during early postnatal life.

journal_name

Pediatr Res

journal_title

Pediatric research

authors

Pácha J,Vagnerová R,Bryndová J

doi

10.1203/01.PDR.0000058923.08017.6F

subject

Has Abstract

pub_date

2003-05-01 00:00:00

pages

808-13

issue

5

eissn

0031-3998

issn

1530-0447

pii

01.PDR.0000058923.08017.6F

journal_volume

53

pub_type

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