Effects of dexamethasone on antral mucosal protein and gastric development in postnatal rats

The rat stomach undergoes major developmental changes postnatally. An antral mucosal protein (AMP-18) with in vitro mitogenic activity has recently been found in the mammalian stomach.

To evaluate the role of AMP-18 in gastric development in postnatal rats, the AMP-18 content of glandular stomach extracts from postnatal rats at different ages were measured by Western blots using anti-AMP-18 specific serum. Dexamethasone administration was used to evaluate the corticosteroid regulation of AMP-18 expression.

AMP-18 was detected only in glandular stomach homogenate and gastric mucus. AMP-18 and pepsin levels were high at birth. Both decreased postnatally to low levels at 7 days of age, then increased at 10-15 days of age and reached peak levels around weaning (18-21 days of age). The glandular stomach showed stepwise growth relative to body weight, with a significant increase at 18-20 days of age. The forestomach showed a decrease in growth relative to body weight during the same period. Dexamethasone given to pups before 7 days of age induced the accumulation of AMP-18 and pepsin. Induction of AMP-18 by dexamethasone was evident by 7 hours with a delayed increase in glandular stomach mass 30 hours after dexamethasone injection. Induction of AMP-18 by dexamethasone was attenuated by RU-486 but not by spironolactone.

Increases in AMP-18, pepsin and glandular stomach mass during normal postnatal development suggest that AMP-18 might be involved in gastric maturation, at least in the glandular portion. Dexamethasone induction of pepsin and AMP-18 and the subsequent increase in glandular stomach mass also suggest a possible role for AMP-18 in glandular stomach maturation. Dexamethasone apparently acts through the type II corticosteroid receptor to induce AMP-18.