Postnatal development of jejunal sucrase: independence from cyclic AMP.
It has previously been shown that jejunal sucrase activity becomes increasingly responsive to glucocorticoids between the postnatal ages of 4 and 15 days. This study examines the possibility that cyclic AMP is the mediator of the increasing responsiveness. When dibutyryl cyclic AMP was administered concomitantly with glucocorticoid to rat pups aged 6 days, there was no enhancement of sucrase activity in pups sacrificed either 30 or 54 h later. To check for short-lived effects of cyclic AMP, pups aged 5 days were pretreated with glucocorticoid for 2 days to elicit sucrase activity, then received dibutyryl cyclic AMP by injection and were sacrificed 1, 3 and 6 h later. Once again there was no effect of cyclic AMP on sucrase activity. The final approach was to use cholera enterotoxin to stimulate epithelial adenylyl cyclase in jejunal segments in vivo. Under these conditions the stimulation of fluid secretion served as positive evidence that intracellular concentrations of cyclic AMP were elevated. However, once again there was no stimulation of sucrase activity. It is concluded that cyclic AMP does not mediate the increasing responsiveness of the developing intestine to glucocorticoids.
D000818:Animals; D000831:Animals, Newborn; D002771:Cholera; D000242:Cyclic AMP / Q000494:pharmacology*; D003907:Dexamethasone / Q000494:pharmacology; D004768:Enterotoxins / Q000494:pharmacology; D006854:Hydrocortisone / Q000031:analogs & derivatives / Q000494:pharmacology; D007583:Jejunum / Q000187:drug effects / Q000201:enzymology*; D051381:Rats; D013393:Sucrase / Q000096:biosynthesis*
D004768:Enterotoxins; C021650:hydrocortisone acetate; D003907:Dexamethasone; D000242:Cyclic AMP; D013393:Sucrase; D006854:Hydrocortisone