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To determine whether a factor appearing in the milk at the beginning of the 3rd postnatal week elicits the appearance of jejunal sucrase activity in the pups, pups were raised with dams that had been lactating for either a week less or a week more than their natural mothers. Pups were sacrificed at 15, 17, 19, 21 and 23 days of age for assay of jejunal sucrase and for measurement of the proportion of chow in the stomachs. Sucrase activity appeared at the same age in all pups (day 17); however, at days 21 and 23 the enzyme activity was higher in the pups cross-fostered to the longer-lactating dams. Correspondingly, the analysis of stomach contents showed that these pups had almost completed weaning by day 21 whereas the other pups were still taking 40–50% milk. It is concluded that neither the appearance of jejunal sucrase nor the onset of weaning is cued by the appearance of a factor in the milk at the beginning of the 3rd postnatal week. However, the lactational stage of the dam can affect the rate of completion of weaning and, secondarily, the terminal portion of the sucrase rise.

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.