Ontogeny of sucrase-isomaltase gene expression in rat intestine: responsiveness to glucocorticoids.

The goal of our study was to determine how sucrase-isomaltase (SI) gene expression in the rat small intestine is modulated by glucocorticoids during the second and third postnatal weeks. SI mRNA was quantitated by Northern blot and was compared with sucrase activities in the same tissue samples. The role of endogenous glucocorticoids was assessed by measuring SI mRNA and enzyme activity in rat pups adrenalectomized (ADX) on postnatal day 9. ADX pups showed a retarded appearance of sucrase activity compared with sham-operated control pups, and the appearance of SI mRNA paralleled the enzyme activity. To determine the role of exogenous glucocorticoids, a saturating dose of dexamethasone (Dex) was administered daily in three series of experiments starting on days 10, 16, and 18. In the day 10 series, Dex caused precocious appearance of both SI mRNA and sucrase activity. In the day 16 series, Dex accelerated the rate of rise of the two parameters, whereas by day 18 there was no significant effect of Dex. To investigate whether the accelerated rise in the day 16 series was associated with changes in epithelial cell kinetics, the location of SI protein was assessed by immunofluorescence staining. The results indicated that the effect of Dex at this age was due to faster emergence of SI-bearing enterocytes from the intestinal crypts.(ABSTRACT TRUNCATED AT 250 WORDS)