The development of gastric H,K-ATPase from fetal to adult life was studied in the rat. The α and β H,K-ATPase mRNA abundance, the protein abundance, and the enzyme activity increased postnatally. The sharpest increase in mRNA and enzyme activity was observed in the weaning period. Several intestinal enzymes are known to be stimulated by glucocorticoids at the time of weaning. To study the role of glucocorticoids in the maturation of gastric H,K-ATPase, we treated 10-d-old rats with a single injection of betamethasone. Twenty-four hours after betamethasone injection, the enzyme activity was significantly higher than in the control animals (2.6-fold, p < 0.05). The abundance of catalytic α H,K-ATPase protein was also increased (2.5-fold, p < 0.01). The time-dependent effect of betamethasone on α H,K- ATPase mRNA was determined from 6 to 24 h after treatment. Glucocorticoids did not significantly alter the mRNA abundance within 18 h. Twenty four hours after injection, the gastric H,K-ATPase mRNA was significantly increased compared with controls (2.8- and 2.2-fold increase for α and β subunits, respectively, p < 0.01 for both). In conclusion this study indicates that glucocorticoids may regulate the long term maturation of gastric H,K-ATPase by indirectly stimulating enzyme synthesis.
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