R. Dimaline et al., FOOD STIMULATION OF HISTIDINE-DECARBOXYLASE MESSENGER-RNA ABUNDANCE IN RAT GASTRIC FUNDUS, Journal of physiology, 465, 1993, pp. 449-458
1. Histidine decarboxylase in the enterochromaffin-like cells of the g
astric corpus mucosa converts histidine to histamine which in turn sti
mulates gastric acid secretion. The control of histidine decarboxylase
activity is poorly understood. We have examined how fasting and refee
ding influence the abundance of the messenger RNA encoding histidine d
ecarboxylase in the gastric corpus of the rat. 2. The polymerase chain
reaction was used to generate a probe for detection of histidine deca
rboxylase messenger RNA in Northern and slot blots of total RNA from t
he gastric corpus of rats fasted for up to 48 h, or fasted and then re
fed. A gastrin monoclonal antibody was used to neutralize the action o
f endogenous gastrin. 3. Fasting progressively reduced histidine decar
boxylase messenger RNA abundance by 3- to 4-fold after 48 h. Refeeding
induced a rapid increase in histidine decarboxylase messenger RNA abu
ndance which was detectable after 30 min. 4. There was a significant c
orrelation between histidine decarboxylase messenger RNA abundance and
plasma gastrin. Administration of gastrin antibody inhibited the incr
ease in histidine decarboxylase activity after 6 h refeeding, but not
after refeeding for 30 min. 5. The results suggest that histamine-medi
ated changes in postprandial acid secretion depend on control of histi
dine decarboxylase mRNA levels, and that gastrin regulates production
of this enzyme in the rat over periods of a few hours.