The activity of N-acetylglucosamine kinase in rat gastric mucosa.

The activity of N-acetylglucosamine kinase in the rat glandular stomach was studied to elucidate its participation in aspirin-induced ulcers, and the effect of proglumide, an anti-ulcer agent which was found to increase gastric mucosal hexosamine, on this enzymatic activity was also studied. N-Acetylglucosamine kinase activity was found to be significantly higher in the antrum than in the corpus, the antrum being 1.3--1.9 times as active as the corpus. The mucosal layer itself was about 1.8--2.0 times as active as the whole tissue of the glandular stomach. This enzymatic activity in the glandular stomach was found to decrease slightly after fasting and to further decrease after intragastric administration of aspirin (100 mg/kg). The pylorus-ligated rats showed a significant decline of this enzymatic activity following the administration of aspirin. Acceleration of N-acetylglucosamine kinase activity with proglumide was demonstrated in vivo and in vitro experiments. Prior treatment with proglumide prevented aspirin-induced ulcers and correspondingly stimulated this enzymatic activity. These results suggest that the activity of N-acetylglucosamine kinase in the rat glandular stomach closely parallels the distribution and localization of gastric hexosamine, glycosaminoglycans, and glycoproteins. A decrease of this enzymatic activity correlates with the production of ulcers by aspirin. The mechanism by which proglumide increases gastric hexosamine is at least partly attributed to the activation of N-acetylglucosamine kinase in the glandular stomach.