Effect of cholecystokinin and 16,16-dimethyl prostaglandin E2 on RNA and DNA of gastric and duodenal mucosa

L R Johnson , P Guthrie

Gastroenterology +

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January 1, 1976

View abstract on PubMed

Summary

Pentagastrin significantly boosted DNA synthesis and content in rat gastric and duodenal mucosa. Cholecystokinin-octopeptide (CCK-OP) showed weak duodenal trophic effects and inhibited gastrin

Area Of Science

Gastroenterology
Cell Biology
Endocrinology

Background

Gastrin and cholecystokinin (CCK) are gastrointestinal hormones with potential trophic effects.
Understanding their roles in mucosal growth is crucial for digestive health.
Prostaglandins also influence gastrointestinal function and mucosal integrity.

Purpose Of The Study

To investigate the comparative trophic effects of pentagastrin, CCK-OP, and 16,16-dimethyl PGE2 on gastric and duodenal mucosa in rats.
To determine the impact of these agents on DNA synthesis and nucleic acid content.
To assess potential interactions between CCK-OP and pentagastrin.

Main Methods

Rats were administered pentagastrin, CCK-OP, 16,16-dimethyl PGE2, or saline every 8 hours for 48 hours.
DNA synthesis was measured using [3H]thymidine incorporation.
Total DNA and RNA content in gastric and duodenal mucosa were quantified.

Main Results

Pentagastrin significantly increased DNA synthesis and content in both gastric and duodenal mucosa.
CCK-OP demonstrated weak trophic effects in the duodenum but not the stomach, and stimulated pancreatic DNA synthesis.
16,16-dimethyl PGE2 did not stimulate mucosal growth but increased duodenal RNA content, suggesting potential hypertrophy.

Conclusions

Pentagastrin is a potent trophic hormone for gastric and duodenal mucosa.
CCK-OP has limited trophic effects on the stomach and duodenum, and can inhibit gastrin's effects.
16,16-dimethyl PGE2 may promote duodenal mucosal activity and hypertrophy without interfering with gastrin's growth-promoting actions.

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