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Reversible drug-induced oxyntic atrophy in rats.
J R Goldenring1, G S Ray, R J Coffey
1Augusta Veterans Affairs Medical Center, Institute of Molecular Medicine, Department of Medicine, Medical College of Georgia, Augusta, Georgia, USA. jgolden@mail.mcg.edu
Gastroenterology
|June 2, 2000
Summary
High doses of DMP 777 in rats cause reversible oxyntic atrophy by specifically targeting parietal cells. Withdrawal of DMP 777 allows for complete restoration of normal gastric mucosal lineages.
Area of Science:
- Gastroenterology
- Cell Biology
- Pharmacology
Background:
- Oxyntic atrophy, a key feature of chronic gastritis, lacks effective reversible animal models.
- Previous models for oxyntic atrophy have not demonstrated reversibility.
Purpose of the Study:
- To investigate the effects of DMP 777 on gastric oxyntic atrophy in rats.
- To determine if DMP 777-induced oxyntic atrophy is reversible.
Main Methods:
- CD-1 rats were administered high-dose DMP 777 orally.
- Evaluated serum gastrin, in vivo acid secretion, and gastric histology.
- Assessed DMP 777's direct effects on isolated rabbit parietal cells and H(+),K(+)-ATPase activity.
Main Results:
- DMP 777 induced rapid hypochlorhydria and loss of parietal cells.
- Observed foveolar hyperplasia and sustained oxyntic atrophy with extended dosing.
- Drug withdrawal led to complete restoration of normal mucosal lineages within 3 months.
Conclusions:
- DMP 777 acts as a protonophore, specifically targeting parietal cell membranes.
- High-dose DMP 777 causes specific parietal cell loss, leading to foveolar hyperplasia and altered mucosal lineages.
- Parietal cells are crucial for maintaining normal gastric mucosal lineage repertoire.
