Effects of Dexamethasone on Antral Mucosal Protein and Gastric Development in Postnatal Rats

• Published in: Journal of pediatric gastroenterology and nutrition Vol. 40; no. 4; pp. 461 - 466
• Main Authors: Petri, Michael K, Lee, Ping C
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins, Inc 01.04.2005; Lippincott
• Subjects: Aging - physiology; Animals; Animals, Newborn; Antrum mucosal protein; Biological and medical sciences; Bones, joints and connective tissue. Antiinflammatory agents; Dexamethasone - pharmacology; Female; Gastric development; Gastric Mucosa - drug effects; Gastric Mucosa - growth & development; Gene Expression Regulation, Developmental; Glucocorticoids - pharmacology; Hormone; Immunohistochemistry; Male; Medical sciences; Mitogens - metabolism; Pepsin; Pepsin A - metabolism; Peptide Hormones; Peptides; Pharmacology. Drug treatments; Rats; Rats, Sprague-Dawley; Receptors, Glucocorticoid - drug effects; Receptors, Glucocorticoid - metabolism; Stomach - drug effects; Stomach - growth & development; Corticosteroid; Stomach; Dexamethasone; Rat; Steroid hormone; Rodentia; Antiinflammatory agent; Antrum mucosal protein- Pepsin-Gastric development-Hormone; Postnatal development; Protein; Vertebrata; Antrum pyloricum; Mammalia; Animal
• ISSN: 0277-2116; 1536-4801
• DOI: 10.1097/01.MPG.0000155565.64279.05

ABSTRACT Background: The rat stomach undergoes major developmental changes postnatally. An antral mucosal protein (AMP‐18) with in vitro mitogenic activity has recently been found in the mammalian stomach. Methods: To evaluate the role of AMP‐18 in gastric development in postnatal rats, the AMP‐18 content of glandular stomach extracts from postnatal rats at different ages were measured by Western blots using anti‐AMP‐18 specific serum. Dexamethasone administration was used to evaluate the corticosteroid regulation of AMP‐18 expression. Results: AMP‐18 was detected only in glandular stomach homogenate and gastric mucus. AMP‐18 and pepsin levels were high at birth. Both decreased postnatally to low levels at 7 days of age, then increased at 10‐15 days of age and reached peak levels around weaning (18‐21 days of age). The glandular stomach showed stepwise growth relative to body weight, with a significant increase at 18‐20 days of age. The forestomach showed a decrease in growth relative to body weight during the same period. Dexamethasone given to pups before 7 days of age induced the accumulation of AMP‐18 and pepsin. Induction of AMP‐18 by dexamethasone was evident by 7 hours with a delayed increase in glandular stomach mass 30 hours after dexamethasone injection. Induction of AMP‐18 by dexamethasone was attenuated by RU‐486 but not by spironolactone. Conclusion: Increases in AMP‐18, pepsin and glandular stomach mass during normal postnatal development suggest that AMP‐18 might be involved in gastric maturation, at least in the glandular portion. Dexamethasone induction of pepsin and AMP‐18 and the subsequent increase in glandular stomach mass also suggest a possible role for AMP‐18 in glandular stomach maturation. Dexamethasone apparently acts through the type II corticosteroid receptor to induce AMP‐18.