Original Articles
Copyright ©The Author(s) 2000. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 15, 2000; 6(5): 704-708
Published online Oct 15, 2000. doi: 10.3748/wjg.v6.i5.704
Ascorbic acid secretion in the human stomach and the effect of gastrin
Bi Guang Tuo, Yong Hui Yan, Zheng Long Ge, Gang Wei Ou, Kui Zhao
Bi Guang Tuo, Yong Hui Yan, Kui Zhao, Department of Gastroenterology, Affiliated Hospital, Zunyi Medical College, Zunyi 563003, Guizhou Province, China
Zheng Long Ge, Gang Wei Ou, Department of Biochemiology, Zunyi Medical College, Zunyi, Guizhou Province, China
Bi Guang Tuo, graduated from Beijing Medical University as a postgraduate in 1992, associate professor of gastroenterology, having 14 papers published.
Author contributions: All authors contributed equally to the work.
Supported by the Youth Scientific Found of Ministry of Healthy.
Correspondence to: Dr. Bi Guang Tuo, Department of Gastroenterology, Affiliated Hospital, Zunyi Medical College, 143 Dalian Road, Zunyi 563003, Guizhou Province, China
Received: May 30, 2000
Revised: June 16, 2000
Accepted: June 23, 2000
Published online: October 15, 2000
Abstract

AIM: To investigate the changes of gastric mucosal ascorbic acid secretion in patients with nonulcer dyspepsia and the effect of gastrin on it, and to relate any observed changes to H. pylori infection and mucosal histology.

METHODS: Ascorbic acid secretions in patients were examined by collecting continuously gastric juice for one hour after having aspirated and discarded fasting gastric juice. Using the clearance rate (mL/min) of ascorbic acid from blood to gastric juice represented ascorbic acid secretion in the gastric mucosa. Ascorbic acid concentrations in plasma and juice were measured by ferric reduced method.

RESULTS: Gastric ascorbic acid secretions in H. pylori -positive patients (1.46 mL/min, range 0.27-3.78) did not significantly differ from those in H. pylori -negative patients (1.25 mL/min, 0.47-3.14) (P > 0.05). There were no significant differences in ascorbic acid secretions between patients with mild (1.56 mL/min, 0.50-3.30), moderate (1.34 mL/min, 0.27-2.93) and severe (1.36 mL/min, 0.47-3.78) inflammation (P > 0.05). There were no significant differences in ascorbic acid secretions between patients without activity (1.45 mL/min, 0.27-3.14) and with mild (1.32 mL/min, 0.61-2.93), moderate (1.49 mL/min, 0.50-3.78) and severe (1.43 mL/min, 0.51-3.26) activity of chronic gastritis either (P > 0.05). Ascorbic acid secretions in patients with severe atrophy (0.56 mL/min, 0.27-1.20) were markedly lower than those in patients with out atrophy (1.51 mL/min, 0.59-3.30) and with mild (1.43 mL/min, 0.53-3.78) and moderate (1.31 mL/min, 0.47-3.16) atrophy (P < 0.005). There was a significant negative correlation between ascorbic acid secretion and severity of atrophy (correlation coefficient = -0.43, P < 0.005). After administration of pentagastrin, ascorbic acid secretions were markedly elevated (from 1.39 mL/min, 0.36-2.96 to 3.53 mL/min, 0.84-5.91) (P < 0.001).

CONCLUSION: Ascorbic acid secretion in gastric mucosa is not affected by H. pylori infection. Gastric ascorbic acid secretion is markedly related to the severity of atrophy, whereas not related to the severity of inflammation and activity. Gastrin may stimulate gastric ascorbic acid secretion. A decreased ascorbic acid secretion may be an important factor in the link between atrophic gastritis and gastric carcinogenesis.

Keywords: gastric mucosa; gastrins; vitaminc; plasma; gastric juice; Helicobacter pylori