Abstract
Helicobacter pylori (H. pylori) alters metabolism during the gastric carcinogenesis process. This study aimed to determine the metabolites in the gastric mucosa according to the status of the H. pylori infection. Patients who visited the outpatient clinic for a gastroscopy and H. pylori tests were included. Gas chromatography–time-of-flight mass spectrometry (GC-TOF-MS) analysis was performed using gastric biopsied specimens from the corpus. Twenty-eight discriminative metabolites were found in the gastric mucosa of 10 patients with current H. pylori infection, in 15 with past infection, and in five with no infection history. The relative abundances (RAs) of amino acids and sugars/sugar alcohols were higher in patients with no infection history than in patients with current or past infection. The current infection group showed higher RAs of organic acids and lower RAs of fatty acids and lipids compared with the other groups. The RA of inosine was highest in the past infection group. Based on GC-TOF-MS analysis findings, metabolites differed not only between the infected and non-infected patients, but also between those with and without infection history. Amino acid and sugars/sugar alcohol metabolites decreased in patients with current or past infection, whereas fatty acid and lipid metabolites decreased only during current infection.
Highlights
Helicobacter pylori (H. pylori) infection induces the carcinogenesis process in the human stomach
We found significant differences in fatty acid/lipid, amino acid, and sugar/sugar alcohol metabolites between patients with current infection, past infection, and no infection history
Non-targeted metabolite profiling of gastric mucosa tissues reveals that the loss of amino acids and sugar/sugar alcohols is observed in patients with current or past infection
Summary
Helicobacter pylori (H. pylori) infection induces the carcinogenesis process in the human stomach. Some precancerous lesions including gastric atrophy and intestinal metaplasia (IM) may persist even after the regression of H. pylori; the risk of gastric cancer is higher in stomachs with infection history than in H. pylori-naive stomachs [1,2]. The risk increases with the degree of atrophy and IM, which extends from the antrum to the corpus [3,4]. H. pylori alters metabolism after infection and changes metabolic dynamics when eradicated [5]. H. pylori infection leads to the loss of carboxylic acids and amino acids in the corpus and antrum [6]. The corpus exhibited significant metabolite changes related to stress, tissue damage, and nutrient depletion in contrast to the antrum. 43 plasma metabolites involved in amino acid, lipid, and fatty acid metabolism differed between H. pylori-infected, non-infected, and gastric cancer patients [7]
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