Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Jul 17;14:1217306. doi: 10.3389/fphar.2023.1217306

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2023 Tian, Huang, Fu, Gao, Mi, Bai, Ma, Zhang, Lu, Zhao, Zhang, Jiang, Lin, Yue, Yuan and Meng.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Mechanisms of PPI altering intestinal flora. PPIs reduce gastric acid secretion by inhibiting H⁺/K⁺ ATPase on gastric parietal cells. Lower PH levels compromise the gastric acid barrier, allowing exogenous bacteria to enter the intestine more easily. It also has a prominent effect on microorganisms with specific PH requirements, such as Helicobacter pylori. Reduced gastric PH stimulates gastric G-cells to secrete more gastrin, resulting in hypergastrinemia and hyperparathyroidism. This can disrupt the intestinal flora by interfering with the metabolism of calcium and phosphorus in the digestive tract. PPI can also interfere with the P-type ATPase of some gut microorganisms, such as fungi and Helicobacter pylori. Above mechanisms work in concert to for PPI to have a considerable effect on the gut flora.