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©The Author(s) 2026. Published by Baishideng Publishing Group Inc. All rights reserved.
Pathological effects of diabetic mice with Helicobacter pylori infection
Wan-Ping Yang, Jin-Hai Zeng, Biao-Liang Wu, Wen-Ting Zhou, Jia-Zi Luo, Yuan-Yuan Dai, Shi-Xian Yang, Zan-Song Huang, Yan-Qiang Huang
Wan-Ping Yang, Jin-Hai Zeng, Biao-Liang Wu, Wen-Ting Zhou, Jia-Zi Luo, Yan-Qiang Huang, Guangxi Technology Innovation Cooperation Base of Prevention and Control Pathogenic Microbes with Drug Resistance, Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Jin-Hai Zeng, Department of Endocrinology and Rheumatology & Immunology, Beiliu People's Hospital, Beiliu 537400, Guangxi Zhuang Autonomous Region, China
Biao-Liang Wu, Department of Endocrinology, The Affiliated Hospital of Youjiang University for Nationalities; Key Laboratory of Medical Research Basic Guarantee for Immune-Related Diseases Research of Guangxi (Cultivation), Baise 533000, Guangxi Zhuang Autonomous Region, China
Yuan-Yuan Dai, Shi-Xian Yang, Zan-Song Huang, Guangxi Clinical Medical Research Center for Hepatobiliary Diseases, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Zan-Song Huang, Guangxi Key Laboratory of Basic Research in Prevention and Treatment for Helicobacter pylori, Baise 533000, Guangxi Zhuang Autonomous Region, China
Yan-Qiang Huang, Key Laboratory of the Prevention and Treatment of Drug Resistant Microbial Infecting, Youjiang Medical University for Nationalities, Education Department of Guangxi Zhuang Autonomous Region, Baise 533000, Guangxi Zhuang Autonomous Region, China
Co-first authors: Wan-Ping Yang and Jin-Hai Zeng.
Co-corresponding authors: Zan-Song Huang and Yan-Qiang Huang.
Author contributions: Yang WP, Zeng JH and Wu BL performed the experiments, acquired and analyzed data; Zhou WT, Luo JZ, Dai YY, and Yang SX interpreted the data; Huang YQ and Huang ZS designed, wrote, guided writing the manuscript; all authors approved the final version of the article. Yang WP and Zeng JH contributed equally to this work as co-first authors. The designation of two corresponding authors is rooted in their complementary academic contributions and research management responsibilities. First, they assume distinct yet critical roles across research dimensions: One leads experimental design, oversees data curation, and ensures methodological rigor, while the other focuses on theoretical frameworks, provides critical analysis, and offers expert guidance on manuscript composition. Second, their responsibilities extend to research coordination. The author with laboratory management expertise standardizes experimental protocols, safeguards data integrity, and coordinates team workflows to optimize timelines. Concurrently, the other author-with profound academic insight-steers the research direction, resolves analytical challenges, and meticulously validates the manuscript’s technical accuracy, ensuring precise terminology and logically sound conclusions.
Supported by Guangxi Science and Technology Major Projects, No. AA23073012; and National Natural Science Foundation of China, No. 32360035 and No. 32060018.
Institutional animal care and use committee statement: This study was reviewed and review approved by the Youjiang Medical University for Nationalities Institution Board. All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Youjiang Medical University for Nationalities.
Conflict-of-interest statement: The authors declare that they have no conflicts of interest.
ARRIVE guidelines statement: The authors have read the ARRIVE Guidelines, and the manuscript was prepared and revised according to the ARRIVE Guidelines.
Data sharing statement: All relevant data are included in the manuscript. Additionally, raw data are available from the corresponding author upon reasonable request.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
https://creativecommons.org/Licenses/by-nc/4.0/ Corresponding author: Yan-Qiang Huang, MD, Professor, Key Laboratory of the Prevention and Treatment of Drug Resistant Microbial Infecting, Youjiang Medical University for Nationalities, Education Department of Guangxi Zhuang Autonomous Region, No. 98 Countryside Road, Baise 533000, Guangxi Zhuang Autonomous Region, China.
hyq77615@163.com
Received: August 8, 2025
Revised: September 8, 2025
Accepted: December 16, 2025
Published online: February 15, 2026
Processing time: 182 Days and 1 Hours
BACKGROUND
Helicobacter pylori (H. pylori) is widely present in the human gastric mucosa and is closely associated with a variety of gastric diseases. Recent studies have found that H. pylori infection is closely associated with diabetic patients and may adversely affect their glucose metabolism and organ function. However, the effect of H. pylori infection on pathological changes in the body during a diabetic state remains unclear.
AIM
To investigate the effects of H. pylori infection on the physiology and pathological changes in the organs of diabetic mice.
METHODS
The diabetic mice models were established using streptozotocin (STZ). The mice were infected with H. pylori through oral gavage, with their fasting blood glucose (FBG) and body weight monitored dynamically over a period of 1 to 13 months after infection. Pathological changes in major organs (including the pancreas, stomach, liver, and kidneys) were assessed, along with apoptosis levels in these tissues. The expression of H. pylori virulence factors in the liver and alterations in the intestinal microbiota were also analyzed.
RESULTS
H. pylori infection led to significant fluctuations in FBG in diabetic mice from the 1st to 9th month, with FBG levels remaining consistently elevated. Body weight increased gradually but remained significantly lower than that of both uninfected diabetic mice and non-diabetic controls. Pancreatic islet cell numbers decreased, accompanied by persistent inflammation and tissue damage for over 9 months. H. pylori colonized the stomach for at least 7 months, causing irreversible gastric mucosal inflammation; by the 13th month, diffuse dense inflammatory infiltration occupying the entire submucosal layer was observed. Progressive damage was observed in liver and kidney tissues, with marked expression of H. pylori virulence factors in the liver by the 9th month. Additionally, significant gut microbiota dysbiosis was observed.
CONCLUSION
The STZ-induced diabetic mouse model with H. pylori infection can significantly prolong the colonization time of H. pylori in the stomach and exacerbate the degree of damage to the stomach, liver, and kidney organs.
Core Tip: This study investigates the effects of Helicobacter pylori (H. pylori) infection on physiological functions and multiorgan pathology in diabetic mice. By establishing diabetic mouse models and subsequently performing H. pylori gavage, we monitored dynamic changes in blood glucose, organ damage, histopathology, and gut microbiota over a 13-month infection period. These findings may provide new insights for clinical interventions in patients with comorbid diabetes and H. pylori infection.
