{"title":"Pathological effects of diabetic mice with <i>Helicobacter pylori</i> infection.","authors":"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","doi":"10.4239/wjd.v17.i2.112534","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong><i>Helicobacter pylori</i> (<i>H. pylori</i>) is widely present in the human gastric mucosa and is closely associated with a variety of gastric diseases. Recent studies have found that <i>H. pylori</i> infection is closely associated with diabetic patients and may adversely affect their glucose metabolism and organ function. However, the effect of <i>H. pylori</i> infection on pathological changes in the body during a diabetic state remains unclear.</p><p><strong>Aim: </strong>To investigate the effects of <i>H. pylori</i> infection on the physiology and pathological changes in the organs of diabetic mice.</p><p><strong>Methods: </strong>The diabetic mice models were established using streptozotocin (STZ). The mice were infected with <i>H. pylori</i> 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 <i>H. pylori</i> virulence factors in the liver and alterations in the intestinal microbiota were also analyzed.</p><p><strong>Results: </strong><i>H. pylori</i> infection led to significant fluctuations in FBG in diabetic mice from the 1<sup>st</sup> to 9<sup>th</sup> 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. <i>H. pylori</i> colonized the stomach for at least 7 months, causing irreversible gastric mucosal inflammation; by the 13<sup>th</sup> 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 <i>H. pylori</i> virulence factors in the liver by the 9<sup>th</sup> month. Additionally, significant gut microbiota dysbiosis was observed.</p><p><strong>Conclusion: </strong>The STZ-induced diabetic mouse model with <i>H. pylori</i> infection can significantly prolong the colonization time of <i>H. pylori</i> in the stomach and exacerbate the degree of damage to the stomach, liver, and kidney organs.</p>","PeriodicalId":48607,"journal":{"name":"World Journal of Diabetes","volume":"17 2","pages":"112534"},"PeriodicalIF":5.1000,"publicationDate":"2026-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12897513/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"World Journal of Diabetes","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.4239/wjd.v17.i2.112534","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0
Abstract
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.
期刊介绍：
The WJD is a high-quality, peer reviewed, open-access journal. The primary task of WJD is to rapidly publish high-quality original articles, reviews, editorials, and case reports in the field of diabetes. In order to promote productive academic communication, the peer review process for the WJD is transparent; to this end, all published manuscripts are accompanied by the anonymized reviewers’ comments as well as the authors’ responses. The primary aims of the WJD are to improve diagnostic, therapeutic and preventive modalities and the skills of clinicians and to guide clinical practice in diabetes. Scope: Diabetes Complications, Experimental Diabetes Mellitus, Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus, Diabetes, Gestational, Diabetic Angiopathies, Diabetic Cardiomyopathies, Diabetic Coma, Diabetic Ketoacidosis, Diabetic Nephropathies, Diabetic Neuropathies, Donohue Syndrome, Fetal Macrosomia, and Prediabetic State.
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