Dhotre SV, Dhotre PS, Rao A, Nagoba BS. When metabolic disease rewrites infection biology: Long-term multiorgan consequences of Helicobacter pylori infection in diabetes. World J Diabetes 2026; 17(5): 118333 [DOI: 10.4239/wjd.v17.i5.118333]
Corresponding Author of This Article
Basavraj S Nagoba, PhD, Assistant Dean, Professor, Department of Microbiology, Maharashtra Institute of Medical Sciences and Research (Medical College), Vishwanathpuram, Ambajogai Road, Latur 413531, Maharashtra, India. dr_bsnagoba@yahoo.com
Research Domain of This Article
Infectious Diseases
Article-Type of This Article
Opinion Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Diabetes. May 15, 2026; 17(5): 118333 Published online May 15, 2026. doi: 10.4239/wjd.v17.i5.118333
When metabolic disease rewrites infection biology: Long-term multiorgan consequences of Helicobacter pylori infection in diabetes
Shree V Dhotre, Pradnya S Dhotre, Arunkumar Rao, Basavraj S Nagoba
Shree V Dhotre, Department of Microbiology, Ashwini Rural Medical College, Hospital and Research Centre, Solapur 413006, Maharashtra, India
Pradnya S Dhotre, Department of Biochemistry, Ashwini Rural Medical College, Hospital and Research Centre, Solapur 413001, Maharashtra, India
Arunkumar Rao, Department of Orthopedics, MIMSR Medical College, Latur 413512, India
Basavraj S Nagoba, Department of Microbiology, Maharashtra Institute of Medical Sciences and Research (Medical College), Latur 413531, Maharashtra, India
Author contributions: Nagoba BS conceptualized and designed the study, developed the study outline, and coordinated manuscript preparation; Nagoba BS, Dhotre SV, Dhotre PS, and Rao A made substantial contributions to the study design, data interpretation, and critical discussion of the manuscript; Dhotre SV and Nagoba BS drafted, critically revised, and edited the manuscript for important intellectual content and contributed to the literature review; and all authors approved the final version of the manuscript to be published.
AI contribution statement: Any language refinement during manuscript preparation was limited to minor grammatical or readability improvements, without involvement in content generation, data analysis, or drafting of the manuscript.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Basavraj S Nagoba, PhD, Assistant Dean, Professor, Department of Microbiology, Maharashtra Institute of Medical Sciences and Research (Medical College), Vishwanathpuram, Ambajogai Road, Latur 413531, Maharashtra, India. dr_bsnagoba@yahoo.com
Received: December 30, 2025 Revised: February 11, 2026 Accepted: April 7, 2026 Published online: May 15, 2026 Processing time: 133 Days and 3.2 Hours
Abstract
The interaction between Helicobacter pylori (H. pylori) infection and diabetes mellitus has attracted increasing scientific attention over the past two decades, yet experimental evidence rigorously delineating causality and long-term organ-specific pathology has remained scarce. The study critically appraised herein addresses this important gap using a streptozotocin (STZ)-induced diabetic mouse model chronically infected with H. pylori and followed for 13 months. While this model yields valuable longitudinal insight into the infection-metabolism interface, the STZ-induced paradigm predominantly reflects insulin-deficiency-driven hyperglycemia rather than the insulin resistance-dominated pathophysiology characteristic of human type 2 diabetes mellitus; translational interpretation therefore warrants appropriate caution. By integrating metabolic monitoring, systematic histopathology, apoptosis assessment, virulence factor detection, and gut microbiota profiling, the investigators provide compelling evidence that diabetes fundamentally alters host-pathogen dynamics. H. pylori colonization is substantially prolonged, gastric inflammation progresses toward irreversibility, and progressive injury extends to the pancreas, liver, and kidneys, even as bacterial burden and hyperglycemia exhibit partial improvement over time. This article critically appraises the mechanistic plausibility, diagnostic relevance, and translational implications of these findings within the evolving framework of infection-driven metabolic and systemic disease. Current advances, controversies in the field, the authors’ perspectives, and priority directions for future research are also discussed.
Core Tip: This long-term experimental study demonstrates that diabetes transforms Helicobacter pylori infection from a largely gastric disease into a systemic pathological modifier. Prolonged colonization, persistent inflammation, extra-gastric dissemination of virulence factors, and compounded disruption of gut microbiota collectively drive irreversible multiorgan injury, even after partial improvement in bacterial load and glycemic status. These findings carry important implications for infection screening, eradication timing, and organ surveillance in diabetic patients, and open novel avenues for therapeutic intervention targeting the inflammation-microbiota-metabolic axis.
