# Glucolipid Metabolic Disorders and Helicobacter pylori Infection

## TL;DR

This paper explores how Helicobacter pylori infection may contribute to glucolipid metabolic disorders through inflammation and insulin issues.

## Contribution

The study provides a systematic review linking Helicobacter pylori infection to multiple glucolipid metabolic disorders.

## Key findings

- H. pylori infection may induce inflammatory responses and impair insulin sensitivity.
- The infection influences diseases like T2DM, MASLD, and atherosclerosis through oxidative stress and cytokine regulation.
- Bacterial virulence factors and exosomes play roles in metabolic dysfunction.

## Abstract

Due to its high incidence and severe consequences, glucolipid metabolic disorders (GLMD) remain a significant challenge for the global medical community. Helicobacter pylori (H. pylori), a Gram‐negative bacterium that colonizes the gastric mucosa, has a high infection rate worldwide, exceeding 50% in the global population. Although numerous studies have explored the associations between H. pylori and individual metabolic diseases, a systematic review framework that integrates these findings to provide a comprehensive perspective on GLMD is still lacking. Recent studies have indicated that H. pylori infection can lead to disturbances in lipid and glucose metabolism; however, this area of research is fraught with controversy, even yielding completely opposing conclusions. Based on this, we systematically reviewed the research on the association between H. pylori and type 2 diabetes (T2DM), metabolic dysfunction–associated steatotic liver disease (MASLD), and atherosclerosis (AS). We conducted an in‐depth analysis of how H. pylori infection influences the onset and progression of GLMD through multiple mechanisms, including the induction of inflammatory responses, exacerbation of oxidative stress, and impairment of insulin sensitivity. Simultaneously, we highlighted the roles of bacterial virulence factors and the exosomes they regulate in metabolism. In conclusion, we have determined that H. pylori infection may induce inflammatory responses, exacerbate oxidative stress, and impair insulin sensitivity by regulating the levels of inflammatory cytokines, adiponectin (ADPN), leptin, vitamin D, homocysteine, and exosomes, thereby collectively influencing the occurrence and progression of the aforementioned diseases. Therefore, effective control and treatment of H. pylori infection should not be neglected in the management of GLMD.