When metabolic disease rewrites infection biology: Long-term multiorgan consequences of Helicobacter pylori infection in diabetes

Table 2 Comparison of animal models for studying Helicobacter pylori infection in the context of metabolic disease

Model	Metabolic phenotype	Strengths	Limitations	Suitability for H. pylori co-infection
Low-dose STZ mouse (current study)	Insulin deficiency; hyperglycemia	Reproducible; reversible beta-cell injury; established protocol; long-duration follow-up feasible	Models T1DM physiology; lacks insulin resistance; potential direct STZ organ toxicity	High-established for long-term H. pylori co-infection studies
High-fat diet mouse	Insulin resistance; obesity; T2DM-like	Mimics T2DM pathophysiology; relevant inflammatory milieu; models diet-microbiota interaction	Variable hyperglycemia; strain-dependent; more complex to manage	Moderate-underutilized in H. pylori infection research; high priority for future studies
Db/db mouse (leptin receptor deficient)	Severe obesity; insulin resistance; hyperglycemia	Strong metabolic phenotype; spontaneous diabetes; immune dysregulation	Immune defects may confound infection response; expensive; limited vendor availability	Moderate-potential for severe T2DM and H. pylori interaction studies
Mongolian gerbil	Standard (non-diabetic) unless combined with HFD	Natural H. pylori colonization; gastric pathology closely mirrors human disease	Limited genetic tools; poorly validated metabolic disease protocols	Low-metabolic co-disease protocols not established; requires development
Non-human primate	Diet-inducible; closest to human pathophysiology	Highest translational relevance; natural H. pylori susceptibility; full immune system	Prohibitive cost; ethical constraints; long study duration; limited research use	Aspirational-for validation of high-priority mechanistic findings only

STZ: Streptozotocin; T1DM: Type 1 diabetes mellitus; T2DM: Type 2 diabetes mellitus; HFD: High-fat diet; H. pylori: Helicobacter pylori.