Escherichia coli as a gut microbial marker of obesity and its reduction following bariatric treatment
摘要
Alterations in the gut microbiota have been implicated in obesity-related metabolic disorders; however, the disease-relevant microbial features that link gut dysbiosis to metabolic risk remain incompletely defined. In particular, whether quantitative expansion or strain-level divergence of specific taxa underlie metabolic dysfunction is unclear.
MethodsWe performed cross-sectional and longitudinal metagenomic analyses of fecal samples from 19 patients with severe obesity undergoing bariatric intervention and 30 healthy donors. Whole-genome shotgun sequencing was combined with quantitative PCR to assess both relative and absolute bacterial abundance. Cultured Escherichia coli isolates were further examined by whole-genome sequencing to evaluate strain-level diversity. Associations between microbial features and metabolic parameters were analyzed.
ResultsThe gut microbiota of patients with severe obesity was taxonomically and functionally distinct from that of healthy donors. Among altered taxa, E. coli was significantly enriched in obesity and showed a consistent and marked reduction at 6 months post-intervention, irrespective of procedure type. Absolute E. coli abundance quantified by qPCR decreased significantly following intervention. In contrast, whole-genome analysis revealed no clear genotypic clustering of E. coli strains by host phenotype. Notably, E. coli abundance correlated positively with HbA1c and systolic blood pressure and negatively with serum albumin levels, whereas global microbial diversity and KEGG-based metabolic pathways showed limited longitudinal change.
ConclusionsQuantitative expansion of gut E. coli, rather than strain-specific genomic divergence, is associated with metabolic risk in severe obesity and is consistently reduced at 6 months after bariatric intervention. These findings suggest that microbial load-dependent effects of E. coli may be associated with obesity-related metabolic dysfunction and represent a potential biomarker. This exploratory, single-center study is hypothesis-generating and warrants further validation in larger, multi-center cohorts as well as interventional studies using preclinical animal models.