Type 2 diabetes and insulin resistance are increasingly recognized as conditions influenced not only by genetic and lifestyle factors but also by infectious and microbial exposures. Diarrheagenic pathogens, including enterotoxigenic, enteroaggregative, and enterohemorrhagic Escherichia coli, as well as other enteric microorganisms, disrupt the gut microbiota and compromise intestinal barrier integrity. These alterations promote dysbiosis, increased intestinal permeability, and systemic exposure to lipopolysaccharides and other microbial products, leading to metabolic endotoxemia and chronic low-grade inflammation. In parallel, pathogen-induced modulation of host immune responses contributes to adipose tissue inflammation, mitochondrial dysfunction, and impaired insulin signaling. This review summarizes current evidence linking diarrheagenic pathogens to insulin resistance, with emphasis on the microbiota–immune–metabolism axis. Understanding these interactions highlights novel perspectives on the pathogenesis of insulin resistance and suggests that targeted modulation of the gut microbiota or reduction in pathogen-driven inflammation may represent therapeutic opportunities to improve metabolic outcomes.
Zermeño-Ruiz et al. (Fri,) studied this question.