This may be because H. pylori infection can enhance oxidative stress, subsequently affecting the insulin signaling pathway through multiple ways, such as inhibiting the activation of fatty acyl inositol 3 kinase p85 subunits, preventing the transport of glucose transporter-4 from the vesicle to the plasma membrane, and downregulating the expression of glucose transporter protein-4, thereby leading to IR and eventually causing dyslipidemia and glucose metabolism disorders [27, 28]. This evidence concerns the gene INS and metabolic syndrome.