In this instance, various pathophysiologic pathways have been suggested that induce insulin resistance by H. pylori, such as activation of pro-inflammatory substances (CRP, PAI-1, and TNF-α), production of reactive oxygen species (ROS), alteration of ghrelin and leptin levels, and increased production of lipopolysaccharides [40, 77–79]. Here, SERPINE1 is linked to Insulin resistance.