In the same time, H. pylori-induced gastritis affects the secretion of gastric hormones, including leptin, ghrelin, gastrin, and somatostatin, which could affect insulin sensitivity and glucose homeostasis [37–39]. H. pylori is one of the most infectious agents proposed as an agent triggering an autoimmune response and molecular mimicry is one of the several mechanisms that have been suggested in an attempt to explain the extraintestinal manifestations of H. pylori infections [3, 4]. This evidence concerns the gene LEP and gastritis.