The lower fasting plasma glucose in H. pylori-infected than non-infected diabetics may partly be attributed to alteration in gastric mucosa as high prevalence of severe acute gastritic inflammation/ulcer disease has been reported in diabetic patients with little or no symptoms of dyspepsia.[23] H. pylori gastritis has been found to enhance glucose and meal stimulated insulin release probably by increasing gastrin secretion.[24] However, no association has yet been documented between H. pylori infection and delayed gastric emptying or upper gastrointestinal symptoms in diabetics.[25]. This evidence concerns the gene INS and dyspepsia.