Editorial
Copyright ©The Author(s) 2015.
World J Diabetes. Aug 25, 2015; 6(10): 1122-1131
Published online Aug 25, 2015. doi: 10.4239/wjd.v6.i10.1122
Figure 1
Figure 1 The possible mechanisms of proton pump inhibitors on the improvement of glycemic control. PPIs indirectly elevate serum gastrin levels. Gastrin promotes an increase in β cell mass by neogenesis of the β cells from the pancreatic ductal complex probably promoted by binding the gastrin with CCK-B receptor during pancreatic remodeling. In addition, a modest increase in the replication of pancreatic β cells during pancreatic remodeling is also reported although the mechanisms are not apparent because of the lack of a CCK-B receptor on β cells. Gastrin can enhance the effect of GLP-1 on β cell neogenesis from ductal cells. A synergistic effect may occur even under non-remodeling conditions in the pancreas. These mechanisms appear to contribute to the improvement of glycemic control in both type 1 and type 2 diabetes. Furthermore, a combination of GLP-1 and gastrin may protect from the onset or progression of type 1 diabetes by an immunoregulatory effect. Other possible gastrin-mediated mechanisms independent of the β cell mass increase may include stimulation of insulin secretion, interaction with other hormones such as ghrelin, direct or indirect (via vagal nerve) effects in the central nervous systems, and promotion of GLP-1 secretion by L cells in the intestine. Finally, it may be possible that PPIs affect glycemic control by unknown mechanisms independent of the elevation of serum gastrin levels. PPIs: Proton pump inhibitors; CCK-B: Cholecystokinin-B; GLP-1: Glucagon like-peptide-1.