title: Proton pump inhibitors: impact on glucose metabolism.
abstract: Diabetes mellitus is a complex chronic disease associated with an absolute insulin deficiency in type 1 diabetes (T1D) and a progressive deterioration of β-cell function in type 2 diabetes (T2D). T2D pathophysiology has numerous defects including incretin deficiency/resistance. Gastrin has demonstrated to be an islet growth factor (like glucagon-like peptide-1, epidermal growth factor, transforming growth factor-α,…) and be able to restore a functional β-cell mass in diabetic animals. This hormone is likely to stimulate insulin secretion during an ordinary protein-rich meal, this is, to have an incretin-like effect. Proton pump inhibitors (PPIs) can raise serum gastrin concentration significantly and therefore, affect to glucose metabolism through promoting β-cell regeneration/expansion and also enhancing insulin secretion. The present paper aims to review studies concerning the effect of PPIs on glucose metabolism. Several research groups have recently explored the potential role of this class of drugs on glycemic control, mainly in T2D. The results show antidiabetic properties for the PPIs with a global glucose-lowering power around 0.6-0.7 % points of HbA1c, but the level of evidence for the available literature is still not high. If these data start to become demonstrated in the ongoing clinical trials, PPIs could become a new antidiabetic agent with a good and safe profile for T2D and even useful for T1D, particularly in the area of islet transplantation to preserve β-cell mass.
authors.affiliation: Endocrinology and Nutrition Unit, Hospital Miguel Servet, Paseo Isabel La Católica, 1-3, 50009, Zaragoza, Spain. dianna_bc@hotmail.com
authors.forename: Diana
authors.initials: D
authors.lastname: Boj-Carceller
mesh_terms: D000818:Animals; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000188:drug therapy / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism; D019861:Enterochromaffin-like Cells / Q000187:drug effects / Q000378:metabolism; D005746:Gastric Emptying / Q000187:drug effects; D019863:Gastrin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism; D005755:Gastrins / Q000097:blood / Q000378:metabolism*; D005765:Gastrointestinal Agents / Q000494:pharmacology / Q000627:therapeutic use*; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007003:Hypoglycemia / Q000517:prevention & control; D007004:Hypoglycemic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism; D010295:Parietal Cells, Gastric / Q000187:drug effects / Q000378:metabolism; D054328:Proton Pump Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D013004:Somatostatin / Q000378:metabolism; D019864:Somatostatin-Secreting Cells / Q000187:drug effects / Q000378:metabolism
chemical_list: D005755:Gastrins; D005765:Gastrointestinal Agents; D007004:Hypoglycemic Agents; D007328:Insulin; D054328:Proton Pump Inhibitors; D013004:Somatostatin; D005947:Glucose