title: Pantoprazole may improve beta cell function and diabetes mellitus.
abstract: BACKGROUND
  Proton pump inhibitors induce hypergastrinemia by suppressing gastric acidity. Gastrin has incretin-like stimulating actions on beta cells. Proton pump inhibitors have been shown to decrease glycosylated hemoglobin.
  
  
  OBJECTIVE
  We aimed to observe changes in beta cell function in diabetic and non-diabetic subjects given pantoprazole for an acid-related ailment.
  
  
  METHODS
  Seventy-nine male patients (38 non-diabetic and 41 type-2 diabetic receiving only metformin therapy) were followed for 12 weeks after pantoprazole 40 mg/day was given. Fasting plasma glucose, HbA1c, fasting insulin, Pancreatic B cell function (HOMA-B), proinsulin and c-peptide levels were measured before and after the treatment.
  
  
  RESULTS
  In non-diabetic patients (n = 38), FPG decreased, whereas c-peptide, log-HOMA-B, increased significantly (p = 0.002, p = 0.03, p = 0.042, respectively) after 12 weeks of pantoprazole administration. In type 2 diabetic patients, FPG, HbA1c and weight decreased, whereas log-HOMA-B, c-peptide and log-proinsulin levels increased significantly after pantoprazole treatment (p = 0.003, p = 0.007, p < 0.001; p < 0.001; p = 0.017, p = 0.05, respectively). After pantoprazole treatment, pancreatic B-cell function was correlated with c-peptide and insulin and inversely with FBG and HbA1c levels in the whole group (r = 0.37, p = 0.001; r = 0.60, p < 0.001, r = -0.29, p = 0.011 and r = -0.28, p = 0.013, respectively). After pantoprazole treatment, HbA1c was correlated with FBG (r = 0.75, p < 0.001) and inversely with only log-HOMA-B level (r = -0.28, p = 0.013).
  
  
  CONCLUSIONS
  Pantoprazole administration seems to correlate with increased beta cell function. Pantoprazole administration improves HbA1c, HOMA-B, c-peptide and proinsulin levels. Since beta cell loss plays a significant role in the pathogenesis of type 2 diabetes, PPI-based therapies may be useful in the treatment of diabetes.
authors.affiliation: Department of Internal Medicine, University of Yuzuncu Yil, Van, Turkey.
authors.forename: F
authors.initials: F
authors.lastname: Inci
authors.forename: M
authors.initials: M
authors.lastname: Atmaca
authors.forename: M
authors.initials: M
authors.lastname: Ozturk
authors.forename: S
authors.initials: S
authors.lastname: Yildiz
authors.forename: R
authors.initials: R
authors.lastname: Koceroglu
authors.forename: R
authors.initials: R
authors.lastname: Sekeroglu
authors.forename: S H
authors.initials: SH
authors.lastname: Ipekci
authors.forename: L
authors.initials: L
authors.lastname: Kebapcilar
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles / Q000009:adverse effects / Q000627:therapeutic use*; D000293:Adolescent; D000328:Adult; D000368:Aged; D000897:Anti-Ulcer Agents / Q000009:adverse effects / Q000627:therapeutic use; D015331:Cohort Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D005744:Gastric Acid / Q000378:metabolism; D005756:Gastritis / Q000150:complications / Q000188:drug therapy; D005764:Gastroesophageal Reflux / Q000150:complications / Q000188:drug therapy; D006801:Humans; D006943:Hyperglycemia / Q000517:prevention & control*; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008687:Metformin / Q000627:therapeutic use; D008875:Middle Aged; D000077402:Pantoprazole; D011446:Prospective Studies; D054328:Proton Pump Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D015854:Up-Regulation / Q000187:drug effects*; D055815:Young Adult
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000897:Anti-Ulcer Agents; D007004:Hypoglycemic Agents; D007328:Insulin; D054328:Proton Pump Inhibitors; D008687:Metformin; D000077402:Pantoprazole