Pantoprazole may improve beta cell function and diabetes mellitus

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.

We aimed to observe changes in beta cell function in diabetic and non-diabetic subjects given pantoprazole for an acid-related ailment.

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.

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).

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.