OBJECTIVE: Proton pump inhibitors, by elevating plasma gastrin, can influence glucose-insulin homeostasis. Because there are no controlled clinical trials, the present study was planned to evaluate the effect of pantoprazole, a proton pump inhibitor, on glucose-insulin homeostasis in patients with type 2 diabetes (T2DM). RESEARCH DESIGN AND METHODS: IN this 12-wk, randomized, double-blind, placebo-controlled study, patients with T2DM were allocated to either the pantoprazole or placebo treatment in an equal ratio. Alterations in glycosylated hemoglobin (HbA1c), fasting plasma glucose, insulin, and gastrin were measured at baseline and at 12 wk. RESULTS:Thirty-one eligible patients were randomized to receive either the pantoprazole (n = 16) or placebo (n = 15). Twelve weeks of pantoprazole therapy significantly increased plasma gastrin and insulin levels and improved β-cell function (P < 0.05 for all parameters), along with a significant decrease in HbA1c (7.6 ± 1.17 to 6.8 ± 1.16; P < 0.001). The decrease in HbA1c correlated with an increase in gastrin and insulin (r = 0.54, P =0.010; and r = 0.67, P =0.01, respectively). CONCLUSIONS:Pantoprazole therapy increases plasma gastrin and insulin levels, thereby improving the glycemic control in T2DM. The effect of pantoprazole on glucose-insulin homeostasis requires further study.
RCT Entities:
OBJECTIVE: Proton pump inhibitors, by elevating plasma gastrin, can influence glucose-insulin homeostasis. Because there are no controlled clinical trials, the present study was planned to evaluate the effect of pantoprazole, a proton pump inhibitor, on glucose-insulin homeostasis in patients with type 2 diabetes (T2DM). RESEARCH DESIGN AND METHODS: IN this 12-wk, randomized, double-blind, placebo-controlled study, patients with T2DM were allocated to either the pantoprazole or placebo treatment in an equal ratio. Alterations in glycosylated hemoglobin (HbA1c), fasting plasma glucose, insulin, and gastrin were measured at baseline and at 12 wk. RESULTS: Thirty-one eligible patients were randomized to receive either the pantoprazole (n = 16) or placebo (n = 15). Twelve weeks of pantoprazole therapy significantly increased plasma gastrin and insulin levels and improved β-cell function (P < 0.05 for all parameters), along with a significant decrease in HbA1c (7.6 ± 1.17 to 6.8 ± 1.16; P < 0.001). The decrease in HbA1c correlated with an increase in gastrin and insulin (r = 0.54, P =0.010; and r = 0.67, P =0.01, respectively). CONCLUSIONS:Pantoprazole therapy increases plasma gastrin and insulin levels, thereby improving the glycemic control in T2DM. The effect of pantoprazole on glucose-insulin homeostasis requires further study.
Authors: F Inci; M Atmaca; M Ozturk; S Yildiz; R Koceroglu; R Sekeroglu; S H Ipekci; L Kebapcilar Journal: J Endocrinol Invest Date: 2014-01-09 Impact factor: 4.256