Inci F, Atmaca M, Ozturk M, Yildiz S, Koceroglu R, Sekeroglu R, Ipekci S H, Kebapcilar L
Department of Internal Medicine, University of Yuzuncu Yil, Van, Turkey.
J Endocrinol Invest. 2014 May;37(5):449-54. doi: 10.1007/s40618-013-0040-y. Epub 2014 Jan 9.
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.
质子泵抑制剂通过抑制胃酸分泌诱导高胃泌素血症。胃泌素对β细胞具有肠促胰岛素样刺激作用。已证明质子泵抑制剂可降低糖化血红蛋白水平。
我们旨在观察给予泮托拉唑治疗酸相关疾病的糖尿病和非糖尿病患者β细胞功能的变化。
79例男性患者（38例非糖尿病患者和41例仅接受二甲双胍治疗的2型糖尿病患者）在给予40mg/天泮托拉唑后随访12周。在治疗前后测量空腹血糖、糖化血红蛋白、空腹胰岛素、胰腺B细胞功能（HOMA-B）、胰岛素原和C肽水平。
在非糖尿病患者（n = 38）中，泮托拉唑治疗12周后，空腹血糖降低，而C肽、log-HOMA-B显著升高（分别为p = 0.002、p = 0.03、p = 0.042）。在2型糖尿病患者中，泮托拉唑治疗后空腹血糖、糖化血红蛋白和体重降低，而log-HOMA-B、C肽和log-胰岛素原水平显著升高（分别为p = 0.003、p = 0.007、p < 0.001；p < 0.001；p = 0.017、p = 0.05）。泮托拉唑治疗后，全组胰腺B细胞功能与C肽和胰岛素呈正相关，与空腹血糖和糖化血红蛋白水平呈负相关（分别为r = 0.37，p = 0.001；r = 0.60，p < 0.001，r = -0.29，p = 0.011和r = -0.28，p = 0.013）。泮托拉唑治疗后，糖化血红蛋白与空腹血糖呈正相关（r = 0.75，p < 0.001），与仅log-HOMA-B水平呈负相关（r = -0.28，p = 0.013）。
泮托拉唑的使用似乎与β细胞功能增强相关。泮托拉唑的使用可改善糖化血红蛋白、HOMA-B、C肽和胰岛素原水平。由于β细胞丢失在2型糖尿病发病机制中起重要作用，基于质子泵抑制剂的治疗可能对糖尿病治疗有用。
