| Background: Recently some studies have shown that gastrin could promote the differentiation and regeneration of beta cells. As the first-line drug to treat acid related disease, proton pump inhibitor(PPI) could inhibit acid secretion and increase serum gastrin levels though a feedback way. Therefore, PPI might have a potential hypoglycemic effect.Objective: To investigate the effect of pantoprazole on Type 2 Diabetes and its mechanism.Methods: A total of 96 patients with type 2 diabetes were enrolled. Inclusive criteria:(1)Type 2 diabetes,18≤age≤75 years old;(2) A poor hypoglycemic effect of the original hypoglycemic therapy regimens;(3) 7%<Hemoglobin A1c< 8.5%. The subjects were randomly divided into two groups of 48 each: pantoprazole group and control group. Pantoprazole(40 mg, bid) combined with oral antidiabetic agents was given to the patients of pantoprazole group, whereas the control group maintain their original hypoglycemic therapy regimens only. Detailed demographic characteristics, diseases history and hypoglycemic drugs were recorded. Besides, fasting blood glucose(FBG), glycosylated hemoglobin(Hb A1c), homeostasis model assessment-insulin resistance, homeostasis model assessment-insulin secretion index, BMI, waist hip ratio, 2 h postprandial peripheral blood glucose(PBG), fasting insulin(INS.), fasting C peptide, total cholesterol(TC), triglycerides(TG), low density lipoprotein(LDL),high density lipoprotein(HDL) and total bile acid were also measured. Record their BMI, waist-to-hip ratio.Homeostasis model assessment-insulin resistance(HOMA-IR) and homeostasis model assessment-insulin secretion index(HOMA-HBCI) calculated according to the blood glucose and serum insulin level(as shown in the formula 1,2)). Blood specimens were centrifuged and it was used for testing the level of serum gastrin and glucagon peptide 1(GLP-1). Patients were followed up by telephone once a week, reminding them to take medicines. Twelve weeks later, all the indexes mentioned above were measured again in the two groups.Results: Eighteen cases were lost during follow-up(7 cases has poor compliance, 4 cases caught a hyperglycemia(> 33.3mmol/L) or hypoglycemia(< 3.9 mmol/L),2 cases renal function deteriorated, 5 cases stop taking medicine because of gastrointestinal symptoms was improved).There were 40 cases in group pantoprazole and 38 cases in control group complete the follow-up.(2)After treatment with pantoprazole(40 mg, bid) for 12-wks, fasting blood glucose decreased from 9.12±2.30mmol/L to 7.68±1.48mmol/L,(P=0.01),glycosylated hemoglobin decreased from7.78±0.46% to 7.24±0.87%,(P= 0.02). After treatment with pantoprazole,the level of serum gastrin increased significantly(200±16.66ng/L VS. 90.83±8.72ng/L,P=0.00),and log HOMA–IR(0.50±0.26 VS. 0.65±0.28,P=0.01) decreased significantly as compared with that before treatment. While in the control group there were no obvious change in serum gastrin, log HOMA–IR, fasting blood glucose andglycosylated hemoglobin before and after the treatment. As for log HOMA-HBCI, there has no significant difference in pantoprazole group(1.65±0.34 VS. 1.63±0.46,P=0.67),but in the control group it has a decrease(1.64±0.46 VS. 1.65±0.45,P=0.04).(3)As for 2h postprandial blood glucose, fasting insulin, fasting C peptide, total cholesterol, triglycerides, total bile acid, high density lipoprotein, low density lipoprotein, glucagon-like peptide-1, BMI and waist/hip, there were no significant difference before and after the treatment in the two groups(P>0.05).Conclusion: Pantoprazole combined with original hypoglycemic drugs can improve blood glucose metabolism, insulin resistance and β-cell function in patients with type 2 diabetes. Its mechanism may correlated with an increased serum gastrin level. |
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