Randomized controlled trial for an effect of green tea-extract powder supplementation on glucose abnormalities.

OBJECTIVE: We examined whether green tea-extract powder supplementation improves glucose abnormality. METHODS: The study was conducted for volunteers who resided in eastern communities of Shizuoka Prefecture and who had fasting blood glucose levels of >or=6.1 mmol/l or nonfasting blood glucose levels of >or=7.8 mmol/l in a recent health check-up. Sixty subjects aged 32-73 years (49 males and 11 females) participated in the trial. The Early intervention group consumed a packet of green tea-extract powder containing 544 mg polyphenols (456 mg catechins) daily for the first 2 months and then entered the 2-month nonintervention period. The Later intervention group was observed for the first 2 months and then consumed green tea-extract powder as described above for the subsequent 2 months. Using the two-period crossover design, we analyzed the changes in fasting hemoglobin A1c level and other biomarkers in blood samples collected at baseline, 2 months and 4 months. RESULTS: A significant reduction in hemoglobin A1c level and a borderline significant reduction in diastolic blood pressure were associated with the intervention. The intervention caused no significant changes in weight, body mass index, body fat, systolic blood pressure, fasting serum glucose level, homeostasis model assessment index, serum lipid level or hypersensitive C-reactive protein. CONCLUSION: Daily supplementary intake of green tea-extract powder lowered the hemoglobin A1c level in individuals with borderline diabetes.

Effects of pirenzepine on omeprazole-induced hypergastrinemia and acid suppression in peptic ulcer patients.

Omeprazole effectively suppresses acid secretion, resulting in the long-term elevation of intragastric pH and serum gastrin level. Pirenzepine has been reported to inhibit gastrin secretion. This study was carried out to examine the effects of additional pirenzepine treatment on the hypergastrinemia and gastric acid suppression induced by omeprazole. Concentrations of serum gastrin and plasma somatostatin were measured in 28 peptic ulcer patients before treatment, after omeprazole treatment (20 mg/day) for 2 weeks, and after omeprazole and pirenzepine (100 mg/day) treatment for 2 weeks. The acid inhibitory effect of pirenzepine treatment in addition to omeprazole was evaluated by 24-h intragastric pH measurement in six healthy volunteers. Serum gastrin level was increased significantly, to 2.4-fold the pretreatment level, by omeprazole treatment. Additional treatment with pirenzepine suppressed serum gastrin level to 0.6-fold the omeprazole-treatment level. The serum somatostatin level was not altered significantly either by omeprazole treatment or by omeprazole and pirenzepine treatment. In healthy volunteers whose pH 3 holding time on 24-h intragastric pH monitoring was 70% by omeprazole treatment, omeprazole and pirenzepine treatment markedly increased the pH 3 holding time, to 89%. These findings suggest that pirenzepine is useful in reducing the undesirable effects of omeprazole-induced hypergastrinemia, i.e., the excessive trophic effect of omeprazole on the acid-secreting part of the stomach and the overstimulation of acid secretion. The additional pirenzepine treatment is also effective in suppressing acid secretion.

Effects of pirenzepine on omeprazole-induced gastrin gene expression in rat antral tissues.

Pirenzepine has inhibitory effects on gastrin secretion both in vivo and in vitro. The aim of this study was to determine the mechanism responsible for the suppression of omeprazole-induced hypergastrinemia that occurs with pirenzepine treatment. The effects were measured in rats treated with oral omeprazole plus intraperitoneal pirenzepine or saline once daily for seven days in the antrum. The serum gastrin level increased significantly by more than sixfold with omeprazole treatment; additional treatment with pirenzepine suppressed this increase by 48%. Pirenzepine treatment did not change the level of gastrin mRNA but significantly increased the level of somatostatin mRNA. Combination treatment with omeprazole plus pirenzepine significantly decreased the gastrin mRNA level to half and significantly increased the somatostatin mRNA level up to 1.4-fold of the levels achieved with omeprazole treatment alone. These results suggest that the stimulatory effect of omeprazole on gastrin synthesis is partially blocked by pirenzepine via mediation of somatostatin synthesis in the antrum.

Expression of antral gastrin and somatostatin mRNA in Helicobacter pylori-infected subjects.

OBJECTIVES: We investigated the gene expression of antral gastrin and somatostatin in Helicobacter pylori-infected subjects. Twelve asymptomatic men with normal endoscopic findings participated in this study, four of whom were infected with H. pylori. METHODS: Biopsy specimens of the gastric mucosa were obtained after subjects had fasted overnight. Serum gastrin levels, antral gastrin and somatostatin content, and antral G- and D-cell densities also were measured. RESULTS: Fasting serum gastrin levels were significantly higher in H. pylori-positive subjects than in H. pylori-negative subjects. There were no differences between groups in antral gastrin content, G-cell density, or gastrin mRNA levels. Antral somatostatin content, D-cell density, somatostatin mRNA levels, and the somatostatin mRNA:D-cell density ratio were significantly decreased in H. pylori-positive subjects. CONCLUSIONS: Our results suggest that in addition to reduced antral D-cell density, a suppression of somatostatin synthesis in D-cells may have contributed to the decrease in antral somatostatin in H. pylori-infected subjects.