Influence of gastric inhibitory polypeptide on pentagastrin-stimulated gastric acid secretion in patients with type 2 diabetes and healthy controls.

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Influence of gastric inhibitory polypeptide on pentagastrin-stimulated gastric acid secretion in patients with type 2 diabetes and healthy controls. / Meier, Juris J; Nauck, Michael A; Kask, Bartholomaeus; Holst, Jens J; Deacon, Carolyn F; Schmidt, Wolfgang E; Gallwitz, Baptist.

In: World Journal of Gastroenterology, Vol. 12, No. 12, 2006, p. 1874-80.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Meier, JJ, Nauck, MA, Kask, B, Holst, JJ, Deacon, CF, Schmidt, WE & Gallwitz, B 2006, 'Influence of gastric inhibitory polypeptide on pentagastrin-stimulated gastric acid secretion in patients with type 2 diabetes and healthy controls.', World Journal of Gastroenterology, vol. 12, no. 12, pp. 1874-80.

APA

Meier, J. J., Nauck, M. A., Kask, B., Holst, J. J., Deacon, C. F., Schmidt, W. E., & Gallwitz, B. (2006). Influence of gastric inhibitory polypeptide on pentagastrin-stimulated gastric acid secretion in patients with type 2 diabetes and healthy controls. World Journal of Gastroenterology, 12(12), 1874-80.

Vancouver

Meier JJ, Nauck MA, Kask B, Holst JJ, Deacon CF, Schmidt WE et al. Influence of gastric inhibitory polypeptide on pentagastrin-stimulated gastric acid secretion in patients with type 2 diabetes and healthy controls. World Journal of Gastroenterology. 2006;12(12):1874-80.

Author

Meier, Juris J ; Nauck, Michael A ; Kask, Bartholomaeus ; Holst, Jens J ; Deacon, Carolyn F ; Schmidt, Wolfgang E ; Gallwitz, Baptist. / Influence of gastric inhibitory polypeptide on pentagastrin-stimulated gastric acid secretion in patients with type 2 diabetes and healthy controls. In: World Journal of Gastroenterology. 2006 ; Vol. 12, No. 12. pp. 1874-80.

Bibtex

@article{8967a1b0ab4b11ddb5e9000ea68e967b,
title = "Influence of gastric inhibitory polypeptide on pentagastrin-stimulated gastric acid secretion in patients with type 2 diabetes and healthy controls.",
abstract = "AIM: Gastric inhibitory polypeptide is secreted from intestinal K-cells in response to nutrient ingestion and acts as an incretin hormone in human physiology. While animal experiments suggested a role for GIP as an inhibitor of gastric secretion, the GIP effects on gastric acid output in humans are still controversial. METHODS: Pentagastrin was administered at an infusion rate of 1 microg . kg(-1) . h(-1) over 300 min in 8 patients with type 2 diabetes (2 female, 6 male, 54+/- 10 years, BMI 30.5+/- 2.2 kg/m(2); no history of autonomic neuropathy) and 8 healthy subjects (2/6, 46+/- 6 years., 28.9+/- 5.3 kg/m(2)). A hyperglycaemic clamp (140 mg/dl) was performed over 240 min. Placebo, GIP at a physiological dose (1 pmol . kg(-1) . min(-1)), and GIP at a pharmacological dose (4 pmol . kg(-1) . min(-1)) were administered over 60 min each. Boluses of placebo, 20 pmol GIP/kg, and 80 pmol GIP/kg were injected intravenously at the beginning of each infusion period, respectively. Gastric volume, acid and chloride output were analysed in 15-min intervals. Capillary and venous blood samples were drawn for the determination of glucose and total GIP. Statistics were carried out by repeated-measures ANOVA and one-way ANOVA. RESULTS: Plasma glucose concentrations during the hyperglycaemic clamp experiments were not different between patients with type 2 diabetes and controls. Steady-state GIP plasma levels were 61+/- 8 and 79+/- 12 pmol/l during the low-dose and 327+/- 35 and 327+/- 17 pmol/l during the high-dose infusion of GIP, in healthy control subjects and in patients with type 2 diabetes, respectively (P=0.23 and P=0.99). Pentagastrin markedly increased gastric acid and chloride secretion (P< 0.001). There were no significant differences in the rates of gastric acid or chloride output between the experimental periods with placebo or any dose of GIP. The temporal patterns of gastric acid and chloride secretion were similar in patients with type 2 diabetes and healthy controls (P=0.86 and P=0.61, respectively). CONCLUSION: Pentagastrin-stimulated gastric acid secretion is similar in patients with type 2 diabetes and healthy controls. GIP administration does not influence gastric acid secretion at physiological or pharmacological plasma levels. Therefore, GIP appears to act as an incretin rather than as an enterogastrone in human physiology.",
author = "Meier, {Juris J} and Nauck, {Michael A} and Bartholomaeus Kask and Holst, {Jens J} and Deacon, {Carolyn F} and Schmidt, {Wolfgang E} and Baptist Gallwitz",
note = "Keywords: Adult; Blood Glucose; Case-Control Studies; Chlorides; Diabetes Mellitus, Type 2; Dose-Response Relationship, Drug; Female; Gastric Acid; Gastric Inhibitory Polypeptide; Humans; Insulin; Male; Middle Aged; Pentagastrin",
year = "2006",
language = "English",
volume = "12",
pages = "1874--80",
journal = "World Journal of Gastroenterology",
issn = "1007-9327",
publisher = "Baishideng Publishing Group Co., Limited",
number = "12",

}

RIS

TY - JOUR

T1 - Influence of gastric inhibitory polypeptide on pentagastrin-stimulated gastric acid secretion in patients with type 2 diabetes and healthy controls.

AU - Meier, Juris J

AU - Nauck, Michael A

AU - Kask, Bartholomaeus

AU - Holst, Jens J

AU - Deacon, Carolyn F

AU - Schmidt, Wolfgang E

AU - Gallwitz, Baptist

N1 - Keywords: Adult; Blood Glucose; Case-Control Studies; Chlorides; Diabetes Mellitus, Type 2; Dose-Response Relationship, Drug; Female; Gastric Acid; Gastric Inhibitory Polypeptide; Humans; Insulin; Male; Middle Aged; Pentagastrin

PY - 2006

Y1 - 2006

N2 - AIM: Gastric inhibitory polypeptide is secreted from intestinal K-cells in response to nutrient ingestion and acts as an incretin hormone in human physiology. While animal experiments suggested a role for GIP as an inhibitor of gastric secretion, the GIP effects on gastric acid output in humans are still controversial. METHODS: Pentagastrin was administered at an infusion rate of 1 microg . kg(-1) . h(-1) over 300 min in 8 patients with type 2 diabetes (2 female, 6 male, 54+/- 10 years, BMI 30.5+/- 2.2 kg/m(2); no history of autonomic neuropathy) and 8 healthy subjects (2/6, 46+/- 6 years., 28.9+/- 5.3 kg/m(2)). A hyperglycaemic clamp (140 mg/dl) was performed over 240 min. Placebo, GIP at a physiological dose (1 pmol . kg(-1) . min(-1)), and GIP at a pharmacological dose (4 pmol . kg(-1) . min(-1)) were administered over 60 min each. Boluses of placebo, 20 pmol GIP/kg, and 80 pmol GIP/kg were injected intravenously at the beginning of each infusion period, respectively. Gastric volume, acid and chloride output were analysed in 15-min intervals. Capillary and venous blood samples were drawn for the determination of glucose and total GIP. Statistics were carried out by repeated-measures ANOVA and one-way ANOVA. RESULTS: Plasma glucose concentrations during the hyperglycaemic clamp experiments were not different between patients with type 2 diabetes and controls. Steady-state GIP plasma levels were 61+/- 8 and 79+/- 12 pmol/l during the low-dose and 327+/- 35 and 327+/- 17 pmol/l during the high-dose infusion of GIP, in healthy control subjects and in patients with type 2 diabetes, respectively (P=0.23 and P=0.99). Pentagastrin markedly increased gastric acid and chloride secretion (P< 0.001). There were no significant differences in the rates of gastric acid or chloride output between the experimental periods with placebo or any dose of GIP. The temporal patterns of gastric acid and chloride secretion were similar in patients with type 2 diabetes and healthy controls (P=0.86 and P=0.61, respectively). CONCLUSION: Pentagastrin-stimulated gastric acid secretion is similar in patients with type 2 diabetes and healthy controls. GIP administration does not influence gastric acid secretion at physiological or pharmacological plasma levels. Therefore, GIP appears to act as an incretin rather than as an enterogastrone in human physiology.

AB - AIM: Gastric inhibitory polypeptide is secreted from intestinal K-cells in response to nutrient ingestion and acts as an incretin hormone in human physiology. While animal experiments suggested a role for GIP as an inhibitor of gastric secretion, the GIP effects on gastric acid output in humans are still controversial. METHODS: Pentagastrin was administered at an infusion rate of 1 microg . kg(-1) . h(-1) over 300 min in 8 patients with type 2 diabetes (2 female, 6 male, 54+/- 10 years, BMI 30.5+/- 2.2 kg/m(2); no history of autonomic neuropathy) and 8 healthy subjects (2/6, 46+/- 6 years., 28.9+/- 5.3 kg/m(2)). A hyperglycaemic clamp (140 mg/dl) was performed over 240 min. Placebo, GIP at a physiological dose (1 pmol . kg(-1) . min(-1)), and GIP at a pharmacological dose (4 pmol . kg(-1) . min(-1)) were administered over 60 min each. Boluses of placebo, 20 pmol GIP/kg, and 80 pmol GIP/kg were injected intravenously at the beginning of each infusion period, respectively. Gastric volume, acid and chloride output were analysed in 15-min intervals. Capillary and venous blood samples were drawn for the determination of glucose and total GIP. Statistics were carried out by repeated-measures ANOVA and one-way ANOVA. RESULTS: Plasma glucose concentrations during the hyperglycaemic clamp experiments were not different between patients with type 2 diabetes and controls. Steady-state GIP plasma levels were 61+/- 8 and 79+/- 12 pmol/l during the low-dose and 327+/- 35 and 327+/- 17 pmol/l during the high-dose infusion of GIP, in healthy control subjects and in patients with type 2 diabetes, respectively (P=0.23 and P=0.99). Pentagastrin markedly increased gastric acid and chloride secretion (P< 0.001). There were no significant differences in the rates of gastric acid or chloride output between the experimental periods with placebo or any dose of GIP. The temporal patterns of gastric acid and chloride secretion were similar in patients with type 2 diabetes and healthy controls (P=0.86 and P=0.61, respectively). CONCLUSION: Pentagastrin-stimulated gastric acid secretion is similar in patients with type 2 diabetes and healthy controls. GIP administration does not influence gastric acid secretion at physiological or pharmacological plasma levels. Therefore, GIP appears to act as an incretin rather than as an enterogastrone in human physiology.

M3 - Journal article

C2 - 16609993

VL - 12

SP - 1874

EP - 1880

JO - World Journal of Gastroenterology

JF - World Journal of Gastroenterology

SN - 1007-9327

IS - 12

ER -

ID: 8417171