Hyperglycemia acutely lowers the postprandial excursions of glucagon-like Peptide-1 and gastric inhibitory polypeptide in humans

Research output: Contribution to journalJournal articleResearchpeer-review

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Hyperglycemia acutely lowers the postprandial excursions of glucagon-like Peptide-1 and gastric inhibitory polypeptide in humans. / Vollmer, Kirsten; Gardiwal, Husai; Menge, Bjoern A; Goetze, Oliver; Deacon, Carolyn F; Schmidt, Wolfgang E; Holst, Jens Juul; Meier, Juris J.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 94, No. 4, 2009, p. 1379-85.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Vollmer, K, Gardiwal, H, Menge, BA, Goetze, O, Deacon, CF, Schmidt, WE, Holst, JJ & Meier, JJ 2009, 'Hyperglycemia acutely lowers the postprandial excursions of glucagon-like Peptide-1 and gastric inhibitory polypeptide in humans', Journal of Clinical Endocrinology and Metabolism, vol. 94, no. 4, pp. 1379-85. https://doi.org/10.1210/jc.2008-2197

APA

Vollmer, K., Gardiwal, H., Menge, B. A., Goetze, O., Deacon, C. F., Schmidt, W. E., ... Meier, J. J. (2009). Hyperglycemia acutely lowers the postprandial excursions of glucagon-like Peptide-1 and gastric inhibitory polypeptide in humans. Journal of Clinical Endocrinology and Metabolism, 94(4), 1379-85. https://doi.org/10.1210/jc.2008-2197

Vancouver

Vollmer K, Gardiwal H, Menge BA, Goetze O, Deacon CF, Schmidt WE et al. Hyperglycemia acutely lowers the postprandial excursions of glucagon-like Peptide-1 and gastric inhibitory polypeptide in humans. Journal of Clinical Endocrinology and Metabolism. 2009;94(4):1379-85. https://doi.org/10.1210/jc.2008-2197

Author

Vollmer, Kirsten ; Gardiwal, Husai ; Menge, Bjoern A ; Goetze, Oliver ; Deacon, Carolyn F ; Schmidt, Wolfgang E ; Holst, Jens Juul ; Meier, Juris J. / Hyperglycemia acutely lowers the postprandial excursions of glucagon-like Peptide-1 and gastric inhibitory polypeptide in humans. In: Journal of Clinical Endocrinology and Metabolism. 2009 ; Vol. 94, No. 4. pp. 1379-85.

Bibtex

@article{3733b2b0334111df8ed1000ea68e967b,
title = "Hyperglycemia acutely lowers the postprandial excursions of glucagon-like Peptide-1 and gastric inhibitory polypeptide in humans",
abstract = "INTRODUCTION: Impaired secretion of glucagon-like peptide 1 (GLP-1) has been suggested to contribute to the deficient incretin effect in patients with type 2 diabetes. It is unclear whether this is a primary defect or a consequence of the hyperglycemia in type 2 diabetes. We examined whether acute hyperglycemia reduces the postprandial excursions of gastric inhibitory polypeptide (GIP) and GLP-1, and if so, whether this can be attributed to changes in gastric emptying. PATIENTS AND METHODS: Fifteen nondiabetic individuals participated in a euglycemic clamp and a hyperglycemic clamp experiment, carried out over 285 min. A mixed meal was ingested after 45 min. Plasma concentrations of glucose, insulin, C-peptide, glucagon, triglycerides, GIP, and GLP-1 were determined, and gastric emptying was assessed using a (13)C-octanoate breath test. RESULTS: Glucose levels were 160 +/- 1 mg/dl during the hyperglycemic clamp experiments and 83 +/- 3 mg/dl during the euglycemia (P < 0.0001). Glucose infusion rates were higher during hyperglycemia, but meal ingestion led to a decline in glucose requirements in both experiments (P < 0.0001). Insulin and C-peptide levels were higher during the hyperglycemic clamp experiments (P < 0.0001), whereas glucagon levels were higher during euglycemia (P < 0.0001). The postprandial increases in GIP and GLP-1 concentrations were 46 and 52{\%} lower during the experiments with hyperglycemia (P = 0.0017 and P = 0.021). Hyperglycemia also elicited a significant delay in gastric emptying (P < 0.0001). CONCLUSIONS: Hyperglycemia acutely reduces the postprandial levels of GIP and GLP-1, possibly through a deceleration of gastric emptying. This supports the concept that reduced incretin levels in some patients with type 2 diabetes are a consequence rather than a cause of type 2 diabetes.",
author = "Kirsten Vollmer and Husai Gardiwal and Menge, {Bjoern A} and Oliver Goetze and Deacon, {Carolyn F} and Schmidt, {Wolfgang E} and Holst, {Jens Juul} and Meier, {Juris J}",
note = "Keywords: Adult; Body Mass Index; C-Peptide; Cholesterol, HDL; Female; Gastric Emptying; Gastric Inhibitory Polypeptide; Glucagon; Glucagon-Like Peptide 1; Glucose Clamp Technique; Humans; Hyperglycemia; Kidney Function Tests; Liver Function Tests; Male; Postprandial Period; Reference Values; Young Adult",
year = "2009",
doi = "10.1210/jc.2008-2197",
language = "English",
volume = "94",
pages = "1379--85",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "Oxford University Press",
number = "4",

}

RIS

TY - JOUR

T1 - Hyperglycemia acutely lowers the postprandial excursions of glucagon-like Peptide-1 and gastric inhibitory polypeptide in humans

AU - Vollmer, Kirsten

AU - Gardiwal, Husai

AU - Menge, Bjoern A

AU - Goetze, Oliver

AU - Deacon, Carolyn F

AU - Schmidt, Wolfgang E

AU - Holst, Jens Juul

AU - Meier, Juris J

N1 - Keywords: Adult; Body Mass Index; C-Peptide; Cholesterol, HDL; Female; Gastric Emptying; Gastric Inhibitory Polypeptide; Glucagon; Glucagon-Like Peptide 1; Glucose Clamp Technique; Humans; Hyperglycemia; Kidney Function Tests; Liver Function Tests; Male; Postprandial Period; Reference Values; Young Adult

PY - 2009

Y1 - 2009

N2 - INTRODUCTION: Impaired secretion of glucagon-like peptide 1 (GLP-1) has been suggested to contribute to the deficient incretin effect in patients with type 2 diabetes. It is unclear whether this is a primary defect or a consequence of the hyperglycemia in type 2 diabetes. We examined whether acute hyperglycemia reduces the postprandial excursions of gastric inhibitory polypeptide (GIP) and GLP-1, and if so, whether this can be attributed to changes in gastric emptying. PATIENTS AND METHODS: Fifteen nondiabetic individuals participated in a euglycemic clamp and a hyperglycemic clamp experiment, carried out over 285 min. A mixed meal was ingested after 45 min. Plasma concentrations of glucose, insulin, C-peptide, glucagon, triglycerides, GIP, and GLP-1 were determined, and gastric emptying was assessed using a (13)C-octanoate breath test. RESULTS: Glucose levels were 160 +/- 1 mg/dl during the hyperglycemic clamp experiments and 83 +/- 3 mg/dl during the euglycemia (P < 0.0001). Glucose infusion rates were higher during hyperglycemia, but meal ingestion led to a decline in glucose requirements in both experiments (P < 0.0001). Insulin and C-peptide levels were higher during the hyperglycemic clamp experiments (P < 0.0001), whereas glucagon levels were higher during euglycemia (P < 0.0001). The postprandial increases in GIP and GLP-1 concentrations were 46 and 52% lower during the experiments with hyperglycemia (P = 0.0017 and P = 0.021). Hyperglycemia also elicited a significant delay in gastric emptying (P < 0.0001). CONCLUSIONS: Hyperglycemia acutely reduces the postprandial levels of GIP and GLP-1, possibly through a deceleration of gastric emptying. This supports the concept that reduced incretin levels in some patients with type 2 diabetes are a consequence rather than a cause of type 2 diabetes.

AB - INTRODUCTION: Impaired secretion of glucagon-like peptide 1 (GLP-1) has been suggested to contribute to the deficient incretin effect in patients with type 2 diabetes. It is unclear whether this is a primary defect or a consequence of the hyperglycemia in type 2 diabetes. We examined whether acute hyperglycemia reduces the postprandial excursions of gastric inhibitory polypeptide (GIP) and GLP-1, and if so, whether this can be attributed to changes in gastric emptying. PATIENTS AND METHODS: Fifteen nondiabetic individuals participated in a euglycemic clamp and a hyperglycemic clamp experiment, carried out over 285 min. A mixed meal was ingested after 45 min. Plasma concentrations of glucose, insulin, C-peptide, glucagon, triglycerides, GIP, and GLP-1 were determined, and gastric emptying was assessed using a (13)C-octanoate breath test. RESULTS: Glucose levels were 160 +/- 1 mg/dl during the hyperglycemic clamp experiments and 83 +/- 3 mg/dl during the euglycemia (P < 0.0001). Glucose infusion rates were higher during hyperglycemia, but meal ingestion led to a decline in glucose requirements in both experiments (P < 0.0001). Insulin and C-peptide levels were higher during the hyperglycemic clamp experiments (P < 0.0001), whereas glucagon levels were higher during euglycemia (P < 0.0001). The postprandial increases in GIP and GLP-1 concentrations were 46 and 52% lower during the experiments with hyperglycemia (P = 0.0017 and P = 0.021). Hyperglycemia also elicited a significant delay in gastric emptying (P < 0.0001). CONCLUSIONS: Hyperglycemia acutely reduces the postprandial levels of GIP and GLP-1, possibly through a deceleration of gastric emptying. This supports the concept that reduced incretin levels in some patients with type 2 diabetes are a consequence rather than a cause of type 2 diabetes.

U2 - 10.1210/jc.2008-2197

DO - 10.1210/jc.2008-2197

M3 - Journal article

C2 - 19174495

VL - 94

SP - 1379

EP - 1385

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 4

ER -

ID: 18699485