Effects of endogenous GLP-1 and GIP on glucose tolerance after Roux-en-Y gastric bypass surgery

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Effects of endogenous GLP-1 and GIP on glucose tolerance after Roux-en-Y gastric bypass surgery. / Svane, Maria S; Bojsen-Moller, Kirstine N; Nielsen, Signe; Jørgensen, Nils B; Dirksen, Carsten; Bendtsen, Flemming; Kristiansen, Viggo B; Hartmann, Bolette; Holst, Jens J; Madsbad, Sten.

In: American Journal of Physiology: Endocrinology and Metabolism, Vol. 310, No. 7, 01.04.2016, p. E505-E514.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Svane, MS, Bojsen-Moller, KN, Nielsen, S, Jørgensen, NB, Dirksen, C, Bendtsen, F, Kristiansen, VB, Hartmann, B, Holst, JJ & Madsbad, S 2016, 'Effects of endogenous GLP-1 and GIP on glucose tolerance after Roux-en-Y gastric bypass surgery', American Journal of Physiology: Endocrinology and Metabolism, vol. 310, no. 7, pp. E505-E514. https://doi.org/10.1152/ajpendo.00471.2015

APA

Svane, M. S., Bojsen-Moller, K. N., Nielsen, S., Jørgensen, N. B., Dirksen, C., Bendtsen, F., Kristiansen, V. B., Hartmann, B., Holst, J. J., & Madsbad, S. (2016). Effects of endogenous GLP-1 and GIP on glucose tolerance after Roux-en-Y gastric bypass surgery. American Journal of Physiology: Endocrinology and Metabolism, 310(7), E505-E514. https://doi.org/10.1152/ajpendo.00471.2015

Vancouver

Svane MS, Bojsen-Moller KN, Nielsen S, Jørgensen NB, Dirksen C, Bendtsen F et al. Effects of endogenous GLP-1 and GIP on glucose tolerance after Roux-en-Y gastric bypass surgery. American Journal of Physiology: Endocrinology and Metabolism. 2016 Apr 1;310(7):E505-E514. https://doi.org/10.1152/ajpendo.00471.2015

Author

Svane, Maria S ; Bojsen-Moller, Kirstine N ; Nielsen, Signe ; Jørgensen, Nils B ; Dirksen, Carsten ; Bendtsen, Flemming ; Kristiansen, Viggo B ; Hartmann, Bolette ; Holst, Jens J ; Madsbad, Sten. / Effects of endogenous GLP-1 and GIP on glucose tolerance after Roux-en-Y gastric bypass surgery. In: American Journal of Physiology: Endocrinology and Metabolism. 2016 ; Vol. 310, No. 7. pp. E505-E514.

Bibtex

@article{ee87228567914449a37a1f163b723fc5,
title = "Effects of endogenous GLP-1 and GIP on glucose tolerance after Roux-en-Y gastric bypass surgery",
abstract = "Exaggerated secretion of glucagon-like peptide 1 (GLP-1) is important for postprandial glucose tolerance after Roux-en-Y gastric bypass (RYGB), whereas the role of glucose-dependent insulinotropic polypeptide (GIP) remains to be resolved. We aimed to explore the relative importance of endogenously secreted GLP-1 and GIP on glucose tolerance and beta-cell function after RYGB. We used DPP-4 inhibition to enhance concentrations of intact GIP and GLP-1 and the GLP-1 receptor antagonist exendin 9-39 (Ex-9) for specific blockage of GLP-1 actions. Twelve glucose tolerant patients were studied after RYGB in a randomized, placebo-controlled, four-day, cross-over study with standard mixed meal tests and concurrent administration of: placebo, oral sitagliptin, Ex-9 infusion or combined Ex-9/sitagliptin. GLP-1 receptor antagonism increased glucose excursions, clearly attenuated beta-cell function and aggravated postprandial hyperglucagonaemia compared with placebo, whereas sitagliptin had no effect despite 2-3-fold increased concentrations of intact GLP-1 and GIP. Similarly, sitagliptin did not affect glucose tolerance or beta-cell function during GLP-1R blockage. This study confirms the importance of GLP-1 for glucose tolerance after RYGB via increased insulin and attenuated glucagon secretion in the postprandial state, whereas amplification of the GIP signal (or other DPP-4 sensitive glucose lowering mechanisms) did not appear to contribute to the improved glucose tolerance seen after RYGB.",
author = "Svane, {Maria S} and Bojsen-Moller, {Kirstine N} and Signe Nielsen and J{\o}rgensen, {Nils B} and Carsten Dirksen and Flemming Bendtsen and Kristiansen, {Viggo B} and Bolette Hartmann and Holst, {Jens J} and Sten Madsbad",
note = "Copyright {\textcopyright} 2016, American Journal of Physiology - Endocrinology and Metabolism.",
year = "2016",
month = apr,
day = "1",
doi = "10.1152/ajpendo.00471.2015",
language = "English",
volume = "310",
pages = "E505--E514",
journal = "American Journal of Physiology: Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "7",

}

RIS

TY - JOUR

T1 - Effects of endogenous GLP-1 and GIP on glucose tolerance after Roux-en-Y gastric bypass surgery

AU - Svane, Maria S

AU - Bojsen-Moller, Kirstine N

AU - Nielsen, Signe

AU - Jørgensen, Nils B

AU - Dirksen, Carsten

AU - Bendtsen, Flemming

AU - Kristiansen, Viggo B

AU - Hartmann, Bolette

AU - Holst, Jens J

AU - Madsbad, Sten

N1 - Copyright © 2016, American Journal of Physiology - Endocrinology and Metabolism.

PY - 2016/4/1

Y1 - 2016/4/1

N2 - Exaggerated secretion of glucagon-like peptide 1 (GLP-1) is important for postprandial glucose tolerance after Roux-en-Y gastric bypass (RYGB), whereas the role of glucose-dependent insulinotropic polypeptide (GIP) remains to be resolved. We aimed to explore the relative importance of endogenously secreted GLP-1 and GIP on glucose tolerance and beta-cell function after RYGB. We used DPP-4 inhibition to enhance concentrations of intact GIP and GLP-1 and the GLP-1 receptor antagonist exendin 9-39 (Ex-9) for specific blockage of GLP-1 actions. Twelve glucose tolerant patients were studied after RYGB in a randomized, placebo-controlled, four-day, cross-over study with standard mixed meal tests and concurrent administration of: placebo, oral sitagliptin, Ex-9 infusion or combined Ex-9/sitagliptin. GLP-1 receptor antagonism increased glucose excursions, clearly attenuated beta-cell function and aggravated postprandial hyperglucagonaemia compared with placebo, whereas sitagliptin had no effect despite 2-3-fold increased concentrations of intact GLP-1 and GIP. Similarly, sitagliptin did not affect glucose tolerance or beta-cell function during GLP-1R blockage. This study confirms the importance of GLP-1 for glucose tolerance after RYGB via increased insulin and attenuated glucagon secretion in the postprandial state, whereas amplification of the GIP signal (or other DPP-4 sensitive glucose lowering mechanisms) did not appear to contribute to the improved glucose tolerance seen after RYGB.

AB - Exaggerated secretion of glucagon-like peptide 1 (GLP-1) is important for postprandial glucose tolerance after Roux-en-Y gastric bypass (RYGB), whereas the role of glucose-dependent insulinotropic polypeptide (GIP) remains to be resolved. We aimed to explore the relative importance of endogenously secreted GLP-1 and GIP on glucose tolerance and beta-cell function after RYGB. We used DPP-4 inhibition to enhance concentrations of intact GIP and GLP-1 and the GLP-1 receptor antagonist exendin 9-39 (Ex-9) for specific blockage of GLP-1 actions. Twelve glucose tolerant patients were studied after RYGB in a randomized, placebo-controlled, four-day, cross-over study with standard mixed meal tests and concurrent administration of: placebo, oral sitagliptin, Ex-9 infusion or combined Ex-9/sitagliptin. GLP-1 receptor antagonism increased glucose excursions, clearly attenuated beta-cell function and aggravated postprandial hyperglucagonaemia compared with placebo, whereas sitagliptin had no effect despite 2-3-fold increased concentrations of intact GLP-1 and GIP. Similarly, sitagliptin did not affect glucose tolerance or beta-cell function during GLP-1R blockage. This study confirms the importance of GLP-1 for glucose tolerance after RYGB via increased insulin and attenuated glucagon secretion in the postprandial state, whereas amplification of the GIP signal (or other DPP-4 sensitive glucose lowering mechanisms) did not appear to contribute to the improved glucose tolerance seen after RYGB.

U2 - 10.1152/ajpendo.00471.2015

DO - 10.1152/ajpendo.00471.2015

M3 - Journal article

C2 - 26786780

VL - 310

SP - E505-E514

JO - American Journal of Physiology: Endocrinology and Metabolism

JF - American Journal of Physiology: Endocrinology and Metabolism

SN - 0193-1849

IS - 7

ER -

ID: 160636684