Gastric inhibitory polypeptide does not inhibit gastric emptying in humans

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Gastric inhibitory polypeptide does not inhibit gastric emptying in humans. / Meier, Juris J; Goetze, Oliver; Anstipp, Jens; Hagemann, Dirk; Holst, Jens Juul; Schmidt, Wolfgang E; Gallwitz, Baptist; Nauck, Michael A.

In: American Journal of Physiology: Endocrinology and Metabolism, Vol. 286, No. 4, 04.2004, p. E621-5.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Meier, JJ, Goetze, O, Anstipp, J, Hagemann, D, Holst, JJ, Schmidt, WE, Gallwitz, B & Nauck, MA 2004, 'Gastric inhibitory polypeptide does not inhibit gastric emptying in humans', American Journal of Physiology: Endocrinology and Metabolism, vol. 286, no. 4, pp. E621-5. https://doi.org/10.1152/ajpendo.00499.2003

APA

Meier, J. J., Goetze, O., Anstipp, J., Hagemann, D., Holst, J. J., Schmidt, W. E., Gallwitz, B., & Nauck, M. A. (2004). Gastric inhibitory polypeptide does not inhibit gastric emptying in humans. American Journal of Physiology: Endocrinology and Metabolism, 286(4), E621-5. https://doi.org/10.1152/ajpendo.00499.2003

Vancouver

Meier JJ, Goetze O, Anstipp J, Hagemann D, Holst JJ, Schmidt WE et al. Gastric inhibitory polypeptide does not inhibit gastric emptying in humans. American Journal of Physiology: Endocrinology and Metabolism. 2004 Apr;286(4):E621-5. https://doi.org/10.1152/ajpendo.00499.2003

Author

Meier, Juris J ; Goetze, Oliver ; Anstipp, Jens ; Hagemann, Dirk ; Holst, Jens Juul ; Schmidt, Wolfgang E ; Gallwitz, Baptist ; Nauck, Michael A. / Gastric inhibitory polypeptide does not inhibit gastric emptying in humans. In: American Journal of Physiology: Endocrinology and Metabolism. 2004 ; Vol. 286, No. 4. pp. E621-5.

Bibtex

@article{0607ca6b54a444e39cef3f569438e058,
title = "Gastric inhibitory polypeptide does not inhibit gastric emptying in humans",
abstract = "The insulinotropic gut hormone gastric inhibitory polypeptide (GIP) has been demonstrated to inhibit gastric acid secretion and was proposed to possess {"}enterogastrone{"} activity. GIP effects on gastric emptying have not yet been studied. Fifteen healthy male volunteers (23.9 +/- 3.3 yr, body mass index 23.7 +/- 2.3 kg/m(2)) were studied with the intravenous infusion of GIP (2 pmol.kg(-1).min(-1)) or placebo, each administered to the volunteers on separate occasions from -30 to 360 min in the fasting state. At 0 min, a solid test meal (250 kcal containing [(13)C]sodium octanoate) was served. Gastric emptying was calculated from the (13)CO(2) exhalation rates in breath samples collected over 360 min. Venous blood was drawn in 30-min intervals for the determination of glucose, insulin, C-peptide, and GIP (total and intact). Statistical calculations were made by use of repeated-measures ANOVA and one-way ANOVA. During the infusion, GIP rose to steady-state concentrations of 159 +/- 15 pmol/l for total and 34 +/- 4 pmol/l for intact GIP (P < 0.0001). Meal ingestion further increased GIP concentrations in both groups, reaching peak levels of 265 +/- 20 and 82 +/- 9 pmol/l for total and 67 +/- 7 and 31 +/- 9 pmol/l for intact GIP during the administration of GIP and placebo, respectively (P < 0.0001). There were no differences in glucose, insulin, and C-peptide between the experiments with the infusion of GIP or placebo. Gastric half-emptying times were 120 +/- 9 and 120 +/- 18 min (P = 1.0, with GIP and placebo, respectively). The time pattern of gastric emptying was similar in the two groups (P = 0.98). Endogenous GIP secretion, as derived from the incremental area under the curve of plasma GIP concentrations in the placebo experiments, did not correlate to gastric half-emptying times (r(2) = 0.15, P = 0.15 for intact GIP; r(2) = 0.21, P = 0.086 for total GIP). We conclude that gastric emptying does not appear to be influenced by GIP. The secretion of GIP after meal ingestion is not suppressed by its exogenous administration. The lack of effect of GIP on gastric emptying underlines the differences between GIP and the second incretin glucagon-like peptide 1.",
keywords = "Adult, Area Under Curve, Blood Glucose, C-Peptide, Gastric Emptying, Gastric Inhibitory Polypeptide, Humans, Immunohistochemistry, Injections, Intravenous, Insulin, Male",
author = "Meier, {Juris J} and Oliver Goetze and Jens Anstipp and Dirk Hagemann and Holst, {Jens Juul} and Schmidt, {Wolfgang E} and Baptist Gallwitz and Nauck, {Michael A}",
year = "2004",
month = apr,
doi = "10.1152/ajpendo.00499.2003",
language = "English",
volume = "286",
pages = "E621--5",
journal = "American Journal of Physiology - Endocrinology and Metabolism",
issn = "0193-1849",
publisher = "American Physiological Society",
number = "4",

}

RIS

TY - JOUR

T1 - Gastric inhibitory polypeptide does not inhibit gastric emptying in humans

AU - Meier, Juris J

AU - Goetze, Oliver

AU - Anstipp, Jens

AU - Hagemann, Dirk

AU - Holst, Jens Juul

AU - Schmidt, Wolfgang E

AU - Gallwitz, Baptist

AU - Nauck, Michael A

PY - 2004/4

Y1 - 2004/4

N2 - The insulinotropic gut hormone gastric inhibitory polypeptide (GIP) has been demonstrated to inhibit gastric acid secretion and was proposed to possess "enterogastrone" activity. GIP effects on gastric emptying have not yet been studied. Fifteen healthy male volunteers (23.9 +/- 3.3 yr, body mass index 23.7 +/- 2.3 kg/m(2)) were studied with the intravenous infusion of GIP (2 pmol.kg(-1).min(-1)) or placebo, each administered to the volunteers on separate occasions from -30 to 360 min in the fasting state. At 0 min, a solid test meal (250 kcal containing [(13)C]sodium octanoate) was served. Gastric emptying was calculated from the (13)CO(2) exhalation rates in breath samples collected over 360 min. Venous blood was drawn in 30-min intervals for the determination of glucose, insulin, C-peptide, and GIP (total and intact). Statistical calculations were made by use of repeated-measures ANOVA and one-way ANOVA. During the infusion, GIP rose to steady-state concentrations of 159 +/- 15 pmol/l for total and 34 +/- 4 pmol/l for intact GIP (P < 0.0001). Meal ingestion further increased GIP concentrations in both groups, reaching peak levels of 265 +/- 20 and 82 +/- 9 pmol/l for total and 67 +/- 7 and 31 +/- 9 pmol/l for intact GIP during the administration of GIP and placebo, respectively (P < 0.0001). There were no differences in glucose, insulin, and C-peptide between the experiments with the infusion of GIP or placebo. Gastric half-emptying times were 120 +/- 9 and 120 +/- 18 min (P = 1.0, with GIP and placebo, respectively). The time pattern of gastric emptying was similar in the two groups (P = 0.98). Endogenous GIP secretion, as derived from the incremental area under the curve of plasma GIP concentrations in the placebo experiments, did not correlate to gastric half-emptying times (r(2) = 0.15, P = 0.15 for intact GIP; r(2) = 0.21, P = 0.086 for total GIP). We conclude that gastric emptying does not appear to be influenced by GIP. The secretion of GIP after meal ingestion is not suppressed by its exogenous administration. The lack of effect of GIP on gastric emptying underlines the differences between GIP and the second incretin glucagon-like peptide 1.

AB - The insulinotropic gut hormone gastric inhibitory polypeptide (GIP) has been demonstrated to inhibit gastric acid secretion and was proposed to possess "enterogastrone" activity. GIP effects on gastric emptying have not yet been studied. Fifteen healthy male volunteers (23.9 +/- 3.3 yr, body mass index 23.7 +/- 2.3 kg/m(2)) were studied with the intravenous infusion of GIP (2 pmol.kg(-1).min(-1)) or placebo, each administered to the volunteers on separate occasions from -30 to 360 min in the fasting state. At 0 min, a solid test meal (250 kcal containing [(13)C]sodium octanoate) was served. Gastric emptying was calculated from the (13)CO(2) exhalation rates in breath samples collected over 360 min. Venous blood was drawn in 30-min intervals for the determination of glucose, insulin, C-peptide, and GIP (total and intact). Statistical calculations were made by use of repeated-measures ANOVA and one-way ANOVA. During the infusion, GIP rose to steady-state concentrations of 159 +/- 15 pmol/l for total and 34 +/- 4 pmol/l for intact GIP (P < 0.0001). Meal ingestion further increased GIP concentrations in both groups, reaching peak levels of 265 +/- 20 and 82 +/- 9 pmol/l for total and 67 +/- 7 and 31 +/- 9 pmol/l for intact GIP during the administration of GIP and placebo, respectively (P < 0.0001). There were no differences in glucose, insulin, and C-peptide between the experiments with the infusion of GIP or placebo. Gastric half-emptying times were 120 +/- 9 and 120 +/- 18 min (P = 1.0, with GIP and placebo, respectively). The time pattern of gastric emptying was similar in the two groups (P = 0.98). Endogenous GIP secretion, as derived from the incremental area under the curve of plasma GIP concentrations in the placebo experiments, did not correlate to gastric half-emptying times (r(2) = 0.15, P = 0.15 for intact GIP; r(2) = 0.21, P = 0.086 for total GIP). We conclude that gastric emptying does not appear to be influenced by GIP. The secretion of GIP after meal ingestion is not suppressed by its exogenous administration. The lack of effect of GIP on gastric emptying underlines the differences between GIP and the second incretin glucagon-like peptide 1.

KW - Adult

KW - Area Under Curve

KW - Blood Glucose

KW - C-Peptide

KW - Gastric Emptying

KW - Gastric Inhibitory Polypeptide

KW - Humans

KW - Immunohistochemistry

KW - Injections, Intravenous

KW - Insulin

KW - Male

U2 - 10.1152/ajpendo.00499.2003

DO - 10.1152/ajpendo.00499.2003

M3 - Journal article

C2 - 14678954

VL - 286

SP - E621-5

JO - American Journal of Physiology - Endocrinology and Metabolism

JF - American Journal of Physiology - Endocrinology and Metabolism

SN - 0193-1849

IS - 4

ER -

ID: 132054672