Higher Endogenous Glucose Production during OGTT vs Isoglycemic Intravenous Glucose Infusion

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Higher Endogenous Glucose Production during OGTT vs Isoglycemic Intravenous Glucose Infusion. / Lund, Asger; Bagger, Jonatan I; Christensen, Mikkel Bring; Grøndahl, Magnus; van Hall, Gerrit; Holst, Jens J; Lauritsen, Tina Vilsbøll; Knop, Filip K.

In: The Journal of Clinical Endocrinology & Metabolism, Vol. 101, No. 11, 11.2016, p. 4377-4384.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Lund, A, Bagger, JI, Christensen, MB, Grøndahl, M, van Hall, G, Holst, JJ, Lauritsen, TV & Knop, FK 2016, 'Higher Endogenous Glucose Production during OGTT vs Isoglycemic Intravenous Glucose Infusion', The Journal of Clinical Endocrinology & Metabolism, vol. 101, no. 11, pp. 4377-4384. https://doi.org/10.1210/jc.2016-1948

APA

Lund, A., Bagger, J. I., Christensen, M. B., Grøndahl, M., van Hall, G., Holst, J. J., ... Knop, F. K. (2016). Higher Endogenous Glucose Production during OGTT vs Isoglycemic Intravenous Glucose Infusion. The Journal of Clinical Endocrinology & Metabolism, 101(11), 4377-4384. https://doi.org/10.1210/jc.2016-1948

Vancouver

Lund A, Bagger JI, Christensen MB, Grøndahl M, van Hall G, Holst JJ et al. Higher Endogenous Glucose Production during OGTT vs Isoglycemic Intravenous Glucose Infusion. The Journal of Clinical Endocrinology & Metabolism. 2016 Nov;101(11):4377-4384. https://doi.org/10.1210/jc.2016-1948

Author

Lund, Asger ; Bagger, Jonatan I ; Christensen, Mikkel Bring ; Grøndahl, Magnus ; van Hall, Gerrit ; Holst, Jens J ; Lauritsen, Tina Vilsbøll ; Knop, Filip K. / Higher Endogenous Glucose Production during OGTT vs Isoglycemic Intravenous Glucose Infusion. In: The Journal of Clinical Endocrinology & Metabolism. 2016 ; Vol. 101, No. 11. pp. 4377-4384.

Bibtex

@article{a26a7c2be79d4b69a98f0d32335d585f,
title = "Higher Endogenous Glucose Production during OGTT vs Isoglycemic Intravenous Glucose Infusion",
abstract = "CONTEXT: Oral glucose ingestion elicits a larger insulin response and delayed suppression of glucagon compared to isoglycemic intravenous (iv) glucose infusion (IIGI).OBJECTIVE: We studied whether these differences translate into effects on endogenous glucose production (EGP) and glucose disposal in patients with type 2 diabetes and non-diabetic control subjects.DESIGN: Single-blinded, randomized, crossover study.SETTING: The study was conducted at a specialized research unit.PARTICIPANTS: Ten patients with type 2 diabetes (age [mean ± SD] 57.1 ± 6.7 years; body mass index (BMI) 29.0 ± 4.3 kg/m(2); HbA1c 53.8 ± 11.0 mmol/mol; duration of diabetes 9.2 ± 5.0 years) and 10 matched non-diabetic control subjects (age 56.0±10.7 years; BMI 29.8 ± 2.9 kg/m(2); HbA1c 33.8 ± 5.5 mmol/mol) Interventions: Three experimental days: 75 g-oral glucose tolerance test (OGTT), IIGI and IIGI+glucagon (IIGI with a concomitant iv glucagon infusion (0.8 ng/kg/min from 0 to 25 min) designed to mimic portal glucagon concentrations during OGTT in the type 2 diabetic group).MAIN OUTCOME MEASURES: Glucose kinetics assessed by the double-tracer technique.RESULTS: Glucose rate of disappearance was higher during the OGTT vs IIGIs in the control group, but similar on all days in the diabetic group. Surprisingly, in both groups, EGP was more suppressed during IIGI than during OGTT and exogenous glucagon infusion during IIGI did not restore EGP to the levels observed during OGTT.CONCLUSION: EGP was less suppressed during OGTT than during IIGI in both patients with type 2 diabetes and in non-diabetic control subjects. Based on the present experimental design it was not possible to attribute this difference to the delayed glucagon suppression observed in the initial phase of the OGTT.",
author = "Asger Lund and Bagger, {Jonatan I} and Christensen, {Mikkel Bring} and Magnus Gr{\o}ndahl and {van Hall}, Gerrit and Holst, {Jens J} and Lauritsen, {Tina Vilsb{\o}ll} and Knop, {Filip K}",
year = "2016",
month = "11",
doi = "10.1210/jc.2016-1948",
language = "English",
volume = "101",
pages = "4377--4384",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "Oxford University Press",
number = "11",

}

RIS

TY - JOUR

T1 - Higher Endogenous Glucose Production during OGTT vs Isoglycemic Intravenous Glucose Infusion

AU - Lund, Asger

AU - Bagger, Jonatan I

AU - Christensen, Mikkel Bring

AU - Grøndahl, Magnus

AU - van Hall, Gerrit

AU - Holst, Jens J

AU - Lauritsen, Tina Vilsbøll

AU - Knop, Filip K

PY - 2016/11

Y1 - 2016/11

N2 - CONTEXT: Oral glucose ingestion elicits a larger insulin response and delayed suppression of glucagon compared to isoglycemic intravenous (iv) glucose infusion (IIGI).OBJECTIVE: We studied whether these differences translate into effects on endogenous glucose production (EGP) and glucose disposal in patients with type 2 diabetes and non-diabetic control subjects.DESIGN: Single-blinded, randomized, crossover study.SETTING: The study was conducted at a specialized research unit.PARTICIPANTS: Ten patients with type 2 diabetes (age [mean ± SD] 57.1 ± 6.7 years; body mass index (BMI) 29.0 ± 4.3 kg/m(2); HbA1c 53.8 ± 11.0 mmol/mol; duration of diabetes 9.2 ± 5.0 years) and 10 matched non-diabetic control subjects (age 56.0±10.7 years; BMI 29.8 ± 2.9 kg/m(2); HbA1c 33.8 ± 5.5 mmol/mol) Interventions: Three experimental days: 75 g-oral glucose tolerance test (OGTT), IIGI and IIGI+glucagon (IIGI with a concomitant iv glucagon infusion (0.8 ng/kg/min from 0 to 25 min) designed to mimic portal glucagon concentrations during OGTT in the type 2 diabetic group).MAIN OUTCOME MEASURES: Glucose kinetics assessed by the double-tracer technique.RESULTS: Glucose rate of disappearance was higher during the OGTT vs IIGIs in the control group, but similar on all days in the diabetic group. Surprisingly, in both groups, EGP was more suppressed during IIGI than during OGTT and exogenous glucagon infusion during IIGI did not restore EGP to the levels observed during OGTT.CONCLUSION: EGP was less suppressed during OGTT than during IIGI in both patients with type 2 diabetes and in non-diabetic control subjects. Based on the present experimental design it was not possible to attribute this difference to the delayed glucagon suppression observed in the initial phase of the OGTT.

AB - CONTEXT: Oral glucose ingestion elicits a larger insulin response and delayed suppression of glucagon compared to isoglycemic intravenous (iv) glucose infusion (IIGI).OBJECTIVE: We studied whether these differences translate into effects on endogenous glucose production (EGP) and glucose disposal in patients with type 2 diabetes and non-diabetic control subjects.DESIGN: Single-blinded, randomized, crossover study.SETTING: The study was conducted at a specialized research unit.PARTICIPANTS: Ten patients with type 2 diabetes (age [mean ± SD] 57.1 ± 6.7 years; body mass index (BMI) 29.0 ± 4.3 kg/m(2); HbA1c 53.8 ± 11.0 mmol/mol; duration of diabetes 9.2 ± 5.0 years) and 10 matched non-diabetic control subjects (age 56.0±10.7 years; BMI 29.8 ± 2.9 kg/m(2); HbA1c 33.8 ± 5.5 mmol/mol) Interventions: Three experimental days: 75 g-oral glucose tolerance test (OGTT), IIGI and IIGI+glucagon (IIGI with a concomitant iv glucagon infusion (0.8 ng/kg/min from 0 to 25 min) designed to mimic portal glucagon concentrations during OGTT in the type 2 diabetic group).MAIN OUTCOME MEASURES: Glucose kinetics assessed by the double-tracer technique.RESULTS: Glucose rate of disappearance was higher during the OGTT vs IIGIs in the control group, but similar on all days in the diabetic group. Surprisingly, in both groups, EGP was more suppressed during IIGI than during OGTT and exogenous glucagon infusion during IIGI did not restore EGP to the levels observed during OGTT.CONCLUSION: EGP was less suppressed during OGTT than during IIGI in both patients with type 2 diabetes and in non-diabetic control subjects. Based on the present experimental design it was not possible to attribute this difference to the delayed glucagon suppression observed in the initial phase of the OGTT.

U2 - 10.1210/jc.2016-1948

DO - 10.1210/jc.2016-1948

M3 - Journal article

VL - 101

SP - 4377

EP - 4384

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 11

ER -

ID: 165935915