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 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 nondiabetic control subjects. Design: This was a 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, 29.0±4.3 kg/m2; hemoglobinA1c, 53.8±11.0 mmol/mol; duration of diabetes, 9.2±5.0 years) and 10 matched nondiabetic control subjects (age, 56.0±10.7 years; body mass index, 29.8±2.9 kg/m2; hemoglobin A1c, 33.8 ± 5.5 mmol/mol) participated. 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 minutes] designed to mimic portal glucagon concentrations during OGTT in the type 2 diabetic group) were undertaken. Main Outcome Measures: Glucose kinetics were assessed by tracer methodology. Results: Glucose rate of disappearance was higher during the OGTT vs IIGI 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 nondiabetic 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. (J Clin Endocrinol Metab 101: 4377-4384, 2016).
AB - Context: Oral glucose ingestion elicits a larger insulin response and delayed suppression of glucagon compared to isoglycemic 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 nondiabetic control subjects. Design: This was a 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, 29.0±4.3 kg/m2; hemoglobinA1c, 53.8±11.0 mmol/mol; duration of diabetes, 9.2±5.0 years) and 10 matched nondiabetic control subjects (age, 56.0±10.7 years; body mass index, 29.8±2.9 kg/m2; hemoglobin A1c, 33.8 ± 5.5 mmol/mol) participated. 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 minutes] designed to mimic portal glucagon concentrations during OGTT in the type 2 diabetic group) were undertaken. Main Outcome Measures: Glucose kinetics were assessed by tracer methodology. Results: Glucose rate of disappearance was higher during the OGTT vs IIGI 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 nondiabetic 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. (J Clin Endocrinol Metab 101: 4377-4384, 2016).
U2 - 10.1210/jc.2016-1948
DO - 10.1210/jc.2016-1948
M3 - Journal article
C2 - 27533305
SN - 0021-972X
VL - 101
SP - 4377
EP - 4384
JO - The Journal of Clinical Endocrinology & Metabolism
JF - The Journal of Clinical Endocrinology & Metabolism
IS - 11
ER -
