J Clin Endocrinol Metab
Center for Diabetes Research (A.L., J.I.B., M.C., M.G., T.V., F.K.K.), Gentofte Hospital, University of Copenhagen, Hellerup, Denmark; The NNF Center for Basic Metabolic Research (A.L., J.J.H., F.K.K.), Copenhagen, Denmark; Department of Clinical Medicine (T.V., F.K.K.), Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; Department of Clinical Pharmacology (M.C.), Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark; Department of Biomedical Sciences (G.v.H., J.J.H.), Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark; and Department of Clinical Biochemistry (G.v.H.), Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Published: November 2016
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/m; hemoglobin A, 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/m; hemoglobin A, 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.
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http://dx.doi.org/10.1210/jc.2016-1948 | DOI Listing |
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