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Division of Endocrinology and Metabolism (A.B., E.B., P.N., W.W., M.R.), Department of Internal Medicine III, Medical University of Vienna, A-1090 Vienna, Austria; Metabolic Unit (K.T., G.P.), Institute of Biomedical Engineering, I-35127 Padova, Italy; and First Medical Department (A.B., M.R.), Hanusch Hospital, A-1140 Vienna, Austria
Address all correspondence and requests for reprints to: Michael Roden, M.D., Division of Endocrinology and Metabolism, Department of Internal Medicine 3, Medical University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria, c/o 1. Medical Department, Hanusch Hospital, Heinrich Collin Strasse 30, A-1140 Vienna, Austria. E-mail: michael.roden{at}meduniwien.ac.at.
Context: During insulin-modified frequently sampled iv glucose tolerance tests (IM-FSIGT), which allow assessment of insulin action, plasma glucose can markedly decrease.
Objective: This study aimed to assess the counterregulatory impact of the insulin-induced fall of glucose on minimal model-derived indices of insulin sensitivity (SI) and glucose effectiveness.
Participants: Thirteen nondiabetic volunteers (seven males, six females, aged 26 ± 1 yr, body mass index 22.1 ± 0.7 kg/m2) were studied.
Design: All participants were studied in random order during IM-FSIGT (0.3 g/kg glucose; 0.03 U/kg insulin at 20 min) and during identical conditions but with a variable glucose infusion preventing a decrease of plasma glucose concentration below euglycemia (IM-FSIGT-CLAMP). Five participants additionally underwent euglycemic-hyperinsulinemic (1 mU·kg1·min1) clamp tests.
Results: Plasma glucose declined during IM-FSIGT to its nadir of 50 ± 3 mg/dl at 60 min in parallel to a rise (P < 0.05 vs. basal) of plasma glucagon, cortisol, epinephrine, and GH. Glucose infusion rates of 4.6 ± 0.5 mg·kg1·min1 between 30 and 180 min during IM-FSIGT-CLAMP prevented the decline of plasma glucose and the hypoglycemia counterregulatory hormone response. SI was approximately 68% lower during IM-FSIGT (3.40 ± 0.36 vs. IM-FSIGT-CLAMP: 10.71 ± 1.06 104·min1 per µU/ml, P < 0.0001), whereas glucose effectiveness did not differ between both protocols (0.024 ± 0.002 vs. 0.021 ± 0.003 min1, P = NS). Compared with the euglycemic hyperinsulinemic clamp test, SI expressed in identical units from IM-FSIGT was approximately 66% (P < 0.001) lower but did not differ between the euglycemic hyperinsulinemic clamp test and the IM-FSIGT-CLAMP (P = NS).
Conclusions: The transient fall of plasma glucose during IM-FSIGT results in lower estimates of SI, which can be explained by hormonal response to hypoglycemia.
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