Abstracts of the IDF Congress in Paris 2003

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Background and Aims: The GLP-1 derivative NN2211 is being evaluated as a new treatment for type 2 diabetes. Glucagon secretion is suppressed by GLP-1, therefore, NN2211 could disturb hypoglycemia counterregulation. This trial examined counterregulation during treatment with NN2211 vs. placebo. Materials and Methods: Eleven subjects with type 2 diabetes (3F, age 56± 9 yrs, BMI 30.4±3.4 kg/m2, diabetes duration 6±3 yrs, fasting plasma glucose (FG) 8.4±2.6 mM, HbA1c 7.5±1.1 %) treated with diet (n=3) or with oral antidiabetic drugs (n=8) were studied in a placebo-controlled cross-over design. NN2211 (7.5μg/kg) was administered as a single s.c. dose at midnight. In the morning, regular insulin infusions (2 mU.kg-1.min-1) were given to achieve fasting euglycemia. Capillary glucose was consecutively clamped for 240 min at levels of 78, 66, 54, and 42 mg/dL for 60 min each. Glucose, insulin, C-peptide, glucagon, cortisol, growth hormone (GH) and catecholamines were determined. Insulin secretion rates (ISR) were derived by deconvolution of C-peptide profiles. Results: NN2211 at mean concentrations of 7.9±1.8 nM reduced FG to 7.5±2.4 mM (placebo: 8.1±3.0 mM). At steady state insulin concentrations of ~1000 pmol/L, glucose infusion rates were similar with NN2211 vs. placebo (p=0.27). Exposure to hypoglycemia led to clear counterregulatory responses of glucagon (1.6 fold), cortisol (2.2 fold), GH (6.6 fold), adrenaline (14 fold) and noradrenaline (2.3 fold; all p

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