Results
Subjects were 17 ± 1 years (range 15.8–18), had diabetes for 5 ± 3.3 years, weighed 67 ± 8.7 kg, had a BMI of 23.8 ± 2.1 kg/m2, had an A1C of 7.4 ± 0.7%, and had a total daily insulin dose of 0.9 ± 0.2 units/kg/day.
Postprandial hyperglycemia was reduced with 1.25 and 2.5 μg adjunctive exenatide versus insulin monotherapy (P < 0.0001) (Fig. 1). Delta plasma glucose area under the curve (AUC0–120) was reduced in the early postprandial period in studies with 1.25 μg (49 ± 156 mmol/l per min) (P < 0.008) and 2.5 μg (44 ± 281 mmol/l per min) exenatide versus insulin alone (379 ± 259 mmol/l per min) (P < 0.007).
Figure 1.
Glucose (A), breath analysis (B), glucagon (C), GLP-1 (D), C-peptide (E), and insulin (F) concentrations with insulin monotherapy (●), 1.25 μg (■) and 2.5 μg of exenatide (□) after a mixed meal.
Gastric emptying as measured by 13CO2 in breath was significantly delayed with 1.25 μg exenatide versus insulin alone (P < 0.004) and 2.5 μg exenatide when compared with insulin monotherapy (P < 0.0001).
Glucagon and C-peptide concentrations were not statistically different between studies using exenatide versus insulin alone (P < 0.1 and P < 0.06, respectively). GLP-1 was lower with 2.5 μg exenatide compared with insulin (P < 0.0001) but not with 1.25 μg exenatide (P < 0.2).
Insulin levels were lower between exenatide groups versus insulin alone (P < 0.0001), as expected with a 20% reduction in insulin.
Adverse Events
One subject had nausea with both exenatide doses and received ondansetron, and another had nausea with the 2.5-μg dose; none had emesis. One subject who was hypoglycemic at the outset of the study (3.3 mmol/l) had further hypoglycemia after injection of 1.25 μg exenatide, reaching a nadir of 3.1 mmol/l, and received one intravenous bolus of glucose.
Diabetes Care. 2010;33(6):1294-1296. © 2010 American Diabetes Association, Inc.
Cite this: The Role of Adjunctive Exenatide Therapy in Pediatric Type 1 Diabetes - Medscape - Jun 01, 2010.
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