Postprandial Hypoglycemia Clinical Trial
Official title:
Role of Glucagon-Like Peptide-1 in Postprandial Hypoglycemia After Nissen Fundoplication: Studies With the GLP-1 Receptor Antagonist Exendin-(9-39)
It has been proposed that the rapid gastric emptying of carbohydrate containing fluids into
the intestine causes hyperglycemia followed by reactive hypoglycemia. The investigators have
shown that glucagon-like peptide-1 (GLP-1) secretion in response to a glucose load is
increased in children with Post-prandial hypoglycemia (PPH). This is a proof of concept study
to investigate the causative role of GLP-1 in the pathophysiology of PPH after fundoplication
by evaluating the effects of GLP-1 receptor antagonism on metabolic variables after a mixed
meal.
Hypothesis: In children with post-prandial hypoglycemia after fundoplication, antagonism of
the GLP-1 receptor by exendin-(9-39) will elevate nadir blood glucose levels after a meal
challenge and prevent post-prandial hypoglycemia.
PPH is a frequent complication of fundoplication in children. The mechanism responsible for the PPH is poorly understood, but involves an exaggerated insulin response to a meal and subsequent hypoglycemia. We have shown that children with PPH after Nissen fundoplication have abnormally exaggerated secretion of GLP-1, an incretin hormone with multiple glucose lowering effects including stimulation of insulin secretion and suppression of glucagon secretion. In this study we seek to examine the causal role of endogenous GLP-1 in PPH after fundoplication by evaluating the effects of antagonizing the GLP-1 receptor with exendin-(9-39) on key metabolic features of PPH. ;
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