Increased Glucagon-Like Peptide-1 Secretion and Postprandial Hypoglycemia in Children after Nissen Fundoplication

The Children's Hospital of Philadelphia, Abramson Research Center, Room 802A, 3615 Civic Center Boulevard, Philadelphia, Pennsylvania 19104, USA.
Journal of Clinical Endocrinology & Metabolism (Impact Factor: 6.21). 10/2008; 94(1):39-44. DOI: 10.1210/jc.2008-1263
Source: PubMed


Postprandial hypoglycemia (PPH) is a frequent complication of Nissen 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 hypothesize that increased glucagon-like peptide-1 (GLP-1) secretion contributes to the exaggerated insulin surge and plays a role in the pathophysiology of this disorder.
The aim of the study was to characterize glucose, insulin, and GLP-1 response to an oral glucose load in children with symptoms of PPH after Nissen fundoplication.
Ten patients with suspected PPH and a history of Nissen fundoplication and eight control subjects underwent a standard oral glucose tolerance test at The Children's Hospital of Philadelphia. Blood glucose (BG), insulin, and intact GLP-1 levels were obtained at various time points.
Children ages 4 months to 13 years old were studied.
Change scores for glucose, insulin, and intact GLP-1 were recorded after an oral glucose tolerance test.
All cases had hypoglycemia after the glucose load. Mean BG at nadir (+/- sd) was 46.7 +/- 11 mg/dl for cases (vs. 85.9 +/- 21.3 mg/dl; P < 0.0005). Mean change in BG from baseline to peak (+/- sd) was 179.3 +/- 87.4 mg/dl for cases (vs. 57.8 +/- 39.5 mg/dl; P = 0.003). Mean change in BG (+/- sd) from peak to nadir was 214.4 +/- 85.9 mg/dl for cases (vs. 55.9 +/- 41.1 mg/dl, P < 0.0005). Mean change in insulin (+/- sd) from baseline to peak was 224.3 +/- 313.7 microIU/ml for cases (vs. 35.5 +/- 22.2 microIU/ml; P = 0.012). Mean change in GLP-1 (+/- sd) from baseline to peak was 31.2 +/- 24 pm (vs. 6.2 +/- 9.5 pm; P = 0.014).
Children with PPH after Nissen fundoplication have abnormally exaggerated secretion of GLP-1, which may contribute to the exaggerated insulin surge and resultant hypoglycemia.

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