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Increased glucagon-like peptide-1 secretion and postprandial hypoglycemia in children after Nissen fundoplication

Andrew A Palladino1, Samir Sayed, Lorraine E Levitt Katz

  • 1The Children's Hospital of Philadelphia, Abramson Research Center, Room 802A, 3615 Civic Center Boulevard, Philadelphia, Pennsylvania 19104, USA.

The Journal of Clinical Endocrinology and Metabolism
|October 30, 2008
PubMed

Insights

Children with postprandial hypoglycemia after Nissen fundoplication exhibit exaggerated glucagon-like peptide-1 (GLP-1) secretion. This may cause an excessive insulin surge, leading to hypoglycemia.

Area of Science:

  • Pediatric endocrinology
  • Gastroenterology
  • Metabolic disorders

Background:

  • Postprandial hypoglycemia (PPH) is a common complication following Nissen fundoplication in children.
  • The underlying mechanisms of PPH are not fully understood but involve an exaggerated insulin response.
  • Glucagon-like peptide-1 (GLP-1) is hypothesized to contribute to this exaggerated insulin response.

Purpose of the Study:

  • To investigate the role of GLP-1 in children experiencing PPH after Nissen fundoplication.
  • To characterize the glucose, insulin, and GLP-1 responses to an oral glucose load in these children.

Main Methods:

  • A standard oral glucose tolerance test was performed on ten children with suspected PPH post-Nissen fundoplication and eight control subjects.
  • Blood glucose (BG), insulin, and intact GLP-1 levels were measured at various time points.
  • Age range of participants was 4 months to 13 years.

Main Results:

  • Children with PPH demonstrated significantly lower nadir blood glucose levels compared to controls (46.7 vs. 85.9 mg/dl).
  • Cases showed exaggerated increases in insulin (224.3 vs. 35.5 microIU/ml) and GLP-1 (31.2 vs. 6.2 pm) from baseline to peak.
  • The change in BG from peak to nadir was also significantly greater in cases.

Conclusions:

  • Children with PPH following Nissen fundoplication exhibit abnormally exaggerated GLP-1 secretion.
  • Elevated GLP-1 levels may contribute to the excessive insulin surge observed in these patients.
  • This exaggerated GLP-1 and insulin response plays a role in the pathophysiology of PPH after Nissen fundoplication.
Abstract

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