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

Department of Pediatrics (A.A.P., S.S., L.E.L.K., D.D.D.L.), Division of Endocrinology/Diabetes, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104; Department of Pediatrics (L.E.L.K., D.D.D.L.), University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104; and Biostatistics and Data Management Core (P.R.G.), The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104

Address all correspondence and requests for reprints to: Diva D. De León, M.D., The Children’s Hospital of Philadelphia, Abramson Research Center, Room 802A, 3615 Civic Center Boulevard, Philadelphia, Pennsylvania 19104. E-mail: deleon{at}email.chop.edu.

Context: 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.

Objective: 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.

Design: 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.

Participants: Children ages 4 months to 13 years old were studied.

Main Outcome Measures: Change scores for glucose, insulin, and intact GLP-1 were recorded after an oral glucose tolerance test.

Results: 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 µIU/ml for cases (vs. 35.5 ± 22.2 µIU/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).

Conclusions: Children with PPH after Nissen fundoplication have abnormally exaggerated secretion of GLP-1, which may contribute to the exaggerated insulin surge and resultant hypoglycemia.