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Increased glucagon-like peptide-1 secretion and postprandial hypoglycemia in children after Nissen fundoplication.
J Clin Endocrinol Metab. 2009 Jan; 94(1):39-44.JC

Abstract

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 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).

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.

Authors+Show Affiliations

The Children's Hospital of Philadelphia, Abramson Research Center, Room 802A, 3615 Civic Center Boulevard, Philadelphia, Pennsylvania 19104, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18957502

Citation

Palladino, Andrew A., et al. "Increased Glucagon-like Peptide-1 Secretion and Postprandial Hypoglycemia in Children After Nissen Fundoplication." The Journal of Clinical Endocrinology and Metabolism, vol. 94, no. 1, 2009, pp. 39-44.
Palladino AA, Sayed S, Levitt Katz LE, et al. Increased glucagon-like peptide-1 secretion and postprandial hypoglycemia in children after Nissen fundoplication. J Clin Endocrinol Metab. 2009;94(1):39-44.
Palladino, A. A., Sayed, S., Levitt Katz, L. E., Gallagher, P. R., & De León, D. D. (2009). Increased glucagon-like peptide-1 secretion and postprandial hypoglycemia in children after Nissen fundoplication. The Journal of Clinical Endocrinology and Metabolism, 94(1), 39-44. https://doi.org/10.1210/jc.2008-1263
Palladino AA, et al. Increased Glucagon-like Peptide-1 Secretion and Postprandial Hypoglycemia in Children After Nissen Fundoplication. J Clin Endocrinol Metab. 2009;94(1):39-44. PubMed PMID: 18957502.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased glucagon-like peptide-1 secretion and postprandial hypoglycemia in children after Nissen fundoplication. AU - Palladino,Andrew A, AU - Sayed,Samir, AU - Levitt Katz,Lorraine E, AU - Gallagher,Paul R, AU - De León,Diva D, Y1 - 2008/10/28/ PY - 2008/10/30/pubmed PY - 2009/2/13/medline PY - 2008/10/30/entrez SP - 39 EP - 44 JF - The Journal of clinical endocrinology and metabolism JO - J Clin Endocrinol Metab VL - 94 IS - 1 N2 - 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 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). 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. SN - 0021-972X UR - https://www.unboundmedicine.com/medline/citation/18957502/Increased_glucagon_like_peptide_1_secretion_and_postprandial_hypoglycemia_in_children_after_Nissen_fundoplication_ L2 - https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2008-1263 DB - PRIME DP - Unbound Medicine ER -