Blockade of glucagon-like peptide 1 receptor corrects postprandial hypoglycemia after gastric bypass

Gastroenterology. 2014 Mar;146(3):669-680.e2. doi: 10.1053/j.gastro.2013.11.044. Epub 2013 Dec 4.

Abstract

Background & aims: Postprandial glycemia excursions increase after gastric bypass surgery; this effect is even greater among patients with recurrent hypoglycemia. These patients also have increased postprandial levels of insulin and glucagon-like peptide 1 (GLP-1). We performed a clinical trial to determine the role of GLP-1 in postprandial glycemia in patients with hyperinsulinemic hypoglycemia syndrome after gastric bypass.

Methods: Nine patients with recurrent hypoglycemia after gastric bypass (H-GB), 7 patients who were asymptomatic after gastric bypass (A-GB), and 8 healthy control subjects underwent a mixed-meal tolerance test (350 kcal) using a dual glucose tracer method on 2 separate days. On 1 day they received continuous infusion of the GLP-1 receptor antagonist exendin (9-39) (Ex-9), and on the other day they received a saline control. Glucose kinetics and islet and gut hormone responses were measured before and after the meal.

Results: Infusion of Ex-9 corrected hypoglycemia in all patients with H-GB. The reduction in postprandial insulin secretion by Ex-9 was greater in the H-GB group than in the other groups (H-GB, 50% ± 8%; A-GB, 13% ± 10%; controls, 14% ± 10%) (P < .05). The meal-derived glucose appearance was significantly greater in subjects who had undergone gastric bypass compared to the controls and in the H-GB group compared to the A-GB group. Ex-9 shortened the time to reach peak meal-derived glucose appearance in all groups without a significant effect on overall glucose flux. Postprandial glucagon levels were higher among patients who had undergone gastric bypass than controls and increased with administration of Ex-9.

Conclusions: Hypoglycemia after gastric bypass can be corrected by administration of a GLP-1 receptor antagonist, which might be used to treat this disorder. These findings are consistent with reports that increased GLP-1 activity contributes to hypoglycemia after gastric bypass. ClinicalTrials.gov, Number: NCT01803451.

Keywords: Glucagon-like Peptide 1; Hyperinsulinemic Hypoglycemia Syndrome; Islet Function; Roux-en-Y Gastric Bypass Surgery.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Adult
  • Blood Glucose / metabolism
  • Case-Control Studies
  • Female
  • Gastric Bypass / adverse effects*
  • Glucagon / blood
  • Glucagon-Like Peptide 1 / blood
  • Glucagon-Like Peptide-1 Receptor
  • Glucagon-Secreting Cells / physiology
  • Humans
  • Hypoglycemia / blood
  • Hypoglycemia / etiology*
  • Hypoglycemia / prevention & control*
  • Insulin / blood
  • Insulin-Secreting Cells / physiology
  • Male
  • Middle Aged
  • Peptide Fragments / pharmacology
  • Peptide Fragments / therapeutic use*
  • Receptors, Glucagon / antagonists & inhibitors*
  • Receptors, Glucagon / drug effects
  • Treatment Outcome

Substances

  • Blood Glucose
  • GLP1R protein, human
  • Glucagon-Like Peptide-1 Receptor
  • Insulin
  • Peptide Fragments
  • Receptors, Glucagon
  • exendin (9-39)
  • Glucagon-Like Peptide 1
  • Glucagon

Associated data

  • ClinicalTrials.gov/NCT01803451