Evidence map›Paper›PMID 24315990›Full record

ArticleGastroenterology2014

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

Marzieh Salehi, Amalia Gastaldelli, David A D'Alessio

2 registry-linked trialsAbstract read
In one paragraph

Article in Gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 123 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 4 pooled it
19.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT01803451 early_phase1recruitingnot on this map

The Role of Glucagon Like Peptide-1 in Glucose Metabolism and Weight Loss Following Gastric Bypass Surgery

TypeinterventionalSponsorThe University of Texas Health Science Center at San AntonioRan2005 to 2027Enrolled80ConditionsPost-bariatric SurgeryArmsexendin-(9-39), exendin -(9-39)
NCT07580079 phase2not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Anakinra for the Treatment of Recurrent Postprandial Hypoglycemia After Total Gastrectomy in a Patient With End-Stage Renal Disease

TypeinterventionalSponsorMarc DonathRan2026 to 2026Enrolled1ConditionsPostprandial Hypoglycemia, End-stage Renal Disease (ESRD), Gastrectomy, Glucose Metabolism DisordersArmsAnakinra (interleukin-1 receptor antagonist), Placebo Comparator (0.9% NaCl)
3 · Its place in the literature

Who cites it

123 citing papers in PubMed, 4 syntheses or guidelines pooled it, 282 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Guideline
  5. Trial
  6. Trial
  7. Trial
  8. Trial
  9. Trial
  10. Trial
  11. Trial
  12. Trial
  13. Trial
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

63 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Marzieh SalehiDivision of Endocrinology, Diabetes, & Metabolism, Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio. Electronic address: salehim@uc.edu.
Amalia GastaldelliCardiometabolic Risk Unit, CNR Institute of Clinical Physiology, Pisa, Italy.
David A D'AlessioDivision of Endocrinology, Diabetes, & Metabolism, Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio; Cincinnati VA Medical Center, Cincinnati, Ohio.
Cincinnati VA Medical Center · USIstituto di Fisiologia Clinica · ITUniversity of Cincinnati Medical Center · US

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., KISSELA, BRETT M · 2015 to 2024
$37.5M
Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Theresa Alenghat · 2007 to 2026
$24.4M
CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR026314 · NCRR · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E. · 2009 to 2011
$14.3M
Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., TSEVAT, JOEL · 2012 to 2014
$9.9M
The role of GLP-1 in normal and abnormal glucose toleranceR01DK057900 · NIDDK · UNIVERSITY OF CINCINNATI · PI D'ALESSIO, DAVID A. · 1999 to 2013
$3.4M
The Weight-Independent Effects of Bariatric Surgeries on Islet Cell FunctionR01DK105379 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SALEHI, MARZIEH · 2015 to 2020
$2.4M
Hormonal and neural control of insulin secretion following gastric bypass surgeryK23DK083554 · NIDDK · UNIVERSITY OF CINCINNATI · PI SALEHI, MARZIEH · 2009 to 2013
$889k
NCATS NIH HHS 8 UL1 TR000077NCATS NIH HHS UL1 TR001425NCRR NIH HHS UL1 RR026314NIDDK NIH HHS DK083554NIDDK NIH HHS DK57900NIDDK NIH HHS K23 DK083554NIDDK NIH HHS P30 DK078392NIDDK NIH HHS R01 DK057900NIDDK NIH HHS R01 DK105379
6 · The paper itself

Abstract

BACKGROUND &

aimsPostprandial 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.

methodsNine 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.

resultsInfusion 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.

conclusionsHypoglycemia 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.

Indexed as

AdultBlood GlucoseCase-Control StudiesFemaleGastric BypassGlucagonGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorGlucagon-Secreting CellsHumansHypoglycemiaInsulinInsulin-Secreting CellsMaleMiddle AgedPeptide FragmentsBlood Glucoseexendin (9-39)GLP1R protein, humanGlucagonGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorInsulinPeptide FragmentsReceptors, GlucagonGlucagon-like Peptide 1Hyperinsulinemic Hypoglycemia SyndromeIslet FunctionRoux-en-Y Gastric Bypass Surgery

Identifiers

PMID24315990
PMCPMC3943944
OpenAlexW2014019554

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.