Evidence mapPaperPMID 20215429Full record

ArticleDiabetes2010

Effect of endogenous GLP-1 on insulin secretion in type 2 diabetes.

Marzieh Salehi, Benedict Aulinger, Ronald L Prigeon, David A D'Alessio

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07224334 (Alpha to Beta Cell Communication in Health and Disease), which is not on this map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
8.1field-weighted citation impact, top 2% 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.

NCT07224334 phase1recruitingstarted 2025, after this paper: background citation

Alpha to Beta Cell Communication in Health and Disease

Ran2025Enrolled30Registered outcomes3Posted comparisons0ConditionsDiabetes (DM)Armsdexamethasone, Exendin-9 is a 30 amino acid peptide that is an established competitive antagonist of the GLP-1 receptor. Subjects will receive exendin-9 by intravenous infusion at a rate of 600 pmol/kg/min
Open the trial in the graph
3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 124 citations in OpenAlex.

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  12. GLP-1 agonists and the gut microbiome: A bidirectional relationship.British journal of clinical pharmacology · 2026
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  18. Assessment of the incretin effect in healthy subjects: concordance between clamp and OGTT methods.American journal of physiology. Endocrinology and metabolism · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Marzieh SalehiUniversity of Cincinnati, Department of Internal Medicine, Cincinnati, Ohio, USA. salehim@uc.edu
Benedict Aulinger
Ronald L Prigeon
David A D'Alessio
University of Cincinnati · US

Funding

VITAMIN K DEFICIENCY IN CHOLESTATIC LIVER DISEASEM01RR008084 · CHILDREN'S HOSPITAL MED CTR (CINCINNATI) · 1994 to 2005
$12.7M
Role of GLP-1 in Normal and Abnormal Glucose ToleranceR01DK057900 · UNIVERSITY OF CINCINNATI · 1999 to 2005
$1.1M
NCATS NIH HHS UL1 TR000077NCRR NIH HHS M01 RR008084NCRR NIH HHS M01-RR-08084NIDDK NIH HHS DK-57900NIDDK NIH HHS R01 DK057900
6 · The paper itself

Abstract

objectiveThe incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) account for up to 60% of postprandial insulin release in healthy people. Previous studies showed a reduced incretin effect in patients with type 2 diabetes but a robust response to exogenous GLP-1. The primary goal of this study was to determine whether endogenous GLP-1 regulates insulin secretion in type 2 diabetes.

methodsTwelve patients with well-controlled type 2 diabetes and eight matched nondiabetic subjects consumed a breakfast meal containing D-xylose during fixed hyperglycemia at 5 mmol/l above fasting levels. Studies were repeated, once with infusion of the GLP-1 receptor antagonist, exendin-(9-39) (Ex-9), and once with saline.

resultsThe relative increase in insulin secretion after meal ingestion was comparable in diabetic and nondiabetic groups (44 +/- 4% vs. 47 +/- 7%). Blocking the action of GLP-1 suppressed postprandial insulin secretion similarly in the diabetic and nondiabetic subjects (25 +/- 4% vs. 27 +/- 8%). However, Ex-9 also reduced the insulin response to intravenous glucose (25 +/- 5% vs. 26 +/- 7%; diabetic vs. nondiabetic subjects), when plasma GLP-1 levels were undetectable. The appearance of postprandial ingested d-xylose in the blood was not affected by Ex-9.

conclusionsThese findings indicate that in patients with well-controlled diabetes, the relative effects of enteral stimuli and endogenous GLP-1 to enhance insulin release are retained and comparable with those in nondiabetic subjects. Surprisingly, GLP-1 receptor signaling promotes glucose-stimulated insulin secretion independent of the mode of glucose entry. Based on rates of D-xylose absorption, GLP-1 receptor blockade did not affect gastric emptying of a solid meal.

Indexed as

AdultBlood GlucoseBody Mass IndexDiabetes Mellitus, Type 2Dietary CarbohydratesFemaleGlucagon-Like Peptide 1GlucoseHumansInsulinInsulin-Secreting CellsInsulin SecretionMaleMiddle AgedPostprandial PeriodReference ValuesBlood GlucoseDietary CarbohydratesGlucagon-Like Peptide 1GlucoseInsulinXylose

Identifiers

PMID20215429
PMCPMC2874693
OpenAlexW2097159083

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.