Evidence mapPaperPMID 30518693Full record

Trial reportJCI insight2018

Metformin-induced glucagon-like peptide-1 secretion contributes to the actions of metformin in type 2 diabetes.

Emilie Bahne, Emily W L Sun, Richard L Young, Morten Hansen, David P Sonne, Jakob S Hansen, Ulrich Rohde, Alice P Liou, Margaret L Jackson, Dayan de Fontgalland and 10 more

Registry-linked trialOpen access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It reports registered trial NCT02050074. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
11.2field-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.

NCT02050074 phase4completed

The Role of Metformin and Colesevelam in Human GLP-1 Secretion

Ran2014Enrolled12Registered outcomes1Posted comparisons0ConditionsType 2 DiabetesArmsColesevelam, Metformin, Placebo
Open the trial in the graph
3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 167 citations in OpenAlex.

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

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

20 authors at 7 institutions in 3 countries.

Emilie BahneClinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte Hospital, Hellerup, Denmark.
Emily W L SunDiscipline of Human Physiology and Centre for Neuroscience, Flinders University of South Australia, Adelaide, Australia.
Richard L YoungAdelaide Medical School, University of Adelaide, Adelaide, Australia.
Morten HansenClinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte Hospital, Hellerup, Denmark.
David P SonneClinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte Hospital, Hellerup, Denmark.
Jakob S HansenClinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte Hospital, Hellerup, Denmark.
Ulrich RohdeClinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte Hospital, Hellerup, Denmark.
Alice P LiouCardiovascular and Metabolic Diseases Research Unit, Pfizer Worldwide Research and Development, Cambridge, Massachusetts, USA.
Margaret L JacksonCardiovascular and Metabolic Diseases Research Unit, Pfizer Worldwide Research and Development, Cambridge, Massachusetts, USA.
Dayan de FontgallandDiscipline of Surgery, Flinders University, Adelaide, South Australia, Australia.
Philippa RabbittDiscipline of Surgery, Flinders University, Adelaide, South Australia, Australia.
Paul HollingtonDiscipline of Surgery, Flinders University, Adelaide, South Australia, Australia.
Luigi SposatoDiscipline of Surgery, Flinders University, Adelaide, South Australia, Australia.
Steven DueDiscipline of Surgery, Flinders University, Adelaide, South Australia, Australia.
David A WattchowDiscipline of Surgery, Flinders University, Adelaide, South Australia, Australia.
Jens F RehfeldDepartment of Clinical Biochemistry, Rigshospitalet, University Copenhagen, Copenhagen, Denmark.
Jens J HolstNovo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University Copenhagen, Copenhagen, Denmark.
Damien J KeatingDiscipline of Human Physiology and Centre for Neuroscience, Flinders University of South Australia, Adelaide, Australia.
Tina VilsbøllClinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte Hospital, Hellerup, Denmark.
Filip K KnopClinical Metabolic Physiology, Steno Diabetes Center Copenhagen, Gentofte Hospital, Hellerup, Denmark.
Flinders University · AUSteno Diabetes Centers · DKPfizer (United States) · USUniversity of Copenhagen · DKCopenhagen University Hospital · DKNovo Nordisk Foundation · DKSouth Australian Health and Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetformin reduces plasma glucose and has been shown to increase glucagon-like peptide 1 (GLP-1) secretion. Whether this is a direct action of metformin on GLP-1 release, and whether some of the glucose-lowering effect of metformin occurs due to GLP-1 release, is unknown. The current study investigated metformin-induced GLP-1 secretion and its contribution to the overall glucose-lowering effect of metformin and underlying mechanisms in patients with type 2 diabetes.

methodsTwelve patients with type 2 diabetes were included in this placebo-controlled, double-blinded study. On 4 separate days, the patients received metformin (1,500 mg) or placebo suspended in a liquid meal, with subsequent i.v. infusion of the GLP-1 receptor antagonist exendin9-39 (Ex9-39) or saline. During 240 minutes, blood was sampled. The direct effect of metformin on GLP-1 secretion was tested ex vivo in human ileal and colonic tissue with and without dorsomorphin-induced inhibiting of the AMPK activity.

resultsMetformin increased postprandial GLP-1 secretion compared with placebo (P = 0.014), and the postprandial glucose excursions were significantly smaller after metformin + saline compared with metformin + Ex9-39 (P = 0.004). Ex vivo metformin acutely increased GLP-1 secretion (colonic tissue, P < 0.01; ileal tissue, P < 0.05), but the effect was abolished by inhibition of AMPK activity.

conclusionsMetformin has a direct and AMPK-dependent effect on GLP-1-secreting L cells and increases postprandial GLP-1 secretion, which seems to contribute to metformin's glucose-lowering effect and mode of action.

trial registrationNCT02050074 (https://clinicaltrials.gov/ct2/show/NCT02050074).

fundingThis study received grants from the A.P. Møller Foundation, the Novo Nordisk Foundation, the Danish Medical Association research grant, the Australian Research Council, the National Health and Medical Research Council, and Pfizer Inc.

Indexed as

AdultAgedAged, 80 and overAustraliaBlood GlucoseDiabetes Mellitus, Type 2Double-Blind MethodFemaleGlucagon-Like Peptide 1HumansMaleMetforminMiddle AgedPostprandial PeriodBlood GlucoseGlucagon-Like Peptide 1MetforminDiabetesEndocrinologyMetabolism

Identifiers

PMID30518693
PMCPMC6328020
OpenAlexW2903143648

What Socratic holds

Texttitle and abstract
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.