Evidence map›Paper›PMID 26752550›Full record

Trial reportPloS one2016

Minor Contribution of Endogenous GLP-1 and GLP-2 to Postprandial Lipemia in Obese Men.

Niina Matikainen, Elias Björnson, Sanni Söderlund, Christofer Borén, Björn Eliasson, Kirsi H Pietiläinen, Leonie H Bogl, Antti Hakkarainen, Nina Lundbom, Angela Rivellese and 7 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.1field-weighted citation impact, top 8% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 21 citations in OpenAlex.

  1. Trial
  2. Review
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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

17 authors at 7 institutions in 5 countries.

Niina MatikainenResearch programs Unit, Diabetes and Obesity, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.
Elias BjörnsonDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Sanni SöderlundResearch programs Unit, Diabetes and Obesity, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.
Christofer BorénDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Björn EliassonDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Kirsi H PietiläinenResearch programs Unit, Diabetes and Obesity, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.
Leonie H BoglResearch programs Unit, Diabetes and Obesity, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.
Antti HakkarainenDepartment of Radiology, HUS Medical Imaging Center, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.
Nina LundbomDepartment of Radiology, HUS Medical Imaging Center, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.
Angela RivelleseDepartment of Clinical Medicine and Surgery, Federico II University, Naples, Italy.
Gabriele RiccardiDepartment of Clinical Medicine and Surgery, Federico II University, Naples, Italy.
Jean-Pierre DesprésInstitut Universitaire de Cardiologie et de Pneumologie de Québec, Québec City, Québec, Canada.
Natalie AlmérasInstitut Universitaire de Cardiologie et de Pneumologie de Québec, Québec City, Québec, Canada.
Jens Juul HolstNNF Centre for Basic Metabolic Research, and Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Carolyn F DeaconNNF Centre for Basic Metabolic Research, and Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Jan BorénDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Marja-Riitta TaskinenResearch programs Unit, Diabetes and Obesity, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland.
Helsinki University Hospital · FISahlgrenska University Hospital · SEFederico II University Hospital · ITInstitut Universitaire de Cardiologie et de Pneumologie de Québec · CAUniversity of Copenhagen · DKUniversity of Gothenburg · SEUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextGlucose and lipids stimulate the gut-hormones glucagon-like peptide (GLP)-1, GLP-2 and glucose-dependent insulinotropic polypeptide (GIP) but the effect of these on human postprandial lipid metabolism is not fully clarified.

objectiveTo explore the responses of GLP-1, GLP-2 and GIP after a fat-rich meal compared to the same responses after an oral glucose tolerance test (OGTT) and to investigate possible relationships between incretin response and triglyceride-rich lipoprotein (TRL) response to a fat-rich meal.

designGlucose, insulin, GLP-1, GLP-2 and GIP were measured after an OGTT and after a fat-rich meal in 65 healthy obese (BMI 26.5-40.2 kg/m(2)) male subjects. Triglycerides (TG), apoB48 and apoB100 in TG-rich lipoproteins (chylomicrons, VLDL1 and VLDL2) were measured after the fat-rich meal.

main outcome measuresPostprandial responses (area under the curve, AUC) for glucose, insulin, GLP-1, GLP-2, GIP in plasma, and TG, apoB48 and apoB100 in plasma and TG-rich lipoproteins.

resultsThe GLP-1, GLP-2 and GIP responses after the fat-rich meal and after the OGTT correlated strongly (r = 0.73, p<0.0001; r = 0.46, p<0.001 and r = 0.69, p<0.001, respectively). Glucose and insulin AUCs were lower, but the AUCs for GLP-1, GLP-2 and GIP were significantly higher after the fat-rich meal than after the OGTT. The peak value for all hormones appeared at 120 minutes after the fat-rich meal, compared to 30 minutes after the OGTT. After the fat-rich meal, the AUCs for GLP-1, GLP-2 and GIP correlated significantly with plasma TG- and apoB48 AUCs but the contribution was very modest.

conclusionsIn obese males, GLP-1, GLP-2 and GIP responses to a fat-rich meal are greater than following an OGTT. However, the most important explanatory variable for postprandial TG excursion was fasting triglycerides. The contribution of endogenous GLP-1, GLP-2 and GIP to explaining the variance in postprandial TG excursion was minor.

Indexed as

AdultAgedApolipoprotein B-100Apolipoprotein B-48Area Under CurveBlood GlucoseChylomicronsDietary FatsGastric Inhibitory PolypeptideGlucagon-Like Peptide 1Glucagon-Like Peptide 2Glucose Tolerance TestHumansHyperlipidemiasIncretinsLipid MetabolismApolipoprotein B-100Apolipoprotein B-48Blood GlucoseChylomicronsDietary FatsGastric Inhibitory PolypeptideGlucagon-Like Peptide 1Glucagon-Like Peptide 2IncretinsTriglycerides

Identifiers

PMID26752550
PMCPMC4709062
OpenAlexW2233074121

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.