Evidence map›Paper›PMID 31147381›Full record

ArticleGut2020

Donor metabolic characteristics drive effects of faecal microbiota transplantation on recipient insulin sensitivity, energy expenditure and intestinal transit time.

Pieter de Groot, Torsten Scheithauer, Guido J Bakker, Andrei Prodan, Evgeni Levin, Muhammad Tanweer Khan, Hilde Herrema, Mariette Ackermans, Mireille J M Serlie, Maurits de Brauw and 12 more

Abstract read
In one paragraph

Article in Gut, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

188 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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128 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

22 authors.

Pieter de GrootDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.ORCID 0000-0003-3559-0138
Torsten ScheithauerDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Guido J BakkerDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Andrei ProdanDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.ORCID 0000-0003-2789-7789
Evgeni LevinDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Muhammad Tanweer KhanWallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, Goteborgs Universitet, Gothenburg, Sweden.
Hilde HerremaDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Mariette AckermansDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Mireille J M SerlieDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Maurits de BrauwDepartment of Surgery, Spaarne Gasthuis, Haarlem, The Netherlands.
Johannes H M LevelsDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Amber SalesDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Victor E GerdesDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Marcus StåhlmanWallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, Goteborgs Universitet, Gothenburg, Sweden.
Alinda W M SchimmelDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Geesje Dallinga-ThieDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Jacques Jghm BergmanDepartment of Gastroenterology, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Frits HollemanDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Joost B L HoekstraDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Albert GroenDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.
Fredrik BäckhedWallenberg Laboratory, Department of Molecular and Clinical Medicine, Sahlgrenska Academy, Goteborgs Universitet, Gothenburg, Sweden.
Max NieuwdorpDepartment of Internal and Vascular Medicine, Amsterdam University Medical Centres, Amsterdam, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveBariatric surgery improves glucose metabolism. Recent data suggest that faecal microbiota transplantation (FMT) using faeces from postbariatric surgery diet-induced obese mice in germ-free mice improves glucose metabolism and intestinal homeostasis. We here investigated whether allogenic FMT using faeces from post-Roux-en-Y gastric bypass donors (RYGB-D) compared with using faeces from metabolic syndrome donors (METS-D) has short-term effects on glucose metabolism, intestinal transit time and adipose tissue inflammation in treatment-naïve, obese, insulin-resistant male subjects.

designSubjects with metabolic syndrome (n=22) received allogenic FMT either from RYGB-D or METS-D. Hepatic and peripheral insulin sensitivity as well as lipolysis were measured at baseline and 2 weeks after FMT by hyperinsulinaemic euglycaemic stable isotope (

resultsWe observed a significant decrease in insulin sensitivity 2 weeks after allogenic METS-D FMT (median rate of glucose disappearance: from 40.6 to 34.0 µmol/kg/min; p<0.01). Moreover, a trend (p=0.052) towards faster intestinal transit time following RYGB-D FMT was seen. Finally, we observed changes in faecal bile acids (increased lithocholic, deoxycholic and (iso)lithocholic acid after METS-D FMT), inflammatory markers (decreased adipose tissue chemokine ligand 2 (CCL2) gene expression and plasma CCL2 after RYGB-D FMT) and changes in several intestinal microbiota taxa.

conclusionAllogenic FMT using METS-D decreases insulin sensitivity in metabolic syndrome recipients when compared with using post-RYGB-D. Further research is needed to delineate the role of donor characteristics in FMT efficacy in human insulin-resistant subjects. TRIAL REGISTRATION NUMBER: NTR4327.

Indexed as

Fecal Microbiota TransplantationGastric BypassInsulin ResistanceAdultAgedBile Acids and SaltsChemokine CCL2Energy MetabolismFatty Acids, VolatileFecesGastrointestinal MicrobiomeGastrointestinal TransitGene ExpressionGlucoseHumansLipolysisBile Acids and SaltsCCL2 protein, humanChemokine CCL2Fatty Acids, VolatileGlucosebile acid metabolismdiabetes mellitusgastrointestinal transitintestinal microbiology

Identifiers

PMID31147381
PMCPMC7034343

What OpenQuestion holds

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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.