Evidence map›Paper›PMID 33033395›Full record

ArticleInternational journal of obesity (2005)2020

Supplementation with a prebiotic (polydextrose) in obese mouse pregnancy improves maternal glucose homeostasis and protects against offspring obesity.

Xanthi Maragkoudaki, Matthew Naylor, Georgia Papacleovoulou, Emilie Stolarczyk, Douglas Rees, Joaquim M Pombo, Shadi Abu-Hayyeh, Anja Czajka, Jane K Howard, Afshan N Malik and 3 more

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In one paragraph

Article in International journal of obesity (2005), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

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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

13 authors at 1 institution in 1 country.

Xanthi MaragkoudakiDepartment of Women and Children's Health, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Matthew NaylorDepartment of Women and Children's Health, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Georgia PapacleovoulouDepartment of Women and Children's Health, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Emilie StolarczykDepartment of Diabetes Research, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Douglas ReesDepartment of Women and Children's Health, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Joaquim M PomboDepartment of Women and Children's Health, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Shadi Abu-HayyehDepartment of Women and Children's Health, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Anja CzajkaDepartment of Diabetes Research, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Jane K HowardDepartment of Diabetes Research, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Afshan N MalikDepartment of Diabetes Research, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Catherine WilliamsonDepartment of Women and Children's Health, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Lucilla PostonDepartment of Women and Children's Health, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK.
Paul D TaylorDepartment of Women and Children's Health, School of Life Course Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK. Paul.taylor@kcl.ac.uk.ORCID http://orcid.org/0000-0002-4740-4307
King's College London · GB

Funding

Biotechnology and Biological Sciences Research Council BB/G017093/1Medical Research Council MR/K002996/1
6 · The paper itself

Abstract

objectivesWe hypothesised that maternal diet-induced-obesity has adverse consequences for offspring energy expenditure and susceptibility to obesity in adulthood, and that the prebiotic polydextrose (PDX) would prevent the consequences of programming by maternal obesity.

methodsFemale mice were fed a control (Con) or obesogenic diet (Ob) for 6 weeks prior to mating and throughout pregnancy and lactation. Half the obese dams were supplemented with 5% PDX (ObPDX) in drinking water throughout pregnancy and lactation. Offspring were weaned onto standard chow. At 3 and 6 months, offspring energy intake (EI) and energy expenditure (EE by indirect calorimetry) were measured, and a glucose-tolerance test performed. Offspring of control (OffCon), obese (OffOb) and PDX supplemented (OffObP) dams were subsequently challenged for 3 weeks with Ob, and energy balanced reassessed. Potential modifiers of offspring energy balance including gut microbiota and biomarkers of mitochondrial activity were also evaluated.

resultsSix-month-old male OffOb demonstrated increased bodyweight (BW, P < 0.001) and white adipose tissue mass (P < 0.05), decreased brown adipose tissue mass (BAT, P < 0.01), lower night-time EE (P < 0.001) versus OffCon, which were prevented in OffObP. Both male and female OffOb showed abnormal glucose-tolerance test (peak [Glucose] P < 0.001; AUC, P < 0.05) which was prevented by PDX. The Ob challenge resulted in greater BW gain in both male and female OffOb versus OffCon (P < 0.05), also associated with increased EI (P < 0.05) and reduced EE in females (P < 0.01). OffObP were protected from accelerated BW gain on the OB diet compared with controls, associated with increased night-time EE in both male (P < 0.05) and female OffObP (P < 0.001). PDX also prevented an increase in skeletal muscle mtDNA copy number in OffOb versus OffCon (P < 0.01) and increased the percentage of Bacteroides cells in faecal samples from male OffObP relative to controls.

conclusionsMaternal obesity adversely influences adult offspring energy balance and propensity for obesity, which is ameliorated by maternal PDX treatment with associated changes in gut microbiota composition and skeletal muscle mitochondrial function.

Indexed as

Prenatal Exposure Delayed EffectsAnimalsBody CompositionBody WeightDietEnergy IntakeEnergy MetabolismFemaleGastrointestinal MicrobiomeGlucansGlucoseGlucose Tolerance TestHomeostasisMaleMiceMice, Inbred C57BLGlucansGlucosepolydextrosePrebiotics

Identifiers

PMID33033395
OpenAlexW3092339164

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.