Evidence map›Paper›PMID 27681875›Full record

ArticlePloS one

Neuropeptide Y Overexpressing Female and Male Mice Show Divergent Metabolic but Not Gut Microbial Responses to Prenatal Metformin Exposure.

Henriikka Salomäki-Myftari, Laura H Vähätalo, Liisa Ailanen, Sami Pietilä, Asta Laiho, Arno Hänninen, Juha-Pekka Pursiheimo, Eveliina Munukka, Anniina Rintala, Eriika Savontaus and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
1.2field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 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

12 authors at 2 institutions in 1 country.

Henriikka Salomäki-MyftariInstitute of Biomedicine, Department of Pharmacology, Drug Development and Therapeutics, University of Turku, Turku, Finland.
Laura H VähätaloInstitute of Biomedicine, Department of Pharmacology, Drug Development and Therapeutics, University of Turku, Turku, Finland.
Liisa AilanenInstitute of Biomedicine, Department of Pharmacology, Drug Development and Therapeutics, University of Turku, Turku, Finland.
Sami PietiläBioinformatics Unit, Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.
Asta LaihoBioinformatics Unit, Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.
Arno HänninenInstitute of Biomedicine, Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland.
Juha-Pekka PursiheimoTurku Clinical Sequencing Laboratory, Institute of Biomedicine, University of Turku, Turku, Finland.
Eveliina MunukkaInstitute of Biomedicine, Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland.
Anniina RintalaInstitute of Biomedicine, Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland.
Eriika SavontausInstitute of Biomedicine, Department of Pharmacology, Drug Development and Therapeutics, University of Turku, Turku, Finland.
Ullamari PesonenInstitute of Biomedicine, Department of Pharmacology, Drug Development and Therapeutics, University of Turku, Turku, Finland.
Markku KouluInstitute of Biomedicine, Department of Pharmacology, Drug Development and Therapeutics, University of Turku, Turku, Finland.
University of Turku · FIÅbo Akademi University · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrenatal metformin exposure has been shown to improve the metabolic outcome in the offspring of high fat diet fed dams. However, if this is evident also in a genetic model of obesity and whether gut microbiota has a role, is not known.

methodsThe metabolic effects of prenatal metformin exposure were investigated in a genetic model of obesity, mice overexpressing neuropeptide Y in the sympathetic nervous system and in brain noradrenergic neurons (OE-NPYDβH). Metformin was given for 18 days to the mated female mice. Body weight, body composition, glucose tolerance and serum parameters of the offspring were investigated on regular diet from weaning and sequentially on western diet (at the age of 5-7 months). Gut microbiota composition was analysed by 16S rRNA sequencing at 10-11 weeks.

resultsIn the male offspring, metformin exposure inhibited weight gain. Moreover, weight of white fat depots and serum insulin and lipids tended to be lower at 7 months. In contrast, in the female offspring, metformin exposure impaired glucose tolerance at 3 months, and subsequently increased body weight gain, fat mass and serum cholesterol. In the gut microbiota, a decline in Erysipelotrichaceae and Odoribacter was detected in the metformin exposed offspring. Furthermore, the abundance of Sutterella tended to be decreased and Parabacteroides increased. Gut microbiota composition of the metformin exposed male offspring correlated to their metabolic phenotype.

conclusionPrenatal metformin exposure caused divergent metabolic phenotypes in the female and male offspring. Nevertheless, gut microbiota of metformin exposed offspring was similarly modified in both genders.

Identifiers

PMID27681875
PMCPMC5040270
OpenAlexW2524638639

What OpenQuestion holds

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LicenceCC BY
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.