Evidence map›Paper›PMID 28859076›Full record

ArticlePloS one2017

Developmental programming of somatic growth, behavior and endocannabinoid metabolism by variation of early postnatal nutrition in a cross-fostering mouse model.

Felix Schreiner, Merle Ackermann, Michael Michalik, Eva Hucklenbruch-Rother, Andras Bilkei-Gorzo, Ildiko Racz, Laura Bindila, Beat Lutz, Jörg Dötsch, Andreas Zimmer and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. Article
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

11 authors at 4 institutions in 1 country.

Felix SchreinerPediatric Endocrinology Division, Children's Hospital, University of Bonn, Bonn, Germany.ORCID http://orcid.org/0000-0002-4216-2169
Merle AckermannPediatric Endocrinology Division, Children's Hospital, University of Bonn, Bonn, Germany.
Michael MichalikPediatric Endocrinology Division, Children's Hospital, University of Bonn, Bonn, Germany.
Eva Hucklenbruch-RotherDepartment of Pediatric and Adolescent Medicine, Medical Faculty, University of Cologne, Cologne, Germany.
Andras Bilkei-GorzoDepartment of Molecular Psychiatry, University Hospital Bonn, Bonn, Germany.
Ildiko RaczDepartment of Molecular Psychiatry, University Hospital Bonn, Bonn, Germany.
Laura BindilaInstitute for Physiological Chemistry, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Beat LutzInstitute for Physiological Chemistry, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Jörg DötschDepartment of Pediatric and Adolescent Medicine, Medical Faculty, University of Cologne, Cologne, Germany.
Andreas ZimmerDepartment of Molecular Psychiatry, University Hospital Bonn, Bonn, Germany.
Joachim WoelflePediatric Endocrinology Division, Children's Hospital, University of Bonn, Bonn, Germany.
University of Bonn · DEUniversity Hospital Bonn · DEJohannes Gutenberg University Mainz · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNutrient deprivation during early development has been associated with the predisposition to metabolic disorders in adulthood. Considering its interaction with metabolism, appetite and behavior, the endocannabinoid (eCB) system represents a promising target of developmental programming.

methodsBy cross-fostering and variation of litter size, early postnatal nutrition of CB6F1-hybrid mice was controlled during the lactation period (3, 6, or 10 pups/mother). After weaning and redistribution at P21, all pups received standard chow ad libitum. Gene expression analyses (liver, visceral fat, hypothalamus) were performed at P50, eCB concentrations were determined in liver and visceral fat. Locomotor activity and social behavior were analyzed by means of computer-assisted videotracking.

resultsBody growth was permanently altered, with differences for length, weight, body mass index and fat mass persisting beyond P100 (all 3>6>10,p<0.01). This was paralleled by differences in hepatic IGF-I expression (p<0.01). Distinct gene expression patterns for key enzymes of the eCB system were observed in fat (eCB-synthesis: 3>6>10 (DAGLα p<0.05; NAPE-PLD p = 0.05)) and liver (eCB-degradation: 3>6>10 (FAAH p<0.05; MGL p<0.01)). Concentrations of endocannabinoids AEA and 2-AG in liver and visceral fat were largely comparable, except for a borderline significance for higher AEA (liver, p = 0.049) in formerly overfed mice and, vice versa, tendencies (p<0.1) towards lower AEA (fat) and 2-AG (liver) in formerly underfed animals. In the arcuate nucleus, formerly underfed mice tended to express more eCB-receptor transcripts (CB1R p<0.05; CB2R p = 0.08) than their overfed fellows. Open-field social behavior testing revealed significant group differences, with formerly underfed mice turning out to be the most sociable animals (p<0.01). Locomotor activity did not differ.

conclusionOur data indicate a developmental plasticity of somatic growth, behavior and parameters of the eCB system, with long-lasting impact of early postnatal nutrition. Developmental programming of the eCB system in metabolically active tissues, as shown here for liver and fat, may play a role in the formation of the adult cardiometabolic risk profile following perinatal malnutrition in humans.

Indexed as

Nutritional StatusAnimalsBody WeightDisease Models, AnimalEndocannabinoidsFemaleGene ExpressionHumansHypothalamusInsulin-Like Growth Factor IIntra-Abdominal FatLiverMiceOvernutritionPregnancyEndocannabinoidsInsulin-Like Growth Factor I

Identifiers

PMID28859076
PMCPMC5578498
OpenAlexW2508517637

What OpenQuestion holds

Textmetadata
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.