Evidence map›Paper›PMID 25202246›Full record

ArticleFrontiers in behavioral neuroscience2014

Gender-dependent resiliency to stressful and metabolic challenges following prenatal exposure to high-fat diet in the p66(Shc-/-) mouse.

Veronica Bellisario, Alessandra Berry, Sara Capoccia, Carla Raggi, Pamela Panetta, Igor Branchi, Giovanni Piccaro, Marco Giorgio, Pier G Pelicci, Francesca Cirulli

Open access · goldAbstract read
In one paragraph

Article in Frontiers in behavioral neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 25% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  9. Nutrients · 2021
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  16. The effect of dietary fat on behavior in mice.Journal of diabetes and metabolic disorders · 2018
    Article
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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

10 authors at 2 institutions in 1 country.

Veronica BellisarioSection of Behavioral Neurosciences, Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità Rome, Italy.
Alessandra BerrySection of Behavioral Neurosciences, Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità Rome, Italy.
Sara CapocciaSection of Behavioral Neurosciences, Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità Rome, Italy.
Carla RaggiSection of Behavioral Neurosciences, Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità Rome, Italy.
Pamela PanettaSection of Behavioral Neurosciences, Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità Rome, Italy.
Igor BranchiSection of Behavioral Neurosciences, Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità Rome, Italy.
Giovanni PiccaroSection of Bacterial, Respiratory and Systemic Diseases, Department of Infectious, Parasitic and Immune-Mediated Diseases, Istituto Superiore di Sanità Rome, Italy.
Marco GiorgioDepartment of Experimental Oncology, European Institute of Oncology Milan, Italy.
Pier G PelicciDepartment of Experimental Oncology, European Institute of Oncology Milan, Italy.
Francesca CirulliSection of Behavioral Neurosciences, Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità Rome, Italy.
Istituto Superiore di Sanità · ITEuropean Institute of Oncology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic stressful challenges during susceptible time windows, such as fetal life, can have important implications for health throughout life. Deletion of the p66(Shc) gene in mice leads to reduced oxidative stress (OS), resulting in a healthy and lean phenotype characterized by increased metabolic rate, resistance to high-fat diet (HFD)-induced obesity and reduced emotionality at adulthood. Here we hypothesize that p66(Shc-/-) (KO) adult offspring might be protected from the detrimental effects induced by maternal HFD administered before and during pregnancy. To test such hypothesis, we fed p66(Shc+/+) (WT) and KO females with HFD for 13 weeks starting on 5 weeks of age until delivery and tested adult male and female offspring for their metabolic, neuroendocrine, and emotional profile. Prenatal diet affected stress responses and metabolic features in a gender-dependent fashion. In particular, prenatal HFD increased plasma leptin levels and decreased anxiety-like behavior in females, while increasing body weight, particularly in KO subjects. KO mice were overall characterized by metabolic resiliency, showing a blunted change in glycemia levels in response to glucose or insulin challenges. However, in p66(Shc-/-) mice, prenatal HFD affected glucose tolerance response in an opposite manner in the two genders, overriding the resilience in males and exacerbating it in females. Finally, KO females were protected from the disrupting effect of prenatal HFD on neuroendocrine response. These findings indicate that prenatal HFD alters the emotional profile and metabolic functionality of the adult individual in a gender-dependent fashion and suggest that exposure to high-caloric food during fetal life is a stressful condition interfering with the developmental programming of the adult phenotype. Deletion of the p66(Shc) gene attenuates such effects, acting as a protective factor.

Indexed as

adipokinesanimal modelsbiomarkersemotionalitygendermaternal obesityoxidative stressp66Shc gene

Identifiers

PMID25202246
PMCPMC4141279
OpenAlexW2067521078

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.