Evidence map›Paper›PMID 27899042›Full record

ArticleInternational journal of food sciences and nutrition2017

Hepatic rhythmicity of endoplasmic reticulum stress is disrupted in perinatal and adult mice models of high-fat diet-induced obesity.

Junpei Soeda, Paul Cordero, Jiawei Li, Angelina Mouralidarane, Esra Asilmaz, Shuvra Ray, Vi Nguyen, Rebeca Carter, Marco Novelli, Manlio Vinciguerra and 3 more

Open access · hybridAbstract read
In one paragraph

Article in International journal of food sciences and nutrition, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 28 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 4 institutions in 3 countries.

Junpei Soedaa Institute for Liver and Digestive Health, University College London , London , UK.
Paul Corderoa Institute for Liver and Digestive Health, University College London , London , UK.
Jiawei Lia Institute for Liver and Digestive Health, University College London , London , UK.
Angelina Mouralidaranea Institute for Liver and Digestive Health, University College London , London , UK.
Esra Asilmaza Institute for Liver and Digestive Health, University College London , London , UK.
Shuvra Raya Institute for Liver and Digestive Health, University College London , London , UK.
Vi Nguyena Institute for Liver and Digestive Health, University College London , London , UK.
Rebeca Cartera Institute for Liver and Digestive Health, University College London , London , UK.
Marco Novellib Department of Pathology , University College London , London , UK.
Manlio Vinciguerraa Institute for Liver and Digestive Health, University College London , London , UK.
Lucilla Postone Division of Women's Health , King's College London , London , UK.
Paul D Taylore Division of Women's Health , King's College London , London , UK.
Jude A Obena Institute for Liver and Digestive Health, University College London , London , UK.
University College London · GBKing's College London · GBGuy's and St Thomas' NHS Foundation Trust · GBInternational Clinical Research Center, St. Anne's University Hospital Brno · CZ

Funding

Biotechnology and Biological Sciences Research Council BB/H008845/1Wellcome Trust
6 · The paper itself

Abstract

We investigated the regulation of hepatic ER stress in healthy liver and adult or perinatally programmed diet-induced non-alcoholic fatty liver disease (NAFLD). Female mice were fed either obesogenic or control diet before mating, during pregnancy and lactation. Post-weaning, offspring from each maternal group were divided into either obesogenic or control diet. At six months, offspring were sacrificed at 4-h intervals over 24 h. Offspring fed obesogenic diets developed NAFLD phenotype, and the combination of maternal and offspring obesogenic diets exacerbated this phenotype. UPR signalling pathways (IREα, PERK, ATF6) and their downstream regulators showed different basal rhythmicity, which was modified in offspring exposed to obesogenic diet and maternal programming. The double obesogenic hit increased liver apoptosis measured by TUNEL staining, active caspase-3 and phospho-JNK and GRP78 promoter methylation levels. This study demonstrates that hepatic UPR is rhythmically activated. The combination of maternal obesity (MO) and obesogenic diets in offspring triggered altered UPR rhythmicity, DNA methylation and cellular apoptosis.

Indexed as

Animal FeedAnimalsDiet, High-FatEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPFemaleHomeostasisLiverMiceMice, Inbred C57BLObesityPregnancyPrenatal Exposure Delayed EffectsStress, PhysiologicalEndoplasmic Reticulum Chaperone BiPcircadian rhythmdevelopmental programmingER stressNAFLDObesity

Identifiers

PMID27899042
PMCPMC5399811
OpenAlexW2557479424

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.