Evidence map›Paper›PMID 30532187›Full record

ArticlePLoS biology2018

Insulin signaling and reduced glucocorticoid receptor activity attenuate postprandial gene expression in liver.

Adrija Kalvisa, Majken S Siersbæk, Stine M Præstholm, Line J L Christensen, Ronni Nielsen, Oliver Stohr, Sabine Vettorazzi, Jan Tuckermann, Morris White, Susanne Mandrup and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 74 citations in OpenAlex.

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  19. An integrative transcriptional logic model of hepatic insulin resistance.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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

11 authors at 3 institutions in 3 countries.

Adrija KalvisaDepartment of Biochemistry and Molecular Biology, VILLUM Center for Bioanalytical Sciences, University of Southern Denmark, Odense, Denmark.
Majken S SiersbækDepartment of Biochemistry and Molecular Biology, VILLUM Center for Bioanalytical Sciences, University of Southern Denmark, Odense, Denmark.
Stine M PræstholmDepartment of Biochemistry and Molecular Biology, VILLUM Center for Bioanalytical Sciences, University of Southern Denmark, Odense, Denmark.
Line J L ChristensenDepartment of Biochemistry and Molecular Biology, VILLUM Center for Bioanalytical Sciences, University of Southern Denmark, Odense, Denmark.
Ronni NielsenDepartment of Biochemistry and Molecular Biology, VILLUM Center for Bioanalytical Sciences, University of Southern Denmark, Odense, Denmark.
Oliver StohrDivision of Endocrinology, Boston Children's Hospital, Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America.
Sabine VettorazziInstitute of Comparative Molecular Endocrinology, University of Ulm, Ulm, Germany.
Jan TuckermannInstitute of Comparative Molecular Endocrinology, University of Ulm, Ulm, Germany.
Morris WhiteDivision of Endocrinology, Boston Children's Hospital, Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America.
Susanne MandrupDepartment of Biochemistry and Molecular Biology, VILLUM Center for Bioanalytical Sciences, University of Southern Denmark, Odense, Denmark.
Lars GrøntvedDepartment of Biochemistry and Molecular Biology, VILLUM Center for Bioanalytical Sciences, University of Southern Denmark, Odense, Denmark.ORCID 0000-0002-6735-8483
University of Southern Denmark · DKBoston Children's Hospital · USUniversität Ulm · DE

Funding

Metabolic Crosstalk During Hepatic Insulin ResistanceR01DK098655 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI WHITE, MORRIS F. · 2013 to 2020
$4.0M
NIDDK NIH HHS R01 DK098655
6 · The paper itself

Abstract

Hepatic circadian gene transcription is tightly coupled to feeding behavior, which has a profound impact on metabolic disorders associated with diet-induced obesity. Here, we describe a genomics approach to uncover mechanisms controlling hepatic postprandial gene expression. Combined transcriptomic and cistromic analysis identified hundreds of circadian-regulated genes and enhancers controlled by feeding. Postprandial suppression of enhancer activity was associated with reduced glucocorticoid receptor (GR) and Forkhead box O1 (FOXO1) occupancy of chromatin correlating with reduced serum corticosterone levels and increased serum insulin levels. Despite substantial co-occupancy of feeding-regulated enhancers by GR and FOXO1, selective disruption of corticosteroid and/or insulin signaling resulted in dysregulation of specific postprandial regulated gene programs. In combination, these signaling pathways operate a major part of the genes suppressed by feeding. Importantly, the feeding response was disrupted in diet-induced obese animals, which was associated with dysregulation of several corticosteroid- and insulin-regulated genes, providing mechanistic insights to dysregulated circadian gene transcription associated with obesity.

Indexed as

AnimalsForkhead Transcription FactorsGene ExpressionGene Expression RegulationHepatocytesInsulinInsulin ResistanceLiverMaleMiceMice, Inbred C57BLObesityPostprandial PeriodReceptors, GlucocorticoidSignal TransductionForkhead Transcription FactorsInsulinReceptors, Glucocorticoid

Identifiers

PMID30532187
PMCPMC6301715
OpenAlexW2903870788

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.