Evidence map›Paper›PMID 29506485›Full record

ArticleBMC genomics2018

Transcriptional profiling of liver in riboflavin-deficient chicken embryos explains impaired lipid utilization, energy depletion, massive hemorrhaging, and delayed feathering.

Larry A Cogburn, Danielle N Smarsh, Xiaofei Wang, Nares Trakooljul, Wilfrid Carré, Harold B White

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

Article in BMC genomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 37 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

6 authors at 3 institutions in 3 countries.

Larry A CogburnDepartment of Animal and Food Sciences, University of Delaware, Newark, DE, 19716, USA. cogburn@udel.edu.
Danielle N SmarshDepartment of Animal and Food Sciences, University of Delaware, Newark, DE, 19716, USA.
Xiaofei WangDepartment of Animal and Food Sciences, University of Delaware, Newark, DE, 19716, USA.
Nares TrakooljulDepartment of Animal and Food Sciences, University of Delaware, Newark, DE, 19716, USA.
Wilfrid CarréDepartment of Animal and Food Sciences, University of Delaware, Newark, DE, 19716, USA.
Harold B WhiteDepartment of Chemistry and Biochemistry, University of Delaware, Newark, DE, 19716, USA.
University of Delaware · USResearch Institute for Farm Animal Biology (FBN) · DETennessee State University · US

Funding

USDA-National Research Initiative (NRI) 2005-35206-15288U.S. Department of Agriculture (USDA)-Initiative for Future Agriculture and Food Systems (IFAFS) 00-52100-9614
6 · The paper itself

Abstract

backgroundA strain of Leghorn chickens (rd/rd), unable to produce a functional riboflavin-binding protein, lays riboflavin-deficient eggs, in which all embryos suddenly die at mid-incubation (days 13-15). This malady, caused by riboflavin deficiency, leads to excessive lipid accumulation in liver, impaired β-oxidation of lipid, and severe hypoglycemia prior to death. We have used high-density chicken microarrays for time-course transcriptional scans of liver in chicken embryos between days 9-15 during this riboflavin-deficiency-induced metabolic catastrophe. For comparison, half of rd/rd embryos (n = 16) were rescued from this calamity by injection of riboflavin just prior to incubation of fertile eggs from rd/rd hens.

resultsNo significant differences were found between hepatic transcriptomes of riboflavin-deficient and riboflavin-rescued embryos at the first two ages (days 9 and 11). Overall, we found a 3.2-fold increase in the number of differentially expressed hepatic genes between day 13 (231 genes) and day 15 (734 genes). Higher expression of genes encoding the chicken flavoproteome was more evident in rescued- (15 genes) than in deficient-embryos (4 genes) at day 15. Diminished activity of flavin-dependent enzymes in riboflavin-deficient embryos blocks catabolism of yolk lipids, which normally serves as the predominant source of energy required for embryonic development.

conclusionsRiboflavin deficiency in mid-stage embryos leads to reduced expression of numerous genes controlling critical functions, including β-oxidation of lipids, blood coagulation and feathering. Surprisingly, reduced expression of feather keratin 1 was found in liver of riboflavin-deficient embryos at e15, which could be related to their delayed feathering and sparse clubbed down. A large number of genes are expressed at higher levels in liver of riboflavin-deficient embryos; these up-regulated genes control lipid storage/transport, gluconeogenesis, ketogenesis, protein catabolism/ubiquitination and cell death.

Indexed as

ChickensAnimalsChick EmbryoEnergy MetabolismFeathersHemorrhageLipidsLiverPoultry DiseasesRiboflavinRiboflavin DeficiencyLipidsRiboflavinAcetyl CoA deficiencyChicken flavoproteomeCoagulation factorsExpression profilingFeather keratinImpaired lipid metabolismMicroarray analysisProtease inhibitorsProtein catabolismRiboflavin deficiencySudden embryonic deathβ-oxidation

Identifiers

PMID29506485
PMCPMC5836443
OpenAlexW2796952035

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LicenceCC BY
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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.