Evidence map›Paper›PMID 30544931›Full record

ArticleCells2018

Metabolic Signature of Dietary Iron Overload in a Mouse Model.

Chiara Volani, Giuseppe Paglia, Sigurdur V Smarason, Peter P Pramstaller, Egon Demetz, Christa Pfeifhofer-Obermair, Guenter Weiss

Open access · goldAbstract read
In one paragraph

Article in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  4. Review
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  9. Review
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  14. Article
  15. Dietary Iron Overload andAntioxidants (Basel, Switzerland) · 2021
    Article
  16. Article
  17. Amniotic fluid metabolomic and lipidomic alterations associated with hemoglobin Bart's diseases.Metabolomics : Official journal of the Metabolomic Society · 2021
    Article
  18. EnvIRONmental Aspects in Myelodysplastic Syndrome.International journal of molecular sciences · 2021
    Review
  19. Article
  20. 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

7 authors at 2 institutions in 2 countries.

Chiara VolaniDepartment of Internal Medicine II, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria. chiara.volani@i-med.ac.at.ORCID 0000-0003-3600-4735
Giuseppe PagliaInstitute for Biomedicine, Eurac Research, Via Galvani 31, 39100 Bolzano, Italy. beppepaglia@gmail.com.ORCID 0000-0003-4724-6801
Sigurdur V SmarasonInstitute for Biomedicine, Eurac Research, Via Galvani 31, 39100 Bolzano, Italy. sigurdur.smarason@eurac.edu.
Peter P PramstallerInstitute for Biomedicine, Eurac Research, Via Galvani 31, 39100 Bolzano, Italy. Peter.pramstaller@eurac.edu.
Egon DemetzDepartment of Internal Medicine II, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria. Egon.demetz@i-med.ac.at.
Christa Pfeifhofer-ObermairDepartment of Internal Medicine II, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria. Christa.pfeifhofer@i-med.ac.at.
Guenter WeissDepartment of Internal Medicine II, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria. guenter.weiss@i-med.ac.at.ORCID 0000-0003-0709-2158
Eurac Research · ITInnsbruck Medical University · AT

Funding

Austrian Science Fund W-1253Transnational doctoral program BI-DOC between the Innsbruck Medical University, Austria and the Institute of Biomedicine, Eurac, in Bolzano, Italy BIDOC-EURAC
6 · The paper itself

Abstract

Iron is an essential co-factor for several metabolic processes, including the Krebs cycle and mitochondrial oxidative phosphorylation. Therefore, maintaining an appropriate iron balance is essential to ensure sufficient energy production and to avoid excessive reactive oxygen species formation. Iron overload impairs mitochondrial fitness; however, little is known about the associated metabolic changes. Here we aimed to characterize the metabolic signature triggered by dietary iron overload over time in a mouse model, where mice received either a standard or a high-iron diet. Metabolic profiling was assessed in blood, plasma and liver tissue. Peripheral blood was collected by means of volumetric absorptive microsampling (VAMS). Extracted blood and tissue metabolites were analyzed by liquid chromatography combined to high resolution mass spectrometry. Upon dietary iron loading we found increased glucose, aspartic acid and 2-/3-hydroxybutyric acid levels but low lactate and malate levels in peripheral blood and plasma, pointing to a re-programming of glucose homeostasis and the Krebs cycle. Further, iron loading resulted in the stimulation of the urea cycle in the liver. In addition, oxidative stress was enhanced in circulation and coincided with increased liver glutathione and systemic cysteine synthesis. Overall, iron supplementation affected several central metabolic circuits over time. Hence, in vivo investigation of metabolic signatures represents a novel and useful tool for getting deeper insights into iron-dependent regulatory circuits and for monitoring of patients with primary and secondary iron overload, and those ones receiving iron supplementation therapy.

Indexed as

glucoseironmetabolomicsmitochondriaoxidative stressurea cycleVAMS

Identifiers

PMID30544931
PMCPMC6315421
OpenAlexW2904992321

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.