Evidence map›Paper›PMID 28271632›Full record

ReviewIUBMB life2017

The role of insufficient copper in lipid synthesis and fatty-liver disease.

Austin Morrell, Savannah Tallino, Lei Yu, Jason L Burkhead

Open access · bronzeAbstract readReview
In one paragraph

Review in IUBMB life, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 3 pooled it
5.8field-weighted citation impact, top 3% 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

70 citing papers in PubMed, 3 syntheses or guidelines pooled it, 126 citations in OpenAlex.

  1. Pooled it
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  4. Article
  5. Cuproptosis and Diabetic Osteoporosis: Mechanisms and Therapeutic Prospects.International journal of molecular sciences · 2026
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10 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Austin MorrellDepartment of Biological Sciences Anchorage, University of Alaska Anchorage, Anchorage, Alaska.
Savannah TallinoDepartment of Biological Sciences Anchorage, University of Alaska Anchorage, Anchorage, Alaska.
Lei YuDepartment of Medicine, Division of Gastroenterology, University of Washington School of Medicine, Seattle, Washington.
Jason L BurkheadDepartment of Biological Sciences Anchorage, University of Alaska Anchorage, Anchorage, Alaska.ORCID 0000-0001-5457-311X
University of Alaska Anchorage · USUniversity of Washington · US

Funding

The Administrative CoreP20GM103395 · NIGMS · UNIVERSITY OF ALASKA FAIRBANKS · PI BRIAN M BARNES · 2012 to 2026
$66.1M
NIGMS NIH HHS P20 GM103395
6 · The paper itself

Abstract

The essential transition metal copper is important in lipid metabolism, redox balance, iron mobilization, and many other critical processes in eukaryotic organisms. Genetic diseases where copper homeostasis is disrupted, including Menkes disease and Wilson disease, indicate the importance of copper balance to human health. The severe consequences of insufficient copper supply are illustrated by Menkes disease, caused by mutation in the X-linked ATP7A gene encoding a protein that transports copper from intestinal epithelia into the bloodstream and across the blood-brain barrier. Inadequate copper supply to the body due to poor diet quality or malabsorption can disrupt several molecular level pathways and processes. Though much of the copper distribution machinery has been described and consequences of disrupted copper handling have been characterized in human disease as well as animal models, physiological consequences of sub-optimal copper due to poor nutrition or malabsorption have not been extensively studied. Recent work indicates that insufficient copper may be important in a number of common diseases including obesity, ischemic heart disease, and metabolic syndrome. Specifically, marginal copper deficiency (CuD) has been reported as a potential etiologic factor in diseases characterized by disrupted lipid metabolism such as non-alcoholic fatty-liver disease (NAFLD). In this review, we discuss the available data suggesting that a significant portion of the North American population may consume insufficient copper, the potential mechanisms by which CuD may promote lipid biosynthesis, and the interaction between CuD and dietary fructose in the etiology of NAFLD. © 2016 IUBMB Life, 69(4):263-270, 2017.

Indexed as

Adenosine TriphosphatasesBlood-Brain BarrierCation Transport ProteinsCopperCopper-Transporting ATPasesDietHumansIronLipid MetabolismLipidsLiverMenkes Kinky Hair SyndromeNon-alcoholic Fatty Liver DiseaseAdenosine TriphosphatasesATP7A protein, humanCation Transport ProteinsCopperCopper-Transporting ATPasesIronLipidscopper deficiencyfatty acid biosynthesisfructoseinflammationnon-alcoholic fatty-liver diseaseoxidative stress

Identifiers

PMID28271632
PMCPMC5619695
OpenAlexW2594684234

What OpenQuestion holds

Textmetadata
LicenceTDM
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.