Evidence map›Paper›PMID 29320745›Full record

ArticleCell reports2018

The Foxo1-Inducible Transcriptional Repressor Zfp125 Causes Hepatic Steatosis and Hypercholesterolemia.

Gustavo W Fernandes, Barbara M L C Bocco, Tatiana L Fonseca, Elizabeth A McAninch, Sungro Jo, Lattoya J Lartey, InSug O-Sullivan, Terry G Unterman, Nailliw Z Preite, Robin M Voigt and 8 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
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  7. Review
  8. Article
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  11. Article
  12. Article
  13. Frontiers in endocrinology · 2020
    Article
  14. Apolipoprotein C1: Its Pleiotropic Effects in Lipid Metabolism and Beyond.International journal of molecular sciences · 2019
    Review
  15. Thyroid Hormone and Alcoholic Fatty Liver: The Developmental Input.Alcoholism, clinical and experimental research · 2019
    Article
  16. Review
  17. Article
  18. Review
  19. Review
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

18 authors at 5 institutions in 3 countries.

Gustavo W FernandesDivision of Endocrinology and Metabolism, Rush University Medical Center, Chicago, IL; Program in Translational Medicine, Federal University of Sao Paulo, Sao Paulo, Brazil.
Barbara M L C BoccoDivision of Endocrinology and Metabolism, Rush University Medical Center, Chicago, IL; Program in Translational Medicine, Federal University of Sao Paulo, Sao Paulo, Brazil.
Tatiana L FonsecaDivision of Endocrinology and Metabolism, Rush University Medical Center, Chicago, IL.
Elizabeth A McAninchDivision of Endocrinology and Metabolism, Rush University Medical Center, Chicago, IL.
Sungro JoDivision of Endocrinology and Metabolism, Rush University Medical Center, Chicago, IL.
Lattoya J LarteyDivision of Endocrinology and Metabolism, Rush University Medical Center, Chicago, IL.
InSug O-SullivanSection of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Illinois at Chicago College of Medicine, Chicago, IL.
Terry G UntermanSection of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Illinois at Chicago College of Medicine, Chicago, IL.
Nailliw Z PreiteDivision of Digestive Diseases and Nutrition, Rush University Medical Center, Chicago, IL.
Robin M VoigtDivision of Digestive Diseases and Nutrition, Rush University Medical Center, Chicago, IL.
Christopher B ForsythDivision of Digestive Diseases and Nutrition, Rush University Medical Center, Chicago, IL.
Ali KeshavarzianDivision of Digestive Diseases and Nutrition, Rush University Medical Center, Chicago, IL.
Richárd SinkóDepartment of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
Allison B GoldfineJoslin Diabetes Center, Harvard Medical School, Boston, MA.
Mary E PattiJoslin Diabetes Center, Harvard Medical School, Boston, MA.
Miriam O RibeiroDevelopmental Disorders Program, Center of Biological Science and Health, Mackenzie Presbyterian University, Sao Paulo, Brazil.
Balázs GerebenDepartment of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
Antonio C BiancoDivision of Endocrinology and Metabolism, Rush University Medical Center, Chicago, IL. Electronic address: abianco@deiodinase.org.
Rush University Medical Center · USHarvard University · USHUN-REN Institute of Experimental Medicine · HUUniversity of Illinois Chicago · USUniversidade Presbiteriana Mackenzie · BR

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI LAURIE J GOODYEAR · 1986 to 2026
$50.5M
SELENODEIODINAS PROCESSING BY THE PROTEASOME SYSTEMR01DK058538 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BIANCO, ANTONIO C, GEREBEN, BALÁZS · 2001 to 2024
$6.0M
Metabolic and Xenobiotic Control of Thyroid Hormone MetabolismR01DK077148 · NIDDK · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ANTONIO C BIANCO · 2007 to 2026
$4.5M
Thyroid-adrenergic synergism and adaptive thermogenesisR01DK065055 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BIANCO, ANTONIO C · 2005 to 2021
$4.4M
Paternal Contributions to Metabolic Disease in Offspring: Environment, Epigenetics, and SpermR01DK106193 · NIDDK · JOSLIN DIABETES CENTER · PI PATTI, MARY E · 2016 to 2024
$4.3M
Regulation of Hepatic Gene Expression and Metabolism by FoxO ProteinsI01BX001968 · VA · JESSE BROWN VA MEDICAL CENTER · PI UNTERMAN, TERRY G. · 2013 to 2023
–
BLRD VA I01 BX001968NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R01 DK058538NIDDK NIH HHS R01 DK065055NIDDK NIH HHS R01 DK077148NIDDK NIH HHS R01 DK106193
6 · The paper itself

Abstract

Liver-specific disruption of the type 2 deiodinase gene (Alb-D2KO) results in resistance to both diet-induced obesity and liver steatosis in mice. Here, we report that this is explained by an ∼60% reduction in liver zinc-finger protein-125 (Zfp125) expression. Zfp125 is a Foxo1-inducible transcriptional repressor that causes lipid accumulation in the AML12 mouse hepatic cell line and liver steatosis in mice by reducing liver secretion of triglycerides and hepatocyte efflux of cholesterol. Zfp125 acts by repressing 18 genes involved in lipoprotein structure, lipid binding, and transport. The ApoE promoter contains a functional Zfp125-binding element that is also present in 17 other lipid-related genes repressed by Zfp125. While liver-specific knockdown of Zfp125 causes an "Alb-D2KO-like" metabolic phenotype, liver-specific normalization of Zfp125 expression in Alb-D2KO mice rescues the phenotype, restoring normal susceptibility to diet-induced obesity, liver steatosis, and hypercholesterolemia.

Indexed as

AnimalsDNA-Binding ProteinsFatty LiverForkhead Box Protein O1HypercholesterolemiaMiceDNA-Binding ProteinsForkhead Box Protein O1Foxo1 protein, mouseZfp125 protein, mousecholesteroldeiodinasehepatocytesliversteatosistranscriptional repressortriglycerideszinc finger protein 125

Identifiers

PMID29320745
PMCPMC6474669
OpenAlexW2784313606

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.