Evidence map›Paper›PMID 29944391›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2018

ErbB4 deletion predisposes to development of metabolic syndrome in mice.

Fenghua Zeng, Yinqiu Wang, Lance A Kloepfer, Suwan Wang, Raymond C Harris

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 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
1.7field-weighted citation impact, top 16% 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, 56 citations in OpenAlex.

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  11. From fasting to fat reshaping: exploring the molecular pathways of intermittent fasting-induced adipose tissue remodeling.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024
    Review
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  17. Genetic variants ofFrontiers in endocrinology · 2023
    Article
  18. Article
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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

5 authors at 1 institution in 1 country.

Fenghua ZengDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center , Nashville, Tennessee.
Yinqiu WangDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center , Nashville, Tennessee.
Lance A KloepferDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center , Nashville, Tennessee.
Suwan WangDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center , Nashville, Tennessee.
Raymond C HarrisDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University Medical Center , Nashville, Tennessee.
Vanderbilt University Medical Center · US

Funding

Vanderbilt Institute for Clinical and Translational Research (VICTR) -Identifying correlates of functional immunity in SARS-CoV-2 convalescent plasmaUL1TR002243 · NCATS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Paul A. Harris, Wesley H Self · 2017 to 2026
$130.7M
The Role of renal macrophages in recovery from renal injuryR01DK095785 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 2013 to 2026
$6.7M
NCATS NIH HHS UL1 TR002243NIDDK NIH HHS R01 DK095785
6 · The paper itself

Abstract

ErbB4, a member of the EGF receptor family, plays a variety of roles in physiological and pathological states. Genetic studies have indicated a link between ErbB4 and type 2 diabetes and obesity, but its role in metabolic syndrome (MetS) has not been reported. In the current study we found that mice with ErbB4 deletion developed MetS after 24 wk on a medium-fat diet (MFD), as indicated by development of obesity, dyslipidemia, hepatic steatosis, hyperglycemia, hyperinsulinemia, and insulin resistance, compared with wild-type mice. ErbB4 deletion mice also exhibited increased amounts of subcutaneous and visceral fat, with increased serum leptin levels, compared with wild-type mice, whereas levels of adiponectin were not significantly different. Histologically, severe inflammation, indicated by F4/80 immunostaining and M1 macrophage polarization, was detected in inguinal and epididymal white adipose tissue in ErbB4 deletion mice. ErbB4 expression decreased during 3T3-L1 preadipocyte differentiation. Administration of neuroregulin 4, a specific ligand for ErbB4, to 3T3-L1 adipocytes had no effect on adipogenesis and lipolysis but significantly inhibited lipogenesis, promoted browning, induced GLUT4 redistribution to the cell membrane, and increased glucose uptake. Neuroregulin 4 also significantly increased glucose uptake in adipocytes isolated from wild-type mice, while these effects were significantly decreased in adipocytes isolated from ErbB4 deletion mice. In conclusion, our results indicate that ErbB4 may play an important role in glucose homeostasis and lipogenesis. ErbB4 deficiency-related obesity and adipose tissue inflammation may contribute to the development of MetS.

Indexed as

Dietary Fats3T3-L1 CellsAdipogenesisAdiponectinAdipose Tissue, WhiteAnimalsDyslipidemiasFatty LiverGene DeletionGenetic Predisposition to DiseaseGlucose Transporter Type 4HyperglycemiaHyperinsulinismInflammationInsulin ResistanceIntra-Abdominal FatAdiponectinDietary FatsErbb4 protein, mouseGlucose Transporter Type 4Leptinneuregulin-4NeuregulinsReceptor, ErbB-4Slc2a4 protein, mouseErbB4inflammationinsulin resistancelipogenesisneuregulin 4

Identifiers

PMID29944391
PMCPMC6230712
OpenAlexW2810036321

What OpenQuestion holds

Textmetadata
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.