Evidence map›Paper›PMID 37235137›Full record

ArticleJHEP reports : innovation in hepatology2023

Genetic variants in HFE are associated with non-alcoholic fatty liver disease in lean individuals.

Zewen Sun, Xingchen Pan, Aowen Tian, Ida Surakka, Tao Wang, Xu Jiao, Shanshan He, Jinfang Song, Xin Tian, Dan Tong and 4 more

Open access · goldAbstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD.bioRxiv : the preprint server for biology · 2026
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  3. [Research progress on clinical characteristics and pathological mechanisms of lean metabolic-associated fatty liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
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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

14 authors at 4 institutions in 2 countries.

Zewen SunDepartment of Genetics, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Xingchen PanDepartment of Molecular Biology, College of Basic Medical Sciences, Jilin University, Changchun, China.
Aowen TianDepartment of Pathology, College of Basic Medical Sciences, Jilin University, Changchun, China.
Ida SurakkaDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Tao WangSoftware College of Jilin University, Changchun, China.
Xu JiaoSoftware College of Jilin University, Changchun, China.
Shanshan HeSoftware College of Jilin University, Changchun, China.
Jinfang SongDepartment of Pediatrics, The Second Hospital of Jilin University, Changchun, China.
Xin TianDepartment of Pediatrics, The Second Hospital of Jilin University, Changchun, China.
Dan TongDepartment of Radiology, The First Hospital of Jilin University, Changchun, China.
Jianping WenDepartment of Genetics, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Yonggang ZhangThe Key Laboratory of Symbol Computation and Knowledge Engineering of Ministry of Education, Jilin University, Changchun, China.
Wanqing LiuDepartment of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, MI, USA.
Peng ChenDepartment of Genetics, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China.
Jilin University · CNSecond Affiliated Hospital of Jilin University · CNEugene Applebaum College of Pharmacy and Health Sciences · USUniversity of Michigan · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Aims: Around 20% of patients with non-alcoholic fatty liver disease (NAFLD) are lean. Increasing evidence suggests that lean NAFLD is a unique subtype of the disease. We aimed to explore the metabolic profile, genetic basis, causal risk factors, and clinical sequelae underlying lean NAFLD. Methods: NAFLD was diagnosed by whole liver proton density fat fraction ≥5%. Whole liver proton density fat fraction and hepatic iron were quantified using magnetic resonance imaging in the UK Biobank. Individuals in this study were stratified according to the World Health Organization criteria of obesity, into lean, overweight, and obese. Mediation analysis, Mendelian randomisation analysis, and Bayesian networks were used to identify a risk factor or a clinical sequela of lean/obese NAFLD. Results: Lean NAFLD manifested a distinct metabolic profile, featured by elevated hepatic iron and fasting glucose. Four loci, namely, Conclusions: Our study suggested that Impact and implications: Lean NAFLD has a distinct natural history from obese NAFLD. This study underscored liver iron content and the genetic variant of the iron homoeostasis gene HFE as major risks of lean NAFLD, in addition to the unique metabolic profile. The development of type 2 diabetes or liver cirrhosis shall be closely monitored and prevented in patients with lean NAFLD.

Indexed as

BMIGenome-wide association studyHepatic ironMagnetic resonance imagingNon-alcoholic fatty liver disease

Identifiers

PMID37235137
PMCPMC10206181
OpenAlexW4360998805

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.