Evidence map›Paper›PMID 37400922›Full record

ArticleEuropean journal of medical research2023

Association between leptin and NAFLD: a two-sample Mendelian randomization study.

Ziwei Guo, Hongbo Du, Yi Guo, Qian Jin, Ruijia Liu, Zhangjun Yun, Jiaxin Zhang, Xiaoke Li, Yong'an Ye

Open access · goldAbstract read
In one paragraph

Article in European journal of medical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.6field-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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Research Progress on Leptin in Metabolic Dysfunction-associated Fatty Liver Disease.Journal of clinical and translational hepatology · 2025
    Review
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  13. Observational
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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

9 authors at 2 institutions in 1 country.

Ziwei GuoDongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, China.
Hongbo DuDongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, China.
Yi GuoDongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, China.
Qian JinDongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, China.
Ruijia LiuDongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, China.
Zhangjun YunDongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, China.
Jiaxin ZhangDongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, China. happyjiaxin@bucm.edu.cn.
Xiaoke LiDongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, China. lixiaoke@vip.163.com.
Yong'an YeDongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, 100700, China. yeyongan@vip.163.com.
Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine · CNBeijing University of Chinese Medicine · CN

Funding

Xiaoke Li 82174341
6 · The paper itself

Abstract

backgroundThe etiology of nonalcoholic fatty liver disease (NAFLD) involves a complex interaction of genetic and environmental factors. Previous observational studies have revealed that higher leptin levels are related to a lower risk of developing NAFLD, but the causative association remains unknown. We intended to study the causal effect between leptin and NAFLD using the Mendelian randomization (MR) study.

methodsWe performed a two-sample Mendelian randomization (TSMR) analysis using summary GWAS data from leptin (up to 50,321 individuals) and NAFLD (8,434 cases and 770,180 controls) in a European population. Instrumental variables (IVs) that satisfied the three core assumptions of Mendelian randomization were selected. The TSMR analysis was conducted using the inverse variance weighted (IVW) method, MR-Egger regression method, and weighted median (WM) method. To ensure the accuracy and stability of the study results, heterogeneity tests, multiple validity tests, and sensitivity analyses were conducted.

resultsThe findings of the TSMR correlation analysis between NAFLD and leptin were as follows: IVW method (odds ratio (OR) 0.6729; 95% confidence interval (95% CI) 0.4907-0.9235; P = 0.0142), WM method (OR 0.6549; 95% CI 0.4373-0.9806; P = 0.0399), and MR-Egger regression method (P = 0.6920). Additionally, the findings of the TSMR correlation analysis between NAFLD and circulating leptin levels adjusted for body mass index (BMI) were as follows: IVW method (OR 0.5876; 95% CI 0.3781-0.9134; P = 0.0181), WM method (OR 0.6074; 95% CI 0.4231-0.8721; P = 0.0069), and MR-Egger regression method (P = 0.8870). It has also been shown that higher levels of leptin are causally linked to a lower risk of developing NAFLD, suggesting that leptin may serve as a protective factor for NAFLD.

conclusionsUsing TSMR analysis and the GWAS database, we investigated the genetic relationship between elevated leptin levels and lowered risk of NAFLD in this study. However, further research is required to understand the underlying mechanisms.

Indexed as

LeptinNon-alcoholic Fatty Liver DiseaseBody Mass IndexHumansMendelian Randomization AnalysisPolymorphism, Single NucleotideLeptinCausal effectLeptinNonalcoholic fatty liver diseaseTwo-sample Mendelian randomization

Identifiers

PMID37400922
PMCPMC10316638
OpenAlexW4382939517

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.