Evidence map›Paper›PMID 40427382›Full record

ArticleAntioxidants (Basel, Switzerland)2025

Allantoin Serves as a Novel Risk Factor for the Progression of MASLD.

Weiqiang Lv, Xueqiang Wang, Zhaode Feng, Cunxiao Sun, Hansen Wu, Mengqi Zeng, Tianlin Gao, Ke Cao, Jie Xu, Xuan Zou and 6 more

Abstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

16 authors.

Weiqiang LvCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Xueqiang WangSchool of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao 266100, China.
Zhaode FengCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Cunxiao SunFrontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Hansen WuFrontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Mengqi ZengSchool of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao 266100, China.
Tianlin GaoSchool of Public Health, Qingdao University, Qingdao 266071, China.
Ke CaoCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.ORCID 0009-0005-4142-8550
Jie XuCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Xuan ZouDepartment of Geriatrics Cardiology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
Tielin YangBiomedical Informatics & Genomics Center, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Hao LiCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Lei ChenSchool of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao 266100, China.
Jiankang LiuCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.ORCID 0000-0003-1207-5037
Shanshan DongBiomedical Informatics & Genomics Center, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Zhihui FengFrontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.ORCID 0000-0002-2448-6565

Funding

National Natural Science Foundation of China 32071154, 32271184, 32350025 to Z.F.; 82100918 to X.Z.; 32300654 to X.W.; 32300976 to M.Z.; 82300902 to J.X.; 82271727 to K.C.; 82300951 to H.L.; and 32171102, 92249303 to J.LOpening Research Fund from Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University 2023LHM-KFKT001Shandong Provincial Natural Foundation ZR2023JQ011, Z.FUK Biobank resource under application 46387
6 · The paper itself

Abstract

Uric acid (UA), traditionally recognized as an extracellular antioxidant, exhibits paradoxical associations with metabolic disorders such as metabolic dysfunction-associated steatotic liver disease (MASLD), though its mechanistic contributions remain elusive. Here, we integrate multi-modal evidence to explore the role of UA and its oxidative metabolite, allantoin, in MASLD progression. Analysis of UK Biobank data revealed a strong association between elevated UA levels and increased risks of MASLD and type 2 diabetes (T2D). However, Mendelian randomization analysis of over 2 million samples demonstrated causal effects of urate solely on serum triglycerides and T2D risk. Targeted metabolomics in an elderly Chinese cohort identified allantoin, an oxidative by-product of UA, significantly elevated in individuals with dyslipidemia or T2D, with serum allantoin levels positively correlated with fasting glucose, triglycerides, and cholesterol. Animal studies indicated that allantoin exacerbates hepatic lipid accumulation and glucose intolerance in high-fat diet mice, driven by increased hepatic lipid biogenesis and reduced bile acid production. Notably, further research revealed a strong binding affinity of allantoin for PPARα, leading to the suppression of PPARα activity, which promotes the progression of MASLD. These findings underscore the critical role of allantoin, rather than UA, as a critical driver of MASLD development, offering valuable insights for the prediction and management of hepatic metabolic disorders.

Indexed as

allantoinMASLDmendelian randomizationPPARαuric acid

Identifiers

PMID40427382
PMCPMC12108491

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.