Evidence map›Paper›PMID 40163211›Full record

ArticleBiological trace element research2025

The Combined Effect Between SEPS1 Genetic Polymorphisms and Exposure to Metals on the Risk of Gestational Diabetes Mellitus.

Weiwei Wu, Yulin Li, Weixuan Hu, Jing Zhao, Bole Zhang, Yongliang Feng, Yawei Zhang, Suping Wang

Abstract read
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In one paragraph

Article in Biological trace element research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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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

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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

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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

8 authors.

Weiwei Wu *Department of Epidemiology, School of Public Health, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, 56 Xinjian South Road, Shanxi, 030001, China. weiwei.wu@sxmu.edu.cn.
Yulin Li *Department of Epidemiology, School of Public Health, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, 56 Xinjian South Road, Shanxi, 030001, China.
Weixuan Hu *Department of Epidemiology, School of Public Health, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, 56 Xinjian South Road, Shanxi, 030001, China.
Jing ZhaoDepartment of Epidemiology, School of Public Health, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, 56 Xinjian South Road, Shanxi, 030001, China.
Bole ZhangDepartment of Epidemiology, School of Public Health, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, 56 Xinjian South Road, Shanxi, 030001, China.
Yongliang FengDepartment of Epidemiology, School of Public Health, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, 56 Xinjian South Road, Shanxi, 030001, China.
Yawei ZhangNational Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100021, China.
Suping WangDepartment of Epidemiology, School of Public Health, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention, Shanxi Medical University, 56 Xinjian South Road, Shanxi, 030001, China.

Funding

Fund Program for the Scientific Activities of Selected Returned Overseas Professionals in Shanxi Province 20210042National Natural Science Foundation of China 82373677Natural Science Foundation of Shanxi Province of China 202103021224229Research Project Supported by Shanxi Scholarship Council of China 2023-099
6 · The paper itself

Abstract

Environmental metal exposure is a key risk factor for gestational diabetes mellitus (GDM), but the mechanisms remain unclear. The traditional view holds that excessive accumulation of metals directly damages the islets to induce GDM. Recent studies suggest that supplementing with trace elements can alleviate insulin resistance by reducing endoplasmic reticulum stress, indicating that endoplasmic reticulum stress might have a comparable impact in metal-induced GDM. Selenoprotein S (SEPS1), a key regulator of endoplasmic reticulum function, may play a role. This study aims to investigate the interaction between the genetic predisposition of the SEPS1 gene and exposure to metals on GDM from the perspective of endoplasmic reticulum stress. A total of 278 pregnant women with GDM and 278 matched pregnant women without GDM were recruited. Maternal blood samples were collected before delivery to genotype the SEPS1 gene and measure metal levels. We found that rs28533324 and rs894317 were associated with the risk of GDM. The level of chromium (Cr) Q3 in maternal blood increased the risk of GDM, and the level of nickel (Ni) Q4 decreased the risk of GDM. Furthermore, the Q3 and Q4 Cr exhibit a multiplicative interaction with rs894317 in both the codominant and dominant models, and a multiplicative interaction between the Cr Q3 and rs894317 is also observed in the allele model. We found a novel link between SEPS1 gene variation and GDM, with these associations potentially being modified by Cr exposure. Our findings provide new etiological insights into GDM induced by Cr through endoplasmic reticulum stress.

Indexed as

Diabetes, GestationalMembrane ProteinsPolymorphism, Single NucleotideSelenoproteinsAdultEndoplasmic Reticulum StressFemaleGenetic Predisposition to DiseaseHumansPregnancyRisk FactorsMembrane ProteinsSelenoproteinsSELENOS protein, humanEndoplasmic reticulum stressGestational diabetes mellitusMetallic elementsSelenoprotein S

Identifiers

PMID40163211

What Socratic holds

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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 Socratic graph.