Evidence map›Paper›PMID 39859525›Full record

ArticleInternational journal of molecular sciences2025

Subacute PM2.5 Exposure Induces Hepatic Insulin Resistance Through Inflammation and Oxidative Stress.

Yao Lu, Wenke Qiu, Ruiwei Liao, Wenjuan Cao, Feifei Huang, Xinyuan Wang, Ming Li, Yan Li

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
–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

17 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

8 authors.

Yao LuSchool of Basic Medical Sciences, Guangzhou University of Chinese Medicine, No. 232, East Waihuan Road, Guangzhou Higher Education Mega Centre, Panyu District, Guangzhou 510006, China.
Wenke QiuSchool of Basic Medical Sciences, Guangdong Pharmaceutical University, No. 280, East Waihuan Road, Guangzhou Higher Education Mega Centre, Panyu District, Guangzhou 510006, China.
Ruiwei LiaoSchool of Basic Medical Sciences, Guangzhou University of Chinese Medicine, No. 232, East Waihuan Road, Guangzhou Higher Education Mega Centre, Panyu District, Guangzhou 510006, China.
Wenjuan CaoSchool of Basic Medical Sciences, Guangdong Pharmaceutical University, No. 280, East Waihuan Road, Guangzhou Higher Education Mega Centre, Panyu District, Guangzhou 510006, China.
Feifei HuangSchool of Basic Medical Sciences, Guangdong Pharmaceutical University, No. 280, East Waihuan Road, Guangzhou Higher Education Mega Centre, Panyu District, Guangzhou 510006, China.
Xinyuan WangSchool of Basic Medical Sciences, Guangzhou University of Chinese Medicine, No. 232, East Waihuan Road, Guangzhou Higher Education Mega Centre, Panyu District, Guangzhou 510006, China.
Ming LiSchool of Basic Medical Sciences, Guangdong Pharmaceutical University, No. 280, East Waihuan Road, Guangzhou Higher Education Mega Centre, Panyu District, Guangzhou 510006, China.ORCID 0000-0001-9981-0270
Yan LiSchool of Basic Medical Sciences, Guangzhou University of Chinese Medicine, No. 232, East Waihuan Road, Guangzhou Higher Education Mega Centre, Panyu District, Guangzhou 510006, China.

Funding

Medical Scientific Research Foundation of Guangdong Province A2023404Science and Technology Special Project of Qingyuan 2021ZDZX001
6 · The paper itself

Abstract

Epidemiological studies prove that type II diabetes, characterized by insulin resistance (IR), may be caused by fine particulate matter 2.5 (PM2.5). However, underlying mechanisms whereby PM2.5, particularly during short-term exposure, induces liver dysfunction leading to IR remains poorly understood. In the present study, HepG2 cells and the BALB/c mouse model were used to explore how PM2.5 affects insulin sensitivity. The effects of subacute PM2.5 exposure on glucose metabolism were examined using commercial kits. Oxidative stress and inflammation were detected by fluorescent staining and RT-qPCR. The phosphorylation of PI3K/AKT was examined by Western blot. Subacute PM2.5 exposure induced IR, as reflected by increased glucose levels in cell supernatants, elevated insulin levels, and the impaired intraperitoneal glucose tolerance test in mice. PM2.5 induced oxidative stress, as evidenced by increased reactive oxygen species, cytochrome P450 2E1, and malondialdehyde, along with reduced superoxide dismutase 1/2 and silent information regulator 1. IL-6 and TNF-α were found to be upregulated using RT-qPCR. Western blot showed that PM2.5 inhibited the PI3K-AKT signaling pathway, indicated by the decreased phosphorylation of PI3K/AKT in HepG2 cells. Additionally, H&E staining showed only mild hepatic injury in mice liver. These results firmly suggest that subacute PM2.5 exposure induces insulin resistance through oxidative stress, inflammation, and the inhibition of the PI3K-AKT signaling pathway.

Indexed as

InflammationInsulin ResistanceLiverOxidative StressParticulate MatterAnimalsHep G2 CellsHumansMaleMiceMice, Inbred BALB CPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSignal TransductionParticulate MatterPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesChinahepatic insulin resistanceinflammationoxidative stressPI3K-AKT signaling pathwayPM2.5

Identifiers

PMID39859525
PMCPMC11766349

What Socratic holds

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LicenceCC BY
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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 Socratic graph.