Evidence map›Paper›PMID 35907871›Full record

ArticleJournal of translational medicine2022

Reducing VEGFB accelerates NAFLD and insulin resistance in mice via inhibiting AMPK signaling pathway.

Rongrong Li, Yuqi Li, Xueling Yang, Yaorui Hu, Haining Yu, Yana Li

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  10. Role of AMPKZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
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  17. Experimental model and novel therapeutic targets for non-alcoholic fatty liver disease development.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
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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

6 authors at 2 institutions in 1 country.

Rongrong Li *Department of Pathophysiology, School of Basic Medicine, Binzhou Medical University, Yantai, 264000, Shandong, China.
Yuqi Li *Department of Pathophysiology, School of Basic Medicine, Binzhou Medical University, Yantai, 264000, Shandong, China.
Xueling YangShandong Technology Innovation Center of Molecular Targeting and Intelligent Diagnosis and Treatment, Binzhou Medical University, Yantai, 264000, Shandong, China.
Yaorui HuDepartment of Anatomy, School of Basic Medicine, Binzhou Medical University, Yantai, 264000, Shandong, China.
Haining YuStomatology Department, Stomatological College, Binzhou Medical University, Yantai, 264000, Shandong, China.
Yana LiDepartment of Pathophysiology, School of Basic Medicine, Binzhou Medical University, Yantai, 264000, Shandong, China. yaya-698@163.com.
Binzhou Medical University · CNBinzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveVascular endothelial growth factor B (VEGFB) was regarded to improve lipid metabolism and reduce obesity-related hyperlipidemia. Whether VEGFB participates in lipid metabolism in nonalcoholic fatty liver disease (NAFLD) has not been clear yet. This study investigated the involvement of VEGFB in lipid metabolism and insulin resistance via the AMPK signaling pathway in NAFLD.

methodsWe constructed the animal and cell model of NAFLD after VEGFB gene knockout to detect liver damage and metabolism in NAFLD. Bioinformatics analysis of VEGFB and the AMPK signaling pathway relative genes to verify the differential proteins. And mRNA levels of NAFLD fatty acid metabolism-related genes were detected.

resultsAfter the systemic VEGFB knockout mice were fed with high fat, the body fat, serum lipoprotein, NAFLD score, and insulin resistance were increased. Animal and cell experiments showed that the expression levels of phosphorylated proteins of CaMKK2 and AMPK decreased, the expression of proteins related to AMPK/ACC/CPT1 signaling pathway decreased, and the target genes CPT1α and Lcad decreased accordingly, reducing fatty acid oxidation in hepatocyte mitochondria; The expression of AMPK/SREBP1/Scd1 signaling pathway relative proteins increased, ACC1 and FAS increased correspondingly, which increased lipid synthesis in the endoplasmic reticulum.

conclusionVEGFB can participate in lipid metabolism and insulin resistance of NAFLD through the AMPK signaling pathway.

Indexed as

Insulin ResistanceNon-alcoholic Fatty Liver DiseaseAMP-Activated Protein KinasesAnimalsDiet, High-FatFatty AcidsLipid MetabolismLiverMiceMice, Inbred C57BLSignal TransductionVascular Endothelial Growth Factor BAMP-Activated Protein KinasesFatty AcidsVascular Endothelial Growth Factor Bvascular endothelial growth factor B, mouseAMPK/ACCAMPK/SREBP1Lipid metabolismNAFLDVEGFB

Identifiers

PMID35907871
PMCPMC9338666
OpenAlexW4288684323

What OpenQuestion 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 OpenQuestion graph.