Evidence map›Paper›PMID 29113994›Full record

ArticleJournal of lipid research2018

Hepatocyte-specific deletion of BAP31 promotes SREBP1C activation, promotes hepatic lipid accumulation, and worsens IR in mice.

Jia-Lin Xu, Li-Ya Li, Yan-Qing Wang, Ya-Qi Li, Mu Shan, Shi-Zhuo Sun, Yang Yu, Bing Wang

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-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

21 citing papers in PubMed, 44 citations in OpenAlex.

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  11. Long non-coding RNAs: a valuable biomarker for metabolic syndrome.Molecular genetics and genomics : MGG · 2022
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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 at 1 institution in 1 country.

Jia-Lin XuInstitutes of Biochemistry and Molecular Biology Northeastern University, Shenyang 110169, People's Republic of China.
Li-Ya LiMicrobial Pharmaceuticals, College of Life and Health Sciences, Northeastern University, Shenyang 110169, People's Republic of China.
Yan-Qing WangInstitutes of Biochemistry and Molecular Biology Northeastern University, Shenyang 110169, People's Republic of China.
Ya-Qi LiInstitutes of Biochemistry and Molecular Biology Northeastern University, Shenyang 110169, People's Republic of China.
Mu ShanInstitutes of Biochemistry and Molecular Biology Northeastern University, Shenyang 110169, People's Republic of China.
Shi-Zhuo SunInstitutes of Biochemistry and Molecular Biology Northeastern University, Shenyang 110169, People's Republic of China.
Yang YuInstitutes of Biochemistry and Molecular Biology Northeastern University, Shenyang 110169, People's Republic of China.
Bing WangInstitutes of Biochemistry and Molecular Biology Northeastern University, Shenyang 110169, People's Republic of China wangbing@mail.neu.edu.cn.
Northeastern University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Conditional knockout mice with targeted disruption of B-cell associated protein (BAP)31 in adult mouse liver were generated and challenged with a high-fat diet (HFD) for 36 or 96 days and markers of obesity, diabetes, and hepatic steatosis were determined. Mutant mice were indistinguishable from WT littermates, but exhibited increased HFD-induced obesity. BAP31-deletion in hepatocytes increased the expression of SREBP1C and the target genes, including acetyl-CoA carboxylase 1 and stearoyl-CoA desaturase-1, and increased hepatic lipid accumulation and HFD-induced liver steatosis. Immunoprecipitation assay showed that BAP31 interacts with SREBP1C and insulin-induced gene 1 (INSIG1), and BAP31-deletion reduces INSIG1 expression, suggesting that BAP31 may regulate SREBP1C activity by modulating INSIG1 protein levels. Additionally, BAP31-deletion induced glucose and insulin intolerance, decreased Akt and glycogen synthase kinase 3β phosphorylation, and enhanced hepatic glucose production in mice. Expression of endoplasmic reticulum (ER) stress markers was significantly induced in BAP31-mutant mice. HFD-induced inflammation was aggravated in mutant mice, along with increased c-Jun N-terminal kinase and nuclear factor-κB activation. These findings demonstrate that BAP31-deletion induces SREBP activation and promotes hepatic lipid accumulation, reduces insulin signaling, impairs glucose/insulin tolerance, and increases ER stress and hepatic inflammation, explaining the protective roles of BAP31 in the development of liver steatosis and insulin resistance in HFD-induced obesity in animal models.

Indexed as

Insulin ResistanceAnimalsDiet, High-FatHepatocytesHep G2 CellsHumansLipidsLiverMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutObesitySterol Regulatory Element Binding Protein 1Tumor Cells, CulturedBcap31 protein, mouseLipidsMembrane ProteinsSrebf1 protein, mouseSterol Regulatory Element Binding Protein 1B-cell activated protein 31B-cell associated protein 31diabetesendoplasmic reticulum stressinsulin resistanceliver steatosissterol regulatory element-binding protein 1C

Identifiers

PMID29113994
PMCPMC5748495
OpenAlexW2782341951

What OpenQuestion 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 OpenQuestion graph.