Evidence map›Paper›PMID 33051821›Full record

ArticleJournal of physiology and biochemistry2020

JAB1 promotes palmitate-induced insulin resistance via ERK pathway in hepatocytes.

Yun Zhao, Suxian Ma, Xingna Hu, Min Feng, Rong Xiang, Min Li, Chenxiao Liu, Ting Lu, Aijie Huang, Jiaqi Chen and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of physiology and biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Yun ZhaoThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China.
Suxian MaThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China.
Xingna HuThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China.
Min FengThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China.
Rong XiangThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China.
Min LiThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China.
Chenxiao LiuThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China.
Ting LuThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China.
Aijie HuangThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China.
Jiaqi ChenThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China.
Mian WuThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China.
Honghong LuThe Affiliated Suzhou Hospital of Nanjing Medical University, 242 Guangji Road, Suzhou, Jiangsu, 215008, People's Republic of China. szsynfm@163.com.ORCID http://orcid.org/0000-0001-7005-2349
Nanjing Medical University · CNSuzhou Guangji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance (IR) is the primary pathological mechanism underlying Type 2 diabetes mellitus (T2DM). Many researches have reported the relationship between chronic inflammation and IR, while the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway is rapidly activated in inflammatory conditions. However, the functional role of ERK1/2 in IR remains to be identified. We here reported that C-Jun activation domain-binding protein-1 (JAB1) was upregulated in IR. In addition, we showed that depletion of JAB1 led to recovery of insulin sensitivity. Given the fact that JAB1 played as an activator of ERK1/2, we assumed JAB1 was involved in IR through ERK pathway. So we assessed the effects of JAB1 knockdown in palmitate acid (PA) treated HepG2 cells. Importantly, JAB1 siRNA blocked the effect of PA-induced activation of ERK1/2. Furthermore, silencing of JAB1 could reduce the release of inflammatory factors, facilitate hepatic glucose uptake and improve lipid metabolism. All these data implicated that JAB1 knockdown might alleviate PA-induced IR through ERK pathway in hepatocytes.

Indexed as

Insulin ResistanceAnimalsCOP9 Signalosome ComplexDiabetes Mellitus, Type 2Hep G2 CellsHumansInflammationIntracellular Signaling Peptides and ProteinsMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLPalmitic AcidPeptide HydrolasesCOP9 Signalosome ComplexCOPS5 protein, humanIntracellular Signaling Peptides and ProteinsPalmitic AcidPeptide HydrolasesERK pathwayInsulin resistanceJAB1Type 2 diabetes

Identifiers

PMID33051821
OpenAlexW3092275019

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.