Evidence map›Paper›PMID 37461021›Full record

ArticleBMC endocrine disorders2023

Effects of UBE3A on the insulin resistance in polycystic ovary syndrome through the ubiquitination of AMPK.

Ning Ma, Jing Zhou, Zhi Zhou, Bangbei Wan, Weiying Lu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC endocrine disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 35% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Review
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

5 authors at 1 institution in 1 country.

Ning MaReproductive Medical Center, Hainan Women and Children's Medical Center, No.75 Longkun South Road, Haikou, Hainan, 570206, China.
Jing ZhouReproductive Medical Center, Hainan Women and Children's Medical Center, No.75 Longkun South Road, Haikou, Hainan, 570206, China.
Zhi ZhouReproductive Medical Center, Hainan Women and Children's Medical Center, No.75 Longkun South Road, Haikou, Hainan, 570206, China.
Bangbei WanReproductive Medical Center, Hainan Women and Children's Medical Center, No.75 Longkun South Road, Haikou, Hainan, 570206, China.
Weiying LuReproductive Medical Center, Hainan Women and Children's Medical Center, No.75 Longkun South Road, Haikou, Hainan, 570206, China. luweiying_0226@sina.com.
Hainan Medical University · CN

Funding

Grants from Hainan Province Clinical Medical Center (QWYH202175)Grants from Science and Technology Department of Hainan Province (ZDYF2022SHFZ074、ZDYF2022SHFZ280)
6 · The paper itself

Abstract

backgroundPolycystic ovary syndrome (PCOS) is a reproductive hormonal abnormality and a metabolic disorder, which is frequently associated with insulin resistance (IR). We aim to investigate the potential therapeutic effects of Ubiquitin-protein ligase E3A (UBE3A) on IR in the PCOS rats via Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) activation.

methodsThe PCOS and IR rats model was established by dehydroepiandrosterone (DHEA) and high fat diet (HFD) treatment, and the fat rate, glucose tolerance and insulin tolerance were measured. The IR rats numbers were calculated. Besides, the mRNA levels of glucose transporter 4 (GLUT4) and UBE3A were detected by RT-qPCR. Furthermore, the relationship between was demonstrated by co-IP assay. The phosphorylation and ubiquitination of AMPK were analyzed by western blot.

resultsUBE3A was up-regulated in the PCOS rats. UBE3A knockdown significantly decreased the fat rate, glucose tolerance and insulin tolerance in the PCOS and IR rats. Additionally, the GLUT4 levels were significantly increased in PCOS + IR rats. Besides, after UBE3A knockdown, the IR rats were decreased, the p-IRS1 and p-AKT levels were significantly up-regulated. Furthermore, UBE3A knockdown enhanced phosphorylation of AMPK through decreasing the ubiquitination of AMPK. AMPK knockdown reversed the role of UBE3A knockdown in the PCOS + IR rats.

conclusionsUBE3A knockdown inhibited the IR in PCOS rats through targeting AMPK. Our study indicated that UBE3A might become a potential biological target for the clinical treatment of PCOS.

Indexed as

Insulin ResistanceInsulinsPolycystic Ovary SyndromeAMP-Activated Protein KinasesAnimalsFemaleGlucoseRatsUbiquitinationUbiquitin-Protein LigasesAMP-Activated Protein KinasesGlucoseInsulinsUbe3a protein, ratUbiquitin-Protein LigasesDenosine 5‘-monophosphate (AMP)-activated protein kinaseInsulin resistancePolycystic ovary syndromeUbiquitin-protein ligase E3A

Identifiers

PMID37461021
PMCPMC10351129
OpenAlexW4384525222

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.