Evidence map›Paper›PMID 36232686›Full record

ArticleInternational journal of molecular sciences2022

Oxidative Stress as a Contributor to Insulin Resistance in the Skeletal Muscles of Mice with Polycystic Ovary Syndrome.

Qiyang Yao, Xin Zou, Shihe Liu, Haowen Wu, Qiyang Shen, Jihong Kang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 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

6 authors at 1 institution in 1 country.

Qiyang YaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, No.38 Xueyuan Rd., Haidian District, Beijing 100191, China.
Xin ZouDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, No.38 Xueyuan Rd., Haidian District, Beijing 100191, China.
Shihe LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, No.38 Xueyuan Rd., Haidian District, Beijing 100191, China.
Haowen WuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, No.38 Xueyuan Rd., Haidian District, Beijing 100191, China.
Qiyang ShenDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, No.38 Xueyuan Rd., Haidian District, Beijing 100191, China.
Jihong KangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, No.38 Xueyuan Rd., Haidian District, Beijing 100191, China.
Peking University · CN

Funding

National Natural Science Foundation of China 31971068National Natural Science Foundation of China 81670733National Natural Science Foundation of China 82171634
6 · The paper itself

Abstract

Polycystic ovarian syndrome (PCOS) is a reproductive, endocrine, and metabolic disorder. Circulating markers of oxidative stress are abnormal in women with PCOS. There is a close relationship between oxidative stress and insulin resistance (IR). However, little information is available about oxidative stress in the skeletal muscles of those affected by PCOS. In this study, PCOS was induced in prepubertal C57BL/6J mice by injection with dehydroepiandrosterone. Oxidative stress biomarkers were then measured in both serum and skeletal muscles. The underlying mechanisms were investigated in C2C12 myotubes treated with testosterone (T). We discovered increased oxidative biomarkers, increased ROS production, and damaged insulin sensitivity in the skeletal muscles of mice with PCOS. High levels of T caused mitochondrial dysfunction and increased ROS levels through the androgen receptor (AR)-nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) signaling pathway in C2C12 cells. Treatment of C2C12 cells with an antioxidant N-acetylcysteine (NAC) decreased T-induced ROS production, improved mitochondrial function, and reversed IR. Administration of NAC to mice with PCOS improved insulin sensitivity in the skeletal muscles of the animals. Hyperandrogenism caused mitochondrial dysfunction and redox imbalance in the skeletal muscles of mice with PCOS. We discovered that oxidative stress contributed to skeletal muscle IR in PCOS. Reducing ROS levels may improve the insulin sensitivity of skeletal muscles in patients with PCOS.

Indexed as

Insulin ResistancePolycystic Ovary SyndromeAcetylcysteineAnimalsAntioxidantsBiomarkersDehydroepiandrosteroneFemaleHumansMiceMice, Inbred C57BLMuscle, SkeletalNADPOxidative StressOxidoreductasesReactive Oxygen SpeciesAcetylcysteineAntioxidantsBiomarkersDehydroepiandrosteroneNADPOxidoreductasesReactive Oxygen SpeciesReceptors, AndrogenTestosteroneinsulin resistanceoxidative stresspolycystic ovary syndromeskeletal muscle

Identifiers

PMID36232686
PMCPMC9569700
OpenAlexW4297539444

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.