Evidence map›Paper›PMID 29855350›Full record

ArticleSkeletal muscle2018

Dietary supplementation with ketoacids protects against CKD-induced oxidative damage and mitochondrial dysfunction in skeletal muscle of 5/6 nephrectomised rats.

Dongtao Wang, Lianbo Wei, Yajun Yang, Huan Liu

Open access · goldAbstract read
In one paragraph

Article in Skeletal muscle, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 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

4 authors at 4 institutions in 1 country.

Dongtao WangDepartment of Traditional Chinese Medicine, Shenzhen Hospital, Southern Medical University, Shenzhen, 518000, Guangdong, China. 95401864@qq.com.
Lianbo WeiDepartment of Traditional Chinese Medicine, Shenzhen Hospital, Southern Medical University, Shenzhen, 518000, Guangdong, China.
Yajun YangDepartment of Pharmacology, Guangdong Key Laboratory for R&D of Natural Drug, Guangdong Medical University, Zhanjiang, 524023, Guangdong, China.
Huan LiuDepartment of Nephrology, Ruikang Affiliated Hospital, Guangxi University of Chinese Medicine, Nanning, 530011, Guangxi, China.
Guangdong Medical College · CNGuangxi University · CNGuangxi University of Chinese Medicine · CNSouthern Medical University Shenzhen Hospital · CN

Funding

China Postdoctoral Science Foundation 2015M582372Health and Family Planning Commission of Shenzhen Municipality 201605013National Natural Science Foundation of China 81503398Natural Science Foundation of Guangxi Province 2015GXNSFBA139171Natural Science Foundation of Guangxi Province 2016GXNSFAA380005Science and Technology Planning Project of Guangdong Province 2016A020226032Science and Technology Planning Project of Guangdong Province 2017A020213008Shenzhen Science and Technology Project JCYJ20160428175036148
6 · The paper itself

Abstract

backgroundA low-protein diet supplemented with ketoacids (LPD + KA) maintains the nutritional status of patients with chronic kidney disease (CKD). Oxidative damage and mitochondrial dysfunction associated with the upregulation of p66SHC and FoxO3a have been shown to contribute to muscle atrophy. This study aimed to determine whether LPD + KA improves muscle atrophy and attenuates the oxidative stress and mitochondrial damage observed in CKD rats.

methods5/6 nephrectomy rats were randomly divided into three groups and fed with either 22% protein (normal-protein diet; NPD), 6% protein (low-protein diets; LPD) or 5% protein plus 1% ketoacids (LPD + KA) for 24 weeks. Sham-operated rats with NPD intake were used as the control.

resultsKA supplementation improved muscle atrophy and function in CKD + LPD rats. It also reduced the upregulation of genes related to the ubiquitin-proteasome system and 26S proteasome activity, as well as protein and mitochondrial oxidative damage in the muscles of CKD + LPD rats. Moreover, KA supplementation prevented the drastic decrease in activities of mitochondrial electron transport chain complexes, mitochondrial respiration, and content in the muscles of CKD + LPD rats. Furthermore, KA supplementation reversed the elevation in p66Shc and FoxO3a expression in the muscles of CKD + LPD rats.

conclusionsOur results showed that KA supplementation to be beneficial to muscle atrophy in CKD + LPD, which might be associated with improvement of oxidative damage and mitochondrial dysfunction through suppression of p66Shc and FoxO3a.

Indexed as

Dietary SupplementsAnimalsDrug Evaluation, PreclinicalKeto AcidsKidneyMaleMitochondria, MuscleMuscle ProteinsMuscle, SkeletalMuscular AtrophyNephrectomyOxidative StressProteasome Endopeptidase ComplexRats, Sprague-DawleyRenal Insufficiency, ChronicUbiquitinKeto AcidsMuscle ProteinsProteasome Endopeptidase ComplexUbiquitinChronic kidney diseaseKetoacidsMitochondrial dysfunctionMuscle atrophyOxidative stress

Identifiers

PMID29855350
PMCPMC5984473
OpenAlexW2805569140

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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.