Evidence map›Paper›PMID 34556698›Full record

ArticleScientific reports2021

Role of pyruvate in maintaining cell viability and energy production under high-glucose conditions.

Hideji Yako, Naoko Niimi, Ayako Kato, Shizuka Takaku, Yasuaki Tatsumi, Yasumasa Nishito, Koichi Kato, Kazunori Sango

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 58 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

8 authors at 2 institutions in 1 country.

Hideji YakoDiabetic Neuropathy Project, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, 156-8506, Japan. yako-hd@igakuken.or.jp.
Naoko NiimiDiabetic Neuropathy Project, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, 156-8506, Japan.
Ayako KatoLaboratory of Medicine, Aichi Gakuin University, School of Pharmacy, Nagoya, Japan.
Shizuka TakakuDiabetic Neuropathy Project, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, 156-8506, Japan.
Yasuaki TatsumiLaboratory of Medicine, Aichi Gakuin University, School of Pharmacy, Nagoya, Japan.
Yasumasa NishitoBasic Technology Research Center, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Koichi KatoLaboratory of Medicine, Aichi Gakuin University, School of Pharmacy, Nagoya, Japan.
Kazunori SangoDiabetic Neuropathy Project, Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, 156-8506, Japan. sango-kz@igakuken.or.jp.
Tokyo Metropolitan Institute of Medical Science · JPAichi Gakuin University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pyruvate functions as a key molecule in energy production and as an antioxidant. The efficacy of pyruvate supplementation in diabetic retinopathy and nephropathy has been shown in animal models; however, its significance in the functional maintenance of neurons and Schwann cells under diabetic conditions remains unknown. We observed rapid and extensive cell death under high-glucose (> 10 mM) and pyruvate-starved conditions. Exposure of Schwann cells to these conditions led to a significant decrease in glycolytic flux, mitochondrial respiration and ATP production, accompanied by enhanced collateral glycolysis pathways (e.g., polyol pathway). Cell death could be prevented by supplementation with 2-oxoglutarate (a TCA cycle intermediate), benfotiamine (the vitamin B1 derivative that suppresses the collateral pathways), or the poly (ADP-ribose) polymerase (PARP) inhibitor, rucaparib. Our findings suggest that exogenous pyruvate plays a pivotal role in maintaining glycolysis-TCA cycle flux and ATP production under high-glucose conditions by suppressing PARP activity.

Indexed as

Adenosine TriphosphateAnimalsCell LineCell SurvivalCitric Acid CycleDiabetic NephropathiesDisease Models, AnimalFemaleGlucoseGlycolysisHumansHyperglycemiaIndolesMiceNeuronsPoly(ADP-ribose) PolymerasesAdenosine TriphosphatebenphothiamineGlucoseIndolesPoly(ADP-ribose) PolymerasesPyruvic AcidrucaparibThiamine

Identifiers

PMID34556698
PMCPMC8460646
OpenAlexW3199657197

What OpenQuestion holds

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LicenceCC BY
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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.