Evidence map›Paper›PMID 28638045›Full record

ArticleScientific reports2017

Treatment of sarcopenia and glucose intolerance through mitochondrial activation by 5-aminolevulinic acid.

Chikako Fujii, Kazutoshi Miyashita, Masanori Mitsuishi, Masaaki Sato, Kentaro Fujii, Hiroyuki Inoue, Aika Hagiwara, Sho Endo, Asuka Uto, Masaki Ryuzaki and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

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  4. Inhibitory effect of standardizedJournal of traditional and complementary medicine · 2026
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  15. Pilot Trial on the Effect of 5-Aminolevulinic Acid on Glucose Tolerance in Patients with Maternally Inherited Diabetes and Deafness.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2023
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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

16 authors at 2 institutions in 1 country.

Chikako FujiiDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Kazutoshi MiyashitaDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan. miyakaz@z6.keio.jp.
Masanori MitsuishiDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Masaaki SatoDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Kentaro FujiiDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Hiroyuki InoueDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Aika HagiwaraDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Sho EndoDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Asuka UtoDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Masaki RyuzakiDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Motowo NakajimaSBI Pharmaceuticals Co., Ltd., Tokyo, Japan.
Tohru TanakaSBI Pharmaceuticals Co., Ltd., Tokyo, Japan.
Masanori TamakiDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Ayako MurakiDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Toshihide KawaiDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Hiroshi ItohDepartment of Endocrinology, Metabolism and Nephrology, Keio University School of Medicine, Tokyo, Japan.
Keio University · JPSBI Pharmaceuticals (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, sarcopenia has attracted attention as therapeutic target because it constitutes a risk factor for metabolic and cardiovascular diseases. We focused 5-aminolevulinic acid (ALA) which act as electron carriers in the mitochondrial electron transport system. The mice that received ALA for 8 weeks gained muscle strength and endurance, and exhibited increased muscle mass and mitochondrial amount. Administration of ALA to sarcopenia mice aged 100 weeks and chronic kidney disease (CKD) model mice also increased muscle mass and improved physical performance. Metabolome analysis revealed increased branched-chain amino acids (BCAAs) levels in the skeletal muscle of ALA-treated mice. Quantitative PCR analysis revealed decreased expression levels in branched-chain amino acid transaminases (BCATs) that degrade BCAAs and other muscle-degrading factors, and increased levels of mitochondria-activating factors. We also studied in cultured myocytes and obtained compatible results. ALA-treated mice tended to increase body weight, but reduced blood glucose level. These suggested that ALA treatment not only activated muscle mitochondria but also enhanced muscle mass through an increase in BCAAs contents, as to improve muscle strength, endurance and glucose tolerance in mice. In these ways, muscle mitochondrial activation with ALA is suggested to be useful for the treatment of sarcopenia and glucose intolerance.

Indexed as

Aminolevulinic AcidAnimalsBlood GlucoseBody WeightDisease Models, AnimalElectron Transport Complex IGlucose IntoleranceHumansMiceMitochondria, MuscleMuscle StrengthPhysical EnduranceRisk FactorsSarcopeniaAminolevulinic AcidBlood GlucoseElectron Transport Complex I

Identifiers

PMID28638045
PMCPMC5479778
OpenAlexW2625216587

What OpenQuestion holds

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LicenceCC BY
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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.