Evidence map›Paper›PMID 28051178›Full record

ArticleScientific reports2017

Muscle-specific deletion of BDK amplifies loss of myofibrillar protein during protein undernutrition.

Takuya Ishikawa, Yasuyuki Kitaura, Yoshihiro Kadota, Yukako Morishita, Miki Ota, Fumiya Yamanaka, Minjun Xu, Masahito Ikawa, Naokazu Inoue, Fuminori Kawano 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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Trial
  2. A metabolic basis for motor deficits in mice lacking BCKDK.The Journal of nutritional biochemistry · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
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 7 institutions in 1 country.

Takuya IshikawaLaboratory of Nutritional Biochemistry, Department of Applied Molecular Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Yasuyuki KitauraLaboratory of Nutritional Biochemistry, Department of Applied Molecular Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Yoshihiro KadotaLaboratory of Nutritional Biochemistry, Department of Applied Molecular Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Yukako MorishitaLaboratory of Nutritional Biochemistry, Department of Applied Molecular Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Miki OtaLaboratory of Nutritional Biochemistry, Department of Applied Molecular Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Fumiya YamanakaLaboratory of Nutritional Biochemistry, Department of Applied Molecular Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Minjun XuLaboratory of Nutritional Biochemistry, Department of Applied Molecular Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Masahito IkawaAnimal Resource Center for Infectious Diseases, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Naokazu InoueDepartment of Experimental Genome Research, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
Fuminori KawanoGraduate School of Health Sciences, Matsumoto University, Matsumoto, Nagano, Japan.
Naoya NakaiSchool of Human Cultures, University of Shiga Prefecture, Hikone, Shiga, Japan.
Taro MurakamiDepartment of Nutrition, Shigakkan University, Obu, Aichi, Japan.
Shinji MiuraGraduate School of Nutritional and Environmental Sciences, University of Shizuoka, Shizuoka, Japan.
Yukino HatazawaGraduate School of Environmental and Life Science, Kyoto Prefectural University, Kyoto, Japan.
Yasutomi KameiGraduate School of Environmental and Life Science, Kyoto Prefectural University, Kyoto, Japan.
Yoshiharu ShimomuraLaboratory of Nutritional Biochemistry, Department of Applied Molecular Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Nagoya University · JPKyoto Prefectural University · JPOsaka University · JPMatsumoto University · JPShigakkan University · JPUniversity of Shiga Prefecture · JPUniversity of Shizuoka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Branched-chain amino acids (BCAAs) are essential amino acids for mammals and play key roles in the regulation of protein metabolism. However, the effect of BCAA deficiency on protein metabolism in skeletal muscle in vivo remains unclear. Here we generated mice with lower BCAA concentrations by specifically accelerating BCAA catabolism in skeletal muscle and heart (BDK-mKO mice). The mice appeared to be healthy without any obvious defects when fed a protein-rich diet; however, bolus ingestion of BCAAs showed that mTORC1 sensitivity in skeletal muscle was enhanced in BDK-mKO mice compared to the corresponding control mice. When these mice were fed a low protein diet, the concentration of myofibrillar protein was significantly decreased (but not soluble protein) and mTORC1 activity was reduced without significant change in autophagy. BCAA supplementation in drinking water attenuated the decreases in myofibrillar protein levels and mTORC1 activity. These results suggest that BCAAs are essential for maintaining myofibrillar proteins during protein undernutrition by keeping mTORC1 activity rather than by inhibiting autophagy and translation. This is the first report to reveal the importance of BCAAs for protein metabolism of skeletal muscle in vivo.

Indexed as

Diet, Protein-RestrictedAdaptor Proteins, Signal TransducingAmino Acids, Branched-ChainAnimalsCarrier ProteinsCell Cycle ProteinsDietary SupplementsEukaryotic Initiation FactorsKidneyMechanistic Target of Rapamycin Complex 1MiceMice, KnockoutMuscle ProteinsMuscle, SkeletalMyocardiumPhosphoproteins(3-methyl-2-oxobutanoate dehydrogenase (lipoamide)) kinaseAdaptor Proteins, Signal TransducingAmino Acids, Branched-ChainCarrier ProteinsCell Cycle ProteinsEif4ebp1 protein, mouseEukaryotic Initiation FactorsMechanistic Target of Rapamycin Complex 1Muscle ProteinsPhosphoproteinsProtein KinasesRibosomal Protein S6 Kinases, 90-kDaRps6ka1 protein, mouse

Identifiers

PMID28051178
PMCPMC5209746
OpenAlexW2568409718

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.