Evidence map›Paper›PMID 30952864›Full record

ArticleNature communications2019

Autophagy regulates lipid metabolism through selective turnover of NCoR1.

Tetsuya Saito, Akiko Kuma, Yuki Sugiura, Yoshinobu Ichimura, Miki Obata, Hiroshi Kitamura, Shujiro Okuda, Hyeon-Cheol Lee, Kazutaka Ikeda, Yumi Kanegae and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed, 3 pooled it
17.6field-weighted citation impact, top 1% 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

126 citing papers in PubMed, 3 syntheses or guidelines pooled it, 191 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Pooled it
  4. Trial
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  12. Enhanced insulin signaling via circulating ATG7: A potential therapeutic strategy for diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  13. Autophagy in the liver.Autophagy reports · 2026
    Review
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  15. Review
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  17. Article
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66 more citing papers are in PubMed but not listed here.

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

19 authors at 11 institutions in 2 countries.

Tetsuya SaitoDepartment of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Niigata, 951-8510, Japan.
Akiko KumaDepartment of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Yuki SugiuraJapan Science and Technology Agency, PRESTO, Saitama, 332-0012, Japan.
Yoshinobu IchimuraDepartment of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Niigata, 951-8510, Japan.
Miki ObataDepartment of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Niigata, 951-8510, Japan.
Hiroshi KitamuraDepartment of Gene Expression Regulation, Institute of Development, Aging and Cancer, Tohoku University, Sendai, 980-8575, Japan.
Shujiro OkudaBioinformatics Laboratory, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Niigata, 951-8510, Japan.ORCID http://orcid.org/0000-0002-7704-8104
Hyeon-Cheol LeeDepartment of Biochemistry, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, 113-8421, Japan.
Kazutaka IkedaLaboratory for Metabolomics, RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Kanagawa, 230-0045, Japan.
Yumi KanegaeCore Research Facilities of Basic Science (Molecular Genetics), Research Center for Medical Science, Jikei University School of Medicine, Tokyo, 105-8461, Japan.
Izumu SaitoLaboratory of Molecular Genetics, Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
Johan AuwerxLaboratory of Integrative and Systems Physiology, École Polytechnique Fédérale de Lausanne (EPFL), 1015, Lausanne, Switzerland.
Hozumi MotohashiDepartment of Gene Expression Regulation, Institute of Development, Aging and Cancer, Tohoku University, Sendai, 980-8575, Japan.ORCID http://orcid.org/0000-0002-7261-1033
Makoto SuematsuDepartment of Biochemistry, Keio University School of Medicine, Tokyo, 160-8582, Japan.ORCID http://orcid.org/0000-0002-7165-6336
Tomoyoshi SogaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Yamagata, 997-0052, Japan.
Takehiko YokomizoDepartment of Biochemistry, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo, 113-8421, Japan.
Satoshi WaguriDepartment of Anatomy and Histology, Fukushima Medical University School of Medicine, Hikarigaoka, Fukushima, 960-1295, Japan.
Noboru MizushimaDepartment of Biochemistry and Molecular Biology, Graduate School and Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, 113-0033, Japan.ORCID http://orcid.org/0000-0002-6258-6444
Masaaki KomatsuDepartment of Biochemistry, Niigata University Graduate School of Medical and Dental Sciences, Chuo-ku, Niigata, 951-8510, Japan. mkomatsu@juntendo.ac.jp.
Niigata University · JPJuntendo University · JPKeio University · JPTohoku University · JPÉcole Polytechnique Fédérale de Lausanne · CHFukushima Medical University · JPJapan Science and Technology Agency · JPJikei University School of Medicine · JPMicrobial Chemistry Research Foundation · JPRIKEN Center for Integrative Medical Sciences · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Selective autophagy ensures the removal of specific soluble proteins, protein aggregates, damaged mitochondria, and invasive bacteria from cells. Defective autophagy has been directly linked to metabolic disorders. However how selective autophagy regulates metabolism remains largely uncharacterized. Here we show that a deficiency in selective autophagy is associated with suppression of lipid oxidation. Hepatic loss of Atg7 or Atg5 significantly impairs the production of ketone bodies upon fasting, due to decreased expression of enzymes involved in β-oxidation following suppression of transactivation by PPARα. Mechanistically, nuclear receptor co-repressor 1 (NCoR1), which interacts with PPARα to suppress its transactivation, binds to the autophagosomal GABARAP family proteins and is degraded by autophagy. Consequently, loss of autophagy causes accumulation of NCoR1, suppressing PPARα activity and resulting in impaired lipid oxidation. These results suggest that autophagy contributes to PPARα activation upon fasting by promoting degradation of NCoR1 and thus regulates β-oxidation and ketone bodies production.

Indexed as

AutophagyLipid MetabolismAnimalsAutophagy-Related Protein 5Autophagy-Related Protein 7FastingKetone BodiesLiverMiceNuclear Receptor Co-Repressor 1Oxidation-ReductionPPAR alphaAtg5 protein, mouseAtg7 protein, mouseAutophagy-Related Protein 5Autophagy-Related Protein 7Ketone BodiesNuclear Receptor Co-Repressor 1PPAR alpha

Identifiers

PMID30952864
PMCPMC6450892
OpenAlexW2931270080

What Socratic 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 Socratic graph.