Evidence map›Paper›PMID 37488415›Full record

ArticleNature aging2023

Impaired BCAA catabolism in adipose tissues promotes age-associated metabolic derangement.

Hye-Sook Han, Eunyong Ahn, Eun Seo Park, Tom Huh, Seri Choi, Yongmin Kwon, Byeong Hun Choi, Jueun Lee, Yoon Ha Choi, Yujin L Jeong and 9 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Gut microbes · 2026
    Article
  2. Metabolomic Profiling ofJournal of fungi (Basel, Switzerland) · 2026
    Article
  3. Article
  4. BCAA Metabolic Dyshomeostasis in Cardiovascular Disease: Pathogenic Mechanisms and Intervention.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2026
    Review
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  7. Article
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  14. Review
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  16. Thermogenic Adipose ADH5 Counteracts Age-related Metabolic Decline.bioRxiv : the preprint server for biology · 2025
    Article
  17. Article
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 6 institutions in 3 countries.

Hye-Sook Han *Division of Life Sciences, Korea University, Seoul, Korea.
Eunyong Ahn *Integrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul, Korea.ORCID http://orcid.org/0000-0003-0330-0247
Eun Seo Park *Department of New Biology, DGIST, Daegu, Korea.ORCID http://orcid.org/0000-0002-6790-5467
Tom HuhDivision of Life Sciences, Korea University, Seoul, Korea.
Seri ChoiDivision of Life Sciences, Korea University, Seoul, Korea.
Yongmin KwonDivision of Life Sciences, Korea University, Seoul, Korea.
Byeong Hun ChoiDivision of Life Sciences, Korea University, Seoul, Korea.
Jueun LeeIntegrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul, Korea.
Yoon Ha ChoiDepartment of Life Sciences, POSTECH, Pohang, Korea.
Yujin L JeongDepartment of Life Sciences, POSTECH, Pohang, Korea.
Gwang Bin LeeDepartment of Chemistry, Yonsei University, Seoul, Korea.
Minji KimDepartment of Anatomy & Cell Biology, Seoul National University College of Medicine, Seoul, Korea.
Je Kyung SeongKorea Mouse Phenotyping Center, Seoul National University, Seoul, Korea.
Hyun Mu ShinDepartment of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Korea.
Hang-Rae KimDepartment of Anatomy & Cell Biology, Seoul National University College of Medicine, Seoul, Korea.ORCID http://orcid.org/0000-0002-3983-6193
Myeong Hee MoonDepartment of Chemistry, Yonsei University, Seoul, Korea.ORCID http://orcid.org/0000-0002-5454-2601
Jong Kyoung KimDepartment of New Biology, DGIST, Daegu, Korea. blkimjk@postech.ac.kr.ORCID http://orcid.org/0000-0002-0257-0547
Geum-Sook HwangIntegrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul, Korea. gshwang@kbsi.re.kr.
Seung-Hoi KooDivision of Life Sciences, Korea University, Seoul, Korea. koohoi@korea.ac.kr.ORCID http://orcid.org/0000-0001-8769-2879
Korea University · KRSeoul National University · KRKorea Basic Science Institute · KRPohang University of Science and Technology · KRYonsei University · KRDaegu Gyeongbuk Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipose tissues are central in controlling metabolic homeostasis and failure in their preservation is associated with age-related metabolic disorders. The exact role of mature adipocytes in this phenomenon remains elusive. Here we describe the role of adipose branched-chain amino acid (BCAA) catabolism in this process. We found that adipocyte-specific Crtc2 knockout protected mice from age-associated metabolic decline. Multiomics analysis revealed that BCAA catabolism was impaired in aged visceral adipose tissues, leading to the activation of mechanistic target of rapamycin complex (mTORC1) signaling and the resultant cellular senescence, which was restored by Crtc2 knockout in adipocytes. Using single-cell RNA sequencing analysis, we found that age-associated decline in adipogenic potential of visceral adipose tissues was reinstated by Crtc2 knockout, via the reduction of BCAA-mTORC1 senescence-associated secretory phenotype axis. Collectively, we propose that perturbation of BCAA catabolism by CRTC2 is critical in instigating age-associated remodeling of adipose tissue and the resultant metabolic decline in vivo.

Indexed as

Adipose TissueMetabolic DiseasesAdipocytesAmino Acids, Branched-ChainAnimalsMechanistic Target of Rapamycin Complex 1MiceAmino Acids, Branched-ChainMechanistic Target of Rapamycin Complex 1

Identifiers

PMID37488415
OpenAlexW4385212999

What Socratic holds

Textmetadata
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.