Evidence map›Paper›PMID 32146873›Full record

ArticlePhysiological genomics2020

Hepatic proteome analysis reveals altered mitochondrial metabolism and suppressed acyl-CoA synthetase-1 in colon-26 tumor-induced cachexia.

Andy V Khamoui, Dorota Tokmina-Roszyk, Harry B Rossiter, Gregg B Fields, Nishant P Visavadiya

Open access · greenAbstract read
In one paragraph

Article in Physiological genomics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Inflammation-induced cholestasis in cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2021
    Article
  17. Article
  18. Review
  19. Cachexia, a Systemic Disease beyond Muscle Atrophy.International journal of molecular sciences · 2020
    Review
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

5 authors at 3 institutions in 2 countries.

Andy V KhamouiDepartment of Exercise Science and Health Promotion, Florida Atlantic University, Boca Raton, Florida.ORCID 0000-0003-4449-536X
Dorota Tokmina-RoszykInstitute for Human Health & Disease Intervention, Florida Atlantic University, Jupiter, Florida.
Harry B RossiterDivision of Respiratory and Critical Care Physiology and Medicine, Department of Medicine, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, California.ORCID 0000-0002-7884-0726
Gregg B FieldsInstitute for Human Health & Disease Intervention, Florida Atlantic University, Jupiter, Florida.
Nishant P VisavadiyaDepartment of Exercise Science and Health Promotion, Florida Atlantic University, Boca Raton, Florida.
Florida Atlantic University · USScripps Research Institute · USUniversity of Leeds · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cachexia is a life-threatening complication of cancer traditionally characterized by weight loss and muscle dysfunction. Cachexia, however, is a systemic disease that also involves remodeling of nonmuscle organs. The liver exerts major control over systemic metabolism, yet its role in cancer cachexia is not well understood. To advance the understanding of how the liver contributes to cancer cachexia, we used quantitative proteomics and bioinformatics to identify hepatic pathways and cellular processes dysregulated in mice with moderate and severe colon-26 tumor-induced cachexia; ~300 differentially expressed proteins identified during the induction of moderate cachexia were also differentially regulated in the transition to severe cachexia. KEGG pathway enrichment revealed representation by oxidative phosphorylation, indicating altered hepatic mitochondrial function as a common feature across cachexia severity. Glycogen catabolism was also observed in cachexic livers along with decreased pyruvate dehydrogenase protein X component (Pdhx), increased lactate dehydrogenase A chain (Ldha), and increased lactate transporter Mct1. Together this suggests altered lactate metabolism and transport in cachexic livers, which may contribute to energetically inefficient interorgan lactate cycling. Acyl-CoA synthetase-1 (ACSL1), known for activating long-chain fatty acids, was decreased in moderate and severe cachexia based on LC-MS/MS analysis and immunoblotting. ACSL1 showed strong linear relationships with percent body weight change and muscle fiber size (R

Indexed as

AnimalsCachexiaChromatography, LiquidCoenzyme A LigasesColonic NeoplasmsEnergy MetabolismFatty AcidsLiverMiceMice, Inbred BALB CMitochondria, LiverProteomeRandom AllocationTandem Mass SpectrometryWeight LossACSL1 protein, mouseCoenzyme A LigasesFatty AcidsProteomebioinformaticsmitochondrial functionquantitative proteomicsSTRINGTMT

Identifiers

PMID32146873
PMCPMC8526341
OpenAlexW3011817008

What OpenQuestion 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 OpenQuestion graph.