Evidence map›Paper›PMID 32969559›Full record

ArticleCancer science2020

Combined administration of lauric acid and glucose improved cancer-derived cardiac atrophy in a mouse cachexia model.

Shota Nukaga, Takuya Mori, Yoshihiro Miyagawa, Rina Fujiwara-Tani, Takamitsu Sasaki, Kiyomu Fujii, Shiori Mori, Kei Goto, Shingo Kishi, Chie Nakashima and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer science, 2020. 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
1.3field-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

23 citing papers in PubMed, 30 citations in OpenAlex.

  1. Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026
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  9. Effects of Antioxidant Amino Acids on Cancer Sarcopenia.International journal of molecular sciences · 2024
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  11. Review
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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

14 authors at 4 institutions in 2 countries.

Shota NukagaDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Takuya MoriDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Yoshihiro MiyagawaDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Rina Fujiwara-TaniDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Takamitsu SasakiDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Kiyomu FujiiDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Shiori MoriDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Kei GotoDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Shingo KishiDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Chie NakashimaDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Hitoshi OhmoriDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Isao KawaharaDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.
Yi LuoKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Hiroki KuniyasuDepartment of Molecular Pathology, Nara Medical University, Kashihara, Japan.ORCID https://orcid.org/0000-0003-2298-8825
Nara Medical University · JPHakodate Central General Hospital · JPNantong University · CNNishida Hospital · JP

Funding

Ministry of Education, Culture, Sports, Science and Technology 18K10788Ministry of Education, Culture, Sports, Science and Technology 19K16564Ministry of Education, Culture, Sports, Science and Technology 19K19332Ministry of Education, Culture, Sports, Science and Technology 19K19915Ministry of Education, Culture, Sports, Science and Technology 20K11260Ministry of Education, Culture, Sports, Science and Technology 20K18007Ministry of Education, Culture, Sports, Science and Technology 20K19349National Natural Science Foundation of China 81702723Natural Science Foundation of Jiangsu Education Department Project 17KJB320010
6 · The paper itself

Abstract

Cancer-derived myocardial damage is an important cause of death in cancer patients. However, the development of dietary interventions for treating such damage has not been advanced. Here, we investigated the effect of dietary intervention with lauric acid (LAA) and glucose, which was effective against skeletal muscle sarcopenia in a mouse cachexia model, on myocardial damage. Treatment of H9c2 rat cardiomyoblasts with lauric acid promoted mitochondrial respiration and increased ATP production by Seahorse flux analysis, but did not increase oxidative stress. Glycolysis was also promoted by LAA. In contrast, mitochondrial respiration and ATP production were suppressed, and oxidative stress was increased in an in vitro cachexia model in which cardiomyoblasts were treated with mouse cachexia ascites. Ascites-treated H9c2 cells with concurrent treatment with LAA and high glucose showed that mitochondrial respiration and glycolysis were promoted more than that of the control, and ATP was restored to the level of the control. Oxidative stress was also reduced by the combined treatment. In the mouse cachexia model, myocardiac atrophy and decreased levels of a marker of muscle maturity, SDS-soluble MYL1, were observed. When LAA in CE-2 diet was orally administered alone, no significant rescue was observed in the cancer-derived myocardial disorder. In contrast, combined oral administration of LAA and glucose recovered myocardial atrophy and MYL1 to levels observed in the control without increase in the cancer weight. Therefore, it is suggested that dietary intervention using a combination of LAA and glucose for cancer cachexia might improve cancer-derived myocardial damage.

Indexed as

Adenosine TriphosphateAnimalsCachexiaCell LineCell Line, TumorEnergy MetabolismGlucoseGlycolysisLauric AcidsMaleMiceMice, Inbred BALB CMitochondria, HeartMuscular AtrophyMyocytes, CardiacOxidative StressAdenosine TriphosphateGlucoselauric acidLauric AcidsPML protein, humanPromyelocytic Leukemia Proteinatrophycachexiamitochondriamyocardiumoxidative stress

Identifiers

PMID32969559
PMCPMC7734008
OpenAlexW3088781611

What OpenQuestion holds

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LicenceCC BY-NC
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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.