Evidence map›Paper›PMID 38619434›Full record

ArticleHepatology communications2024

Potential utility of l-carnitine for preventing liver tumors derived from metabolic dysfunction-associated steatohepatitis.

Junyan Lyu, Hikari Okada, Hajime Sunagozaka, Kazunori Kawaguchi, Tetsuro Shimakami, Kouki Nio, Kazuhisa Murai, Takayoshi Shirasaki, Mika Yoshida, Kuniaki Arai and 7 more

Open access · goldAbstract read
In one paragraph

Article in Hepatology communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. MASLD/MASH-New mechanisms and treatments.Hepatology communications · 2025
    Article
  9. Targeting Metabolism: Innovative Therapies for MASLD Unveiled.International journal of molecular sciences · 2025
    Review
  10. 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

17 authors at 2 institutions in 1 country.

Junyan LyuDepartment of Clinical Laboratory Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Hikari OkadaDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Hajime SunagozakaDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Kazunori KawaguchiDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Tetsuro ShimakamiDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Kouki NioDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Kazuhisa MuraiDepartment of Clinical Laboratory Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Takayoshi ShirasakiDepartment of Clinical Laboratory Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Mika YoshidaDepartment of Clinical Laboratory Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Kuniaki AraiDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Tatsuya YamashitaDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Takuji TanakaResearch Center of Diagnostic Pathology, Gifu Municipal Hospital, Gifu, Japan.
Kenichi HaradaDepartment of Human Pathology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Toshinari TakamuraDepartment of Endocrinology and Metabolism, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Shuichi KanekoDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Taro YamashitaDepartment of Gastroenterology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.
Masao HondaDepartment of Clinical Laboratory Medicine, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan.ORCID 0000-0003-3050-5854
Kanazawa University · JPGifu Municipal Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent reports have unveiled the potential utility of l-carnitine to alleviate metabolic dysfunction-associated steatohepatitis (MASH) by enhancing mitochondrial metabolic function. However, its efficacy at preventing the development of HCC has not been assessed fully.

methodsl-carnitine (2 g/d) was administered to 11 patients with MASH for 10 weeks, and blood liver function tests were performed. Five patients received a serial liver biopsy, and liver histology and hepatic gene expression were evaluated using this tissue. An atherogenic plus high-fat diet MASH mouse model received long-term l-carnitine administration, and liver histology and liver tumor development were evaluated.

resultsTen-week l-carnitine administration significantly improved serum alanine transaminase and aspartate transaminase levels along with a histological improvement in the NAFLD activity score, while steatosis and fibrosis were not improved. Gene expression profiling revealed a significant improvement in the inflammation and profibrotic gene signature as well as the recovery of lipid metabolism. Long-term l-carnitine administration to atherogenic plus high-fat diet MASH mice substantially improved liver histology (inflammation, steatosis, and fibrosis) and significantly reduced the incidence of liver tumors. l-carnitine directly reduced the expression of the MASH-associated and stress-induced transcriptional factor early growth response 1. Early growth response 1 activated the promoter activity of neural precursor cell expressed, developmentally downregulated protein 9 (NEDD9), an oncogenic protein. Thus, l-carnitine reduced the activation of the NEDD9, focal adhesion kinase 1, and AKT oncogenic signaling pathway.

conclusionsShort-term l-carnitine administration ameliorated MASH through its anti-inflammatory effects. Long-term l-carnitine administration potentially improved the steatosis and fibrosis of MASH and may eventually reduce the risk of HCC.

Indexed as

Carcinoma, HepatocellularFatty LiverLiver NeoplasmsAdaptor Proteins, Signal TransducingAnimalsCarnitineFibrosisHumansInflammationMiceAdaptor Proteins, Signal TransducingCarnitineNEDD9 protein, human

Identifiers

PMID38619434
PMCPMC11019826
OpenAlexW4394807815

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.