Evidence map›Paper›PMID 39718621›Full record

ArticleAmino acids2024

Comprehensive analysis of peripheral blood free amino acids in MASLD: the impact of glycine-serine-threonine metabolism.

Masaaki Mino, Eiji Kakazu, Akitoshi Sano, Mio Tsuruoka, Hiroko Matsubara, Keisuke Kakisaka, Takayuki Kogure, Katsunori Sekine, Yoshihiko Aoki, Masatoshi Imamura and 7 more

Abstract read
In one paragraph

Article in Amino acids, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
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  6. Article
  7. Review
  8. Metabolomics Reveals the Anti-hepatic Fibrosis Mechanisms ofInternational journal of medical sciences · 2026
    Article
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  10. Review
  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

17 authors.

Masaaki MinoDepartment of Gastroenterology and Hepatology, Kohnodai Hospital, National Center for Global Health and Medicine, 1-7-1 Kohnodai, Ichikawa, Chiba, 272-8516, Japan.
Eiji KakazuDepartment of Gastroenterology and Hepatology, Kohnodai Hospital, National Center for Global Health and Medicine, 1-7-1 Kohnodai, Ichikawa, Chiba, 272-8516, Japan. kakazu@coral.ocn.ne.jp.
Akitoshi SanoDivision of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Mio TsuruokaDivision of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Hiroko MatsubaraDepartment of Biobank, Tohoku Medical Megabank Organization, Tohoku University, Sendai, Miyagi, Japan.
Keisuke KakisakaDivision of Gastroenterology and Hepatology, Iwate Medical University School of Medicine, Yahaba, Iwate, Japan.
Takayuki KogureDivision of Gastroenterology Tohoku Medical and Pharmaceutical University, Sendai, Miyagi, Japan.
Katsunori SekineDepartment of Gastroenterology and Hepatology, Kohnodai Hospital, National Center for Global Health and Medicine, 1-7-1 Kohnodai, Ichikawa, Chiba, 272-8516, Japan.
Yoshihiko AokiDepartment of Gastroenterology and Hepatology, Kohnodai Hospital, National Center for Global Health and Medicine, 1-7-1 Kohnodai, Ichikawa, Chiba, 272-8516, Japan.
Masatoshi ImamuraDepartment of Gastroenterology and Hepatology, Kohnodai Hospital, National Center for Global Health and Medicine, 1-7-1 Kohnodai, Ichikawa, Chiba, 272-8516, Japan.
Michitaka MatsudaDepartment of Liver Diseases, The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Ichikawa, Chiba, Japan.
Taiji YamazoeDepartment of Liver Diseases, The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Ichikawa, Chiba, Japan.
Taizo MoriDepartment of Liver Diseases, The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Ichikawa, Chiba, Japan.
Sachiyo YoshioDepartment of Liver Diseases, The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Ichikawa, Chiba, Japan.
Jun InoueDivision of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Atsushi MasamuneDivision of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Tatsuya KantoDepartment of Gastroenterology and Hepatology, Kohnodai Hospital, National Center for Global Health and Medicine, 1-7-1 Kohnodai, Ichikawa, Chiba, 272-8516, Japan.

Funding

Grant-in-Aid for Research from the National Center for Global Health and Medicine 21A2009Japan Agency for Medical Research and Development JP24fk0210114Ministry of Education, Culture, Sports, Science, and Technology of Japan 24K11078
6 · The paper itself

Abstract

Little is known about how blood free amino acids (FAAs) change in metabolic dysfunction-associated steatotic liver disease (MASLD). This study aims to identify the imbalance of FAAs in MASLD and explore its correction as a potential therapeutic target. We analyzed plasma FAAs data from 23,036 individuals with steatosis information from a biobank in Japan, and 310 patients with MASLD were enrolled. According to diagnostic criteria for steatotic liver disease (SLD) or cardiometabolic criteria (CC), we divided the subjects into five groups: MASLD, metabolic dysfunction and alcohol-associated liver disease (MetALD), CC-SLD-, CC + SLD-, and CC-SLD + . Twenty FAAs were compared among these groups and among MASLD patients with pathological information. Among the 20 FAAs, the levels of 16 FAAs increased in CC + SLD- according to the number of matches with CC items associated with insulin resistance (IR). Steatosis enhanced most of these changes but serine (Ser) and threonine (Thr) were unaffected. Glycine (Gly), Ser and Thr were significantly decreased in patients according to steatosis grade. We investigated the association between these FAAs imbalances and pathogenesis using MASLD mouse models. In mice fed a high-fat, fructose, and cholesterol (FFC) diet, metabolomics and RNA sequencing analyses indicated that abnormality in Gly, Ser, and Thr metabolism in the liver was associated with mitochondrial dysfunction and enhanced glycolysis via pyruvate. High-Gly, Ser, and Thr diet ameliorated pathogenesis of MASLD in leptin-deficient mice. Most FAAs increase due to cardiometabolic abnormalities, particularly IR. However, interventions targeting the metabolism of Gly, Ser, and Thr have the potential to improve MASLD.

Indexed as

Fatty LiverGlycineSerineThreonineAgedAmino AcidsAnimalsFemaleHumansInsulin ResistanceLiverMaleMiceMice, Inbred C57BLMiddle AgedAmino AcidsGlycineSerineThreonineCardiometabolic criteriaMASHMetALDNASHSLD

Identifiers

PMID39718621
PMCPMC11668895

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LicenceCC BY-NC-ND
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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.