Evidence map›Paper›PMID 39022853›Full record

ArticleThe Journal of pathology2024

Increased hepatic putrescine levels as a new potential factor related to the progression of metabolic dysfunction-associated steatotic liver disease.

María Ángeles Núñez-Sánchez, María Antonia Martínez-Sánchez, Marta Sierra-Cruz, Ana Lambertos, Sara Rico-Chazarra, Alba Oliva-Bolarín, Andrés Balaguer-Román, José Enrique Yuste, Carlos Manuel Martínez, Adriana Mika and 4 more

Abstract read
In one paragraph

Article in The Journal of pathology, 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
–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

10 citing papers in PubMed.

  1. Trial
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  3. Review
  4. Article
  5. Article
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  7. Review
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  10. 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

14 authors.

María Ángeles Núñez-Sánchez *Obesity, Diabetes and Metabolism Laboratory, Biomedical Research Institute of Murcia (IMIB), Murcia, Spain.ORCID 0000-0002-8938-2767
María Antonia Martínez-Sánchez *Obesity, Diabetes and Metabolism Laboratory, Biomedical Research Institute of Murcia (IMIB), Murcia, Spain.ORCID 0000-0001-9750-4237
Marta Sierra-CruzDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Illinois, Chicago, IL, USA.ORCID 0000-0002-1904-7859
Ana LambertosDepartment of Biochemistry and Molecular Biology B and Immunology, Faculty of Medicine, University of Murcia, Murcia, Spain.ORCID 0000-0001-5616-2218
Sara Rico-ChazarraObesity, Diabetes and Metabolism Laboratory, Biomedical Research Institute of Murcia (IMIB), Murcia, Spain.ORCID 0009-0002-4490-1866
Alba Oliva-BolarínObesity, Diabetes and Metabolism Laboratory, Biomedical Research Institute of Murcia (IMIB), Murcia, Spain.ORCID 0000-0002-9308-1043
Andrés Balaguer-RománObesity, Diabetes and Metabolism Laboratory, Biomedical Research Institute of Murcia (IMIB), Murcia, Spain.ORCID 0000-0002-5297-0194
José Enrique YusteMetabolomics Platform of CEBAS-CSIC, Campus Universitario de Espinardo, Murcia, Spain.ORCID 0000-0002-9847-0275
Carlos Manuel MartínezExperimental Pathology Platform, Biomedical Research Institute of Murcia (IMIB), Murcia, Spain.ORCID 0000-0003-3307-1326
Adriana MikaDepartment of Pharmaceutical Biochemistry, Faculty of Pharmacy, Medical University of Gdansk, Gdansk, Poland.ORCID 0000-0003-2877-5652
María Dolores FrutosDepartment of General and Digestive System Surgery, Virgen de la Arrixaca University Hospital, Murcia, Spain.
Camilo J Llamoza-TorresObesity, Diabetes and Metabolism Laboratory, Biomedical Research Institute of Murcia (IMIB), Murcia, Spain.
José Córdoba-ChacónDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Illinois, Chicago, IL, USA.ORCID 0000-0001-8787-2706
Bruno Ramos-MolinaObesity, Diabetes and Metabolism Laboratory, Biomedical Research Institute of Murcia (IMIB), Murcia, Spain.ORCID 0000-0001-6804-5449

Funding

PPARgamma-regulated mechanisms in hepatocytes that promote NAFLDR01DK131038 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Jose Cordoba-Chacon · 2022 to 2026
$2.1M
Regulation of methionine metabolism in NASH by PPARgammaR03DK129419 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CORDOBA-CHACON, JOSE · 2022 to 2023
$237k
Instituto de Salud Carlos III CP19/00098Instituto de Salud Carlos III CP23/00051Instituto de Salud Carlos III FI21/00003Instituto de Salud Carlos III PI20/00505Instituto de Salud Carlos III PI23/00171National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health (NIH) R01DK131038National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health (NIH) R03DK129419NIDDK NIH HHS R01 DK131038NIDDK NIH HHS R03 DK129419
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic liver condition that often progresses to more advanced stages, such as metabolic dysfunction-associated steatohepatitis (MASH). MASH is characterized by inflammation and hepatocellular ballooning, in addition to hepatic steatosis. Despite the relatively high incidence of MASH in the population and its potential detrimental effects on human health, this liver disease is still not fully understood from a pathophysiological perspective. Deregulation of polyamine levels has been detected in various pathological conditions, including neurodegenerative diseases, inflammation, and cancer. However, the role of the polyamine pathway in chronic liver disorders such as MASLD has not been explored. In this study, we measured the expression of liver ornithine decarboxylase (ODC1), the rate-limiting enzyme responsible for the production of putrescine, and the hepatic levels of putrescine, in a preclinical model of MASH as well as in liver biopsies of patients with obesity undergoing bariatric surgery. Our findings reveal that expression of ODC1 and the levels of putrescine, but not spermidine nor spermine, are elevated in hepatic tissue of both diet-induced MASH mice and patients with biopsy-proven MASH compared with control mice and patients without MASH, respectively. Furthermore, we found that the levels of putrescine were positively associated with higher aspartate aminotransferase concentrations in serum and an increased SAF score (steatosis, activity, fibrosis). Additionally, in in vitro assays using human HepG2 cells, we demonstrate that elevated levels of putrescine exacerbate the cellular response to palmitic acid, leading to decreased cell viability and increased release of CK-18. Our results support an association between the expression of ODC1 and the progression of MASLD, which could have translational relevance in understanding the onset of this disease. © 2024 The Pathological Society of Great Britain and Ireland.

Indexed as

Disease ProgressionLiverOrnithine DecarboxylasePutrescineAdultAnimalsDisease Models, AnimalFatty LiverFemaleHep G2 CellsHumansMaleMiceMice, Inbred C57BLMiddle AgedObesityOrnithine DecarboxylasePutrescineliver metabolismmetabolic dysfunction‐associated steatohepatitismetabolic dysfunction‐associated steatotic liver diseaseobesityornithine decarboxylasepolyamine

Identifiers

PMID39022853
PMCPMC11300153

What Socratic holds

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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.