Evidence map›Paper›PMID 32982112›Full record

ArticleWorld journal of gastroenterology2020

Arachidyl amido cholanoic acid improves liver glucose and lipid homeostasis in nonalcoholic steatohepatitis

David Fernández-Ramos, Fernando Lopitz-Otsoa, Laura Delacruz-Villar, Jon Bilbao, Martina Pagano, Laura Mosca, Maider Bizkarguenaga, Marina Serrano-Macia, Mikel Azkargorta, Marta Iruarrizaga-Lejarreta and 10 more

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

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  12. Carvedilol impairs bile acid homeostasis in mice: implication for nonalcoholic steatohepatitis.Toxicological sciences : an official journal of the Society of Toxicology · 2023
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  15. iScience · 2022
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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

20 authors at 2 institutions in 2 countries.

David Fernández-RamosPrecision Medicine and Metabolism Laboratory, Centro de Investigación Cooperativa en Biociencias (CIC bioGUNE), Derio 48160, Bizkaia, Spain.
Fernando Lopitz-OtsoaPrecision Medicine and Metabolism Laboratory, Centro de Investigación Cooperativa en Biociencias (CIC bioGUNE), Derio 48160, Bizkaia, Spain.
Laura Delacruz-VillarPrecision Medicine and Metabolism Laboratory, Centro de Investigación Cooperativa en Biociencias (CIC bioGUNE), Derio 48160, Bizkaia, Spain.
Jon BilbaoPrecision Medicine and Metabolism Laboratory, Centro de Investigación Cooperativa en Biociencias (CIC bioGUNE), Derio 48160, Bizkaia, Spain.
Martina PaganoDepartment of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples 80138, Italy.
Laura MoscaDepartment of Precision Medicine, University of Campania "Luigi Vanvitelli", Naples 80138, Italy.
Maider BizkarguenagaPrecision Medicine and Metabolism Laboratory, Centro de Investigación Cooperativa en Biociencias (CIC bioGUNE), Derio 48160, Bizkaia, Spain.
Marina Serrano-MaciaLiver Disease Laboratory, Centro de Investigación Cooperativa en Biociencias (CIC bioGUNE), Derio 48160, Spain.
Mikel AzkargortaProteomics Platform, Centro de Investigación Cooperativa en Biociencias (CIC bioGUNE), Derio 48160, Spain.
Marta Iruarrizaga-LejarretaOWL Metabolomics, Derio 48160, Spain.
Jesús SotInstituto Biofisika (UPV/EHU, CSIC), Leioa 48940, Spain; Departamento de Bioquímica y Biología Molecular, Universidad del País Vasco, Leioa 48940, Spain.
Darya TsvirkunPre-clinical and Chemistry, Manufacturing and Controls, Galmed Pharmaceuticals, Tel Aviv 6578317, Israel.
Sebastiaan Martijn van LiempdMetabolomics Platform, Centro de Investigación Cooperativa en Biociencias (CIC bioGUNE), Derio 48160, Spain.
Felix M GoniInstituto Biofisika (UPV/EHU, CSIC), Leioa 48940, Spain; Departamento de Bioquímica y Biología Molecular, Universidad del País Vasco, Leioa 48940, Spain.
Cristina AlonsoOWL Metabolomics, Derio 48160, Spain.
María Luz Martínez-ChantarCIBERehd - Centro de Investigación Biomédica en Red de enfermedades hepáticas y digestivas, Madrid 28029, Spain.
Felix ElortzaProteomics Platform, Centro de Investigación Cooperativa en Biociencias (CIC bioGUNE), Derio 48160, Spain.
Liat HayardenyPre-clinical and Chemistry, Manufacturing and Controls, Galmed Pharmaceuticals, Tel Aviv 6578317, Israel.
Shelly C LuDivision of Digestive and Liver Diseases, Cedars-Sinai Medical Center, Los Angeles, CA 90048, United States.
José M MatoPrecision Medicine and Metabolism Laboratory, Centro de Investigación Cooperativa en Biociencias (CIC bioGUNE), Derio 48160, Bizkaia, Spain.
University of Campania "Luigi Vanvitelli" · ITCedars-Sinai Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundArachidyl amido cholanoic acid (Aramchol) is a potent downregulator of hepatic stearoyl-CoA desaturase 1 (SCD1) protein expression that reduces liver triglycerides and fibrosis in animal models of steatohepatitis. In a phase IIb clinical trial in patients with nonalcoholic steatohepatitis (NASH), 52 wk of treatment with Aramchol reduced blood levels of glycated hemoglobin A1c, an indicator of glycemic control.

aimTo assess lipid and glucose metabolism in mouse hepatocytes and in a NASH mouse model [induced with a 0.1% methionine and choline deficient diet (0.1MCD)] after treatment with Aramchol.

methodsIsolated primary mouse hepatocytes were incubated with 20 μmol/L Aramchol or vehicle for 48 h. Subsequently, analyses were performed including Western blot, proteomics by mass spectrometry, and fluxomic analysis with

resultsCombination of proteomics and Western blot analyses showed increased AMPK activity while the activity of nutrient sensor mTORC1 was decreased by Aramchol in hepatocytes. This translated into changes in the content of their downstream targets including proteins involved in fatty acid (FA) synthesis and oxidation [P-ACCα/β(S79), SCD1, CPT1A/B, HADHA, and HADHB], oxidative phosphorylation (NDUFA9, NDUFB11, NDUFS1, NDUFV1, ETFDH, and UQCRC2), tricarboxylic acid (TCA) cycle (MDH2, SUCLA2, and SUCLG2), and ribosome (P-p70S6K[T389] and P-S6[S235/S236]). Flux experiments with

conclusionAramchol exerts its effect on glucose and lipid metabolism in NASH through activation of AMPK and inhibition of mTORC1, which in turn activate FA β-oxidation and oxidative phosphorylation.

Indexed as

Non-alcoholic Fatty Liver DiseaseAMP-Activated Protein KinasesAnimalsCholic AcidsDisease Models, AnimalGlucoseHomeostasisHumansLipid MetabolismLipidsLiverMaleMethionineMiceMice, Inbred C57BLTOR Serine-Threonine KinasesAMP-Activated Protein KinasesaramcholCholic AcidsGlucoseLipidsMethionineMTOR protein, humanTOR Serine-Threonine KinasesHemoglobin A1cMethionine and choline deficient dietNonalcoholic fatty liver diseaseStearoyl-CoA desaturase 1SteatohepatitisTricarboxylic acid cycle

Identifiers

PMID32982112
PMCPMC7495035
OpenAlexW3083964491

What OpenQuestion holds

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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.