Evidence map›Paper›PMID 38474208›Full record

ArticleInternational journal of molecular sciences2024

Semaglutide Improves Liver Steatosis and De Novo Lipogenesis Markers in Obese and Type-2-Diabetic Mice with Metabolic-Dysfunction-Associated Steatotic Liver Disease.

Manuel Soto-Catalán, Lucas Opazo-Ríos, Hernán Quiceno, Iolanda Lázaro, Juan Antonio Moreno, Carmen Gómez-Guerrero, Jesús Egido, Sebastian Mas-Fontao

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
12.0field-weighted citation impact, top 1% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

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  11. Focus on Semaglutide 2.4 mg/week for the Treatment of Metabolic Dysfunction-Associated Steatohepatitis.Liver international : official journal of the International Association for the Study of the Liver · 2025
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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

8 authors at 5 institutions in 2 countries.

Manuel Soto-CatalánRenal, Vascular and Diabetes Research Laboratory, IIS-Fundación Jiménez Díaz, Spanish Biomedical Universidad Autónoma de Madrid, 28049 Madrid, Spain.
Lucas Opazo-RíosRenal, Vascular and Diabetes Research Laboratory, IIS-Fundación Jiménez Díaz, Spanish Biomedical Universidad Autónoma de Madrid, 28049 Madrid, Spain.ORCID 0000-0003-3586-3319
Hernán QuicenoDepartment of Pathology, Fundación Jiménez Díaz, 28040 Madrid, Spain.
Iolanda LázaroCardiovascular Risk and Nutrition Research Group, Epidemiology and Public Health Program, Hospital del Mar Medical Research Institute (IMIM), 08003 Barcelona, Spain.
Juan Antonio MorenoDepartment of Cell Biology, Physiology and Immunology, University of Cordoba, 140471 Cordoba, Spain.ORCID 0000-0002-7468-2871
Carmen Gómez-GuerreroRenal, Vascular and Diabetes Research Laboratory, IIS-Fundación Jiménez Díaz, Spanish Biomedical Universidad Autónoma de Madrid, 28049 Madrid, Spain.ORCID 0000-0001-9001-5414
Jesús EgidoRenal, Vascular and Diabetes Research Laboratory, IIS-Fundación Jiménez Díaz, Spanish Biomedical Universidad Autónoma de Madrid, 28049 Madrid, Spain.
Sebastian Mas-FontaoRenal, Vascular and Diabetes Research Laboratory, IIS-Fundación Jiménez Díaz, Spanish Biomedical Universidad Autónoma de Madrid, 28049 Madrid, Spain.ORCID 0000-0001-6604-3327
Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESHospital Del Mar · ESHospital Universitario Fundación Jiménez Díaz · ESInstituto Maimónides de Investigación Biomédica de Córdoba · ESUniversity of Concepción · CL

Funding

Instituto de Salud Carlos III PI20/00375Instituto de Salud Carlos III PI23/00119
6 · The paper itself

Abstract

Metabolic-dysfunction-associated steatotic liver disease (MASLD) is a prevalent clinical condition associated with elevated morbidity and mortality rates. Patients with MASLD treated with semaglutide, a glucagon-like peptide-1 receptor agonist, demonstrate improvement in terms of liver damage. However, the mechanisms underlaying this beneficial effect are not yet fully elucidated. We investigated the efficacy of semaglutide in halting MASLD progression using a genetic mouse model of diabesity. Leptin-receptor-deficient mice with obesity and diabetes (BKS db/db) were either untreated or administered with semaglutide for 11 weeks. Changes in food and water intake, body weight and glycemia were monitored throughout the study. Body fat composition was assessed by dual-energy X-ray absorptiometry. Upon sacrifice, serum biochemical parameters, liver morphology, lipidomic profile and liver-lipid-related pathways were evaluated. The semaglutide-treated mice exhibited lower levels of glycemia, body weight, serum markers of liver dysfunction and total and percentage of fat mass compared to untreated db/db mice without a significant reduction in food intake. Histologically, semaglutide reduced hepatic steatosis, hepatocellular ballooning and intrahepatic triglycerides. Furthermore, the treatment ameliorated the hepatic expression of de novo lipogenesis markers and modified lipid composition by increasing the amount of polyunsaturated fatty acids. The administration of semaglutide to leptin-receptor-deficient, hyperphagic and diabetic mice resulted in the amelioration of MASLD, likely independently of daily caloric intake, suggesting a direct effect of semaglutide on the liver through modulation of the lipid profile.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Fatty LiverGlucagon-Like PeptidesNon-alcoholic Fatty Liver DiseaseAnimalsBody WeightHumansLeptinLipogenesisLiverMiceMice, ObeseObesitySemaglutideTriglyceridesGlucagon-Like PeptidesLeptinSemaglutideTriglyceridesdiabetesGLP1 receptor agonistsinsulin resistanceobesitysemaglutidesteatosis

Identifiers

PMID38474208
PMCPMC10932050
OpenAlexW4392375364

What OpenQuestion holds

Texttitle and abstract
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 OpenQuestion graph.