Evidence map›Paper›PMID 38913153›Full record

ArticlePharmacological reports : PR2024

Multi-layered metabolic effects of trehalose on the liver proteome in apoE-knockout mice model of liver steatosis.

Weronika Pogoda, Jakub Koczur, Aneta Stachowicz, Józef Madej, Rafał Olszanecki, Maciej Suski

Abstract read
In one paragraph

Article in Pharmacological reports : PR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Weronika PogodaProteomics Laboratory, Centre for the Development of Therapies for Civilization and Age-Related Diseases, Jagiellonian University Medical College, Krakow, Poland.
Jakub KoczurDepartment of Pharmacology, Faculty of Medicine, Jagiellonian University Medical College, Kraków, Poland.
Aneta StachowiczDepartment of Pharmacology, Faculty of Medicine, Jagiellonian University Medical College, Kraków, Poland.
Józef MadejDepartment of Pharmacology, Faculty of Medicine, Jagiellonian University Medical College, Kraków, Poland.
Rafał OlszaneckiDepartment of Pharmacology, Faculty of Medicine, Jagiellonian University Medical College, Kraków, Poland.
Maciej SuskiProteomics Laboratory, Centre for the Development of Therapies for Civilization and Age-Related Diseases, Jagiellonian University Medical College, Krakow, Poland. maciej.suski@uj.edu.pl.ORCID http://orcid.org/0000-0001-7575-2184

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetabolic dysfunction-associated fatty liver disease has been well documented as a key independent risk factor for the development of atherosclerosis. A growing body of evidence suggests that due to its numerous favorable molecular effects, trehalose may exert beneficial effects in counteracting liver steatosis. In our previous study, we described the antiatherosclerotic and antisteatotic properties of trehalose, which we attributed to the induction of autophagy. Considering the pleiotropic activities of trehalose, our present study aimed to extend our preliminary results with the comprehensive examination of proteome-wide changes in the livers of high-fat-fed apoE-/- mice.

methodsThus, we applied modern, next-generation proteomic methodology to comprehensively analyze the effects of trehalose on the alterations of liver proteins in apoE-/- mice.

resultsOur proteomic analysis showed that the administration of trehalose elicited profound changes in the liver proteome of apoE-/- mice. The collected data allowed the identification and quantitation of 3 681 protein groups of which 129 were significantly regulated in the livers of trehalose-treated apoE-/- mice.

conclusionsThe presented results are the first to highlight the effects of disaccharide on the induction of proteins mainly related to the metabolism and elimination of lipids, especially by peroxisomal β-oxidation. Our study provides evidence for the pleiotropic activity of trehalose, extending our initial observations of its potential mechanisms responsible for mitigating of liver steatosis, which paves the way for new pharmacological strategies in fatty liver disease.

Indexed as

Apolipoproteins EDisease Models, AnimalFatty LiverLiverProteomeTrehaloseAnimalsDiet, High-FatLipid MetabolismMaleMiceMice, Inbred C57BLMice, KnockoutMice, Knockout, ApoEProteomicsApolipoproteins EProteomeTrehaloseApoe-knockout miceBeta-oxidationLiver steatosisProteomicsTrehalose

Identifiers

PMID38913153
PMCPMC11294376

What OpenQuestion 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 OpenQuestion graph.