Evidence map›Paper›PMID 42650746›Full record

ArticleBiomolecules2026

Selective Pharmacological Activation of PPARα/δ/γ Alters the Triglyceride Composition of Fatty Liver in a Diet-Induced MASLD Mouse Model.

Takako Hishiki, Akihiro Honda, Reina Tanaka, Yukiko Minomo, Otoe Minamisawa, Tsubasa Konno, Shotaro Kamata, Waka Kamichatani, Suzumi M Tokuoka, Yoshihiro Kita and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biomolecules, 2026. 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

12 authors.

Takako HishikiDepartment of Health Chemistry, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan.ORCID 0000-0003-3167-6524
Akihiro HondaDepartment of Health Chemistry, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan.ORCID 0009-0005-3611-5584
Reina TanakaDepartment of Health Chemistry, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan.
Yukiko MinomoDepartment of Health Chemistry, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan.
Otoe MinamisawaDepartment of Health Chemistry, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan.
Tsubasa KonnoDepartment of Health Chemistry, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan.
Shotaro KamataDepartment of Health Chemistry, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan.
Waka KamichataniDepartment of Health Chemistry, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan.
Suzumi M TokuokaDepartment of Lipidomics, Graduate School of Medicine, The University of Tokyo, Bunkyo, Tokyo 113-0033, Japan.
Yoshihiro KitaDepartment of Lipidomics, Graduate School of Medicine, The University of Tokyo, Bunkyo, Tokyo 113-0033, Japan.ORCID 0000-0001-7377-5956
Hideo ShindouDepartment of Lipid Life Science, Japan Institute for Health Security, Shinjuku, Tokyo 162-8655, Japan.
Isao IshiiDepartment of Health Chemistry, Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan.ORCID 0000-0002-5367-205X

Funding

Japan Institute for Health Security 22T001Japan Society for the Promotion of Science 22H05577Japan Society for the Promotion of Science 22K15049Japan Society for the Promotion of Science 24K08642
6 · The paper itself

Abstract

Various high-fat diets have been used to create animal models of metabolic dysfunction-associated steatotic liver disease (MASLD) and to evaluate the effect of various therapeutic drugs. We determined the effects of PPARα/δ/γ subtype-selective agonists (pemafibrate, seladelpar, and pioglitazone, respectively) on the hepatic triglyceride (TG) profile using LC-MS in a MASLD mouse model established by administering a high-fat/high-cholesterol/high-cholic acid (HFCC) diet combined with cyclodextrin-containing water, which is thought to induce fatty liver over a short period. The livers of mice fed the HFCC/CDX diet for four weeks exhibited an approximately fivefold increase in the summed TG LC-MS signal per unit liver weight and altered TG composition compared with normal livers of mice administered a standard diet/water. Specifically, the proportion of TG54 (TG with 54 carbon atoms) species doubled, whereas the proportion of TG52 decreased by 38%. Pemafibrate did not alter the relative total TG signal but decreased the proportion of some TG58/TG56 species and increased the proportion of some TG56/TG52 species. Seladelpar did not alter the relative total TG signal, while only slightly altering TG composition. Pioglitazone reduced the relative total TG signal by 44%, which included a decrease in the proportion of polyunsaturated fatty acid-rich TG54 and an increase in the proportion of TG58/TG56 with 1-3 unsaturated bonds. We are the first to demonstrate that selective activation of PPARα/δ/γ has different effects on the TG profile in fatty liver.

Indexed as

Fatty LiverPPAR alphaPPAR gammaTriglyceridesAnimalsBenzoxazolesButyratesDiet, High-FatDisease Models, AnimalLiverMaleMiceMice, Inbred C57BLPioglitazonePPAR-gamma AgonistsBenzoxazolesButyratesPioglitazonePPAR alphaPpara protein, mousePPAR gammaPPAR-gamma Agonists(R)-2-(3-((benzoxazol-2-yl-d4 (3-(4-methoxyphenoxy-d7)propyl)amino)methyl)phenoxy) butanoic acidTriglycerideslipidomicsliquid chromatography–mass spectrometrymetabolic dysfunction-associated steatohepatitismetabolic dysfunction-associated steatotic liver diseasepemafibrateperoxisome proliferator-activated receptorpioglitazoneseladelpartriacylglycerol

Identifiers

PMID42650746
PMCPMC13510052

What OpenQuestion holds

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Read underepoch 390

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.