Evidence map›Paper›PMID 41156495›Full record

ArticleNutrients2025

Sesaminol Inhibits Adipogenesis by Suppressing Mitotic Clonal Expansion and Activating the Nrf2-ARE Pathway.

Saki Nakamatsu, Miki Nakata, Toshio Norikura, Yutaro Sasaki, Isao Matsui-Yuasa, Ayano Omura, Kunio Kiyomoto, Akiko Kojima-Yuasa

Abstract read
In one paragraph

Article in Nutrients, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Saki NakamatsuDepartment of Nutrition, Graduate School of Human Life and Ecology, Osaka Metropolitan University, Osaka 538-8525, Japan.
Miki NakataDepartment of Nutrition, Graduate School of Human Life and Ecology, Osaka Metropolitan University, Osaka 538-8525, Japan.
Toshio NorikuraDepartment of Nutrition, Aomori University of Health and Welfare, Aomori 030-8505, Japan.ORCID 0000-0002-8285-2965
Yutaro SasakiDepartment of Nutrition, Graduate School of Human Life and Ecology, Osaka Metropolitan University, Osaka 538-8525, Japan.
Isao Matsui-YuasaDepartment of Nutrition, Graduate School of Human Life and Ecology, Osaka Metropolitan University, Osaka 538-8525, Japan.
Ayano OmuraKiyomoto Co., Ltd., Miyazaki 889-0595, Japan.
Kunio KiyomotoKiyomoto Co., Ltd., Miyazaki 889-0595, Japan.
Akiko Kojima-YuasaDepartment of Nutrition, Graduate School of Human Life and Ecology, Osaka Metropolitan University, Osaka 538-8525, Japan.ORCID 0000-0001-8167-3693

Funding

Japan Society for the Promotion of Science 20K11626
6 · The paper itself

Abstract

backgroundAs a key contributor to metabolic disorders, obesity is recognized as a critical global health challenge. Adipocyte differentiation depends on the mitotic clonal expansion (MCE) phase, which is controlled by oxidative balance and transcription factors like C/EBPβ. Sesaminol, a lignan derived from

methodsIn the early period of adipogenic induction, 3T3-L1 preadipocytes received treatment with sesaminol. Adipogenic development was evaluated through Oil Red O staining together with the assay of GPDH activity. Assays of cell proliferation and expression of cell cycle-related proteins, along with ROS measurement, qRT-PCR, Western blotting, and immunofluorescence, were performed to evaluate the effects on oxidative stress, transcriptional regulation, and AMPK-Nrf2 signaling.

resultsSesaminol significantly inhibited lipid accumulation and GPDH activity without cytotoxicity. It suppressed MCE by inhibiting DNA synthesis and reducing the expression of cyclin E1/E2 and CDK2. Sesaminol decreased C/EBPβ expression and its nuclear localization, resulting in lower levels of C/EBPα and PPARγ. It also reduced intracellular ROS, promoted nuclear translocation of Nrf2, and upregulated antioxidant genes HO-1 and GCLC. AMPK phosphorylation was concurrently enhanced.

conclusionsSesaminol inhibits early adipogenesis by suppressing ROS-mediated MCE and activating the AMPK-Nrf2-ARE signaling pathway, leading to downregulation of key adipogenic transcription factors. The present study supports the potential of sesaminol as an effective strategy for obesity prevention.

Indexed as

AdipogenesisAntioxidant Response ElementsDioxolesLignansMitosisNF-E2-Related Factor 23T3-L1 CellsAdipocytesAllylbenzene DerivativesAnimalsAntioxidantsCCAAT-Enhancer-Binding Protein-betaCell ProliferationFuransMiceOxidative StressAllylbenzene DerivativesAntioxidantsCCAAT-Enhancer-Binding Protein-betaDioxolesFuransLignansNfe2l2 protein, mouseNF-E2-Related Factor 2Reactive Oxygen Speciessesaminoladipogenesis inhibitionC/EBPβ centromeremitotic clonal expansion (MCE)Nrf2-ARE pathwayreactive oxygen species (ROS)sesaminol

Identifiers

PMID41156495
PMCPMC12567471

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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.