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

Saki Nakamatsu1, Miki Nakata1, Toshio Norikura2

  • 1Department of Nutrition, Graduate School of Human Life and Ecology, Osaka Metropolitan University, Osaka 538-8525, Japan.

Nutrients
|October 29, 2025
PubMed
Abstract

Insights

Sesaminol, an antioxidant from sesame, inhibits obesity by reducing fat cell growth and activating protective pathways. This research supports sesaminol for obesity prevention strategies.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Metabolic Research

Background:

  • Obesity is a major global health issue linked to metabolic disorders.
  • Adipocyte differentiation, crucial for fat development, involves mitotic clonal expansion (MCE) regulated by oxidative balance and transcription factors.
  • Sesaminol, a potent antioxidant from Sesamum indicum, was investigated for its anti-adipogenic effects.

Purpose of the Study:

  • To determine if sesaminol suppresses adipogenesis.
  • To investigate sesaminol's modulation of reactive oxygen species (ROS) signaling, MCE, and the Nrf2-ARE pathway.

Main Methods:

  • 3T3-L1 preadipocytes were treated with sesaminol during adipogenic induction.
  • Evaluated adipogenic markers (Oil Red O, GPDH activity), cell proliferation, cell cycle proteins, ROS levels, and gene/protein expression via qRT-PCR, Western blotting, and immunofluorescence.
  • Assessed effects on oxidative stress, transcriptional regulation, and AMP-activated protein kinase (AMPK)-Nrf2 signaling.

Main Results:

  • Sesaminol inhibited lipid accumulation and GPDH activity without cytotoxicity.
  • Suppressed MCE by reducing DNA synthesis and cyclin E1/E2 and CDK2 expression.
  • Decreased C/EBPβ expression and nuclear localization, lowering C/EBPα and PPARγ levels.
  • Reduced intracellular ROS, enhanced Nrf2 nuclear translocation, upregulated HO-1 and GCLC, and increased AMPK phosphorylation.

Conclusions:

  • Sesaminol effectively inhibits early adipogenesis.
  • Mechanism involves suppressing ROS-mediated MCE and activating the AMPK-Nrf2-ARE pathway.
  • Downregulates key adipogenic transcription factors, supporting sesaminol's potential for obesity prevention.
Keywords:
C/EBPβ centromereNrf2-ARE pathwayadipogenesis inhibitionmitotic clonal expansion (MCE)reactive oxygen species (ROS)sesaminol

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