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Fucosterol Promotes Browning in Mouse 3T3-L1 Adipocytes Through HO-1/Nrf2 and AMPK Pathways
Indyaswan T Suryaningtyas1,2, Won-Kyo Jung1,3,4, Jae-Young Je5
1Research Center for Marine-Integrated Bionics Technology, Pukyong National University, Busan, Republic of Korea.
Biofactors (Oxford, England)
|July 8, 2025
Summary
Fucosterol, a compound from brown seaweed, triggers white fat browning, boosting thermogenesis and lipid breakdown. This discovery offers a new avenue for obesity management by enhancing metabolic health.
Area of Science:
- Biochemistry
- Metabolic Health
- Obesity Research
Background:
- White adipose tissue browning is a key strategy for obesity management.
- Fucosterol, a seaweed phytosterol, has known antioxidant and metabolic benefits.
- Fucosterol's potential to induce adipocyte browning was previously unreported.
Purpose of the Study:
- To investigate the effect of fucosterol on adipocyte browning.
- To elucidate the molecular mechanisms underlying fucosterol-induced browning.
Main Methods:
- 3T3-L1 adipocytes were treated with fucosterol during differentiation.
- Lipid accumulation, adipogenic transcription factors, lipolysis, and browning markers were assessed.
- The roles of HO-1, AMPK, and MAPK pathways were examined.
Main Results:
- Fucosterol suppressed lipid accumulation and downregulated adipogenic factors.
- It upregulated key browning markers (PRDM16, PGC1α, UCP1) dose-dependently.
- Fucosterol activated the Nrf2/HO-1 and AMPK pathways, crucial for thermogenic remodeling.
- Pro-inflammatory cytokines were reduced, and antioxidant enzymes were elevated.
Conclusions:
- Fucosterol effectively induces adipocyte browning in 3T3-L1 cells.
- The HO-1/Nrf2 and AMPK pathways mediate fucosterol's thermogenic effects.
- Fucosterol presents a potential therapeutic agent for obesity and related metabolic disorders.
