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Allyl Isothiocyanate Ameliorates Obesity by Inhibiting Galectin-12
Chia-Wen Lo1, Chih-Sheng Chen2,3,4, Ying-Chi Chen5
1School of Chinese Medicine, China Medical University, Taichung, Taiwan.
Scope:
The aim of this study is to investigate the signaling pathways by which allyl isothiocyanate (AITC) reduces adipocyte differentiation and the efficacy of AITC in suppressing galectin-12 levels as a therapeutic for high fat diet (HFD)-induced obesity.
Methods And Results:
AITC presents anti-adipogenic effects on 3T3-L1 cells by decreasing lipid droplet accumulation in a dose-dependent manner. AITC suppresses 3T3-L1 differentiation into adipocytes by decreasing galectin-12 expression and by downregulating key adipogenic transcription factors. AITC influences the expression of 3T3-L1 pre-adipocytes by modulating adipokine expression (leptin and resistin) and by regulating the protein kinase B (PKB/Akt)/cAMP response element-binding protein (CREB) pathway. In HFD-fed mice, oral administration of AITC reduces the body weight, accumulation of lipid droplets in the liver, and white adipocyte size.
Conclusion:
In summary, the results indicate that AITC inhibits adipocyte differentiation by suppressing galectin-12 levels in 3T3L1 cells and has antiobesity effects in HFD-fed mice.
Insights
Allyl isothiocyanate (AITC) inhibits adipocyte differentiation by reducing galectin-12 levels. This compound also demonstrates anti-obesity effects in high-fat diet-induced obesity models.
Area of Science:
- Biochemistry
- Cell Biology
- Metabolic Research
Background:
- Obesity is a complex metabolic disorder linked to adipocyte dysfunction.
- Galectin-12 plays a role in adipogenesis and obesity.
- Allyl isothiocyanate (AITC) is a natural compound with potential therapeutic properties.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying AITC's anti-adipogenic effects.
- To investigate AITC's impact on galectin-12 expression.
- To evaluate AITC's efficacy in a high-fat diet (HFD)-induced obesity mouse model.
Main Methods:
- 3T3-L1 cells were used to assess AITC's effects on adipocyte differentiation.
- Key adipogenic transcription factors and signaling pathways (PKB/Akt/CREB) were analyzed.
- Mice were fed a HFD and treated with AITC to evaluate its in vivo anti-obesity effects.
Main Results:
- AITC dose-dependently inhibited lipid droplet accumulation in 3T3-L1 cells.
- AITC suppressed adipocyte differentiation by downregulating galectin-12 expression and key transcription factors.
- AITC modulated adipokine expression (leptin, resistin) and the PKB/Akt/CREB pathway.
- In HFD-fed mice, AITC reduced body weight, liver lipid accumulation, and adipocyte size.
Conclusions:
- AITC effectively inhibits adipocyte differentiation, partly through suppressing galectin-12.
- AITC exhibits significant anti-obesity effects in a preclinical model of HFD-induced obesity.
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