Allyl Isothiocyanate Ameliorates Obesity by Inhibiting Galectin-12

Chia Wen Lo; Chih Sheng Chen; Ying Chi Chen; Yu An Hsu; Chi Chun Huang; Ching Yao Chang; Chao Jen Lin; Cheng Wen Lin; Hui Ju Lin; Fu-Tong Liu; Lei Wan

doi:10.1002/mnfr.201700616

Allyl Isothiocyanate Ameliorates Obesity by Inhibiting Galectin-12

Chia Wen Lo, Chih Sheng Chen, Ying Chi Chen, Yu An Hsu, Chi Chun Huang, Ching Yao Chang, Chao Jen Lin, Cheng Wen Lin, Hui Ju Lin, Fu-Tong Liu, Lei Wan

Dermatology

Research output: Contribution to journal › Article

7 Scopus citations

Abstract

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.

Original language	English (US)
Article number	1700616
Journal	Molecular Nutrition and Food Research
Volume	62
Issue number	6
DOIs	https://doi.org/10.1002/mnfr.201700616
State	Published - Mar 1 2018

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Keywords

3T3-L1
adipocytes
Allyl isothiocyanate
galectin-12
obesity

ASJC Scopus subject areas

Biotechnology
Food Science

Cite this

Lo, C. W., Chen, C. S., Chen, Y. C., Hsu, Y. A., Huang, C. C., Chang, C. Y., Lin, C. J., Lin, C. W., Lin, H. J., Liu, F-T., & Wan, L. (2018). Allyl Isothiocyanate Ameliorates Obesity by Inhibiting Galectin-12. Molecular Nutrition and Food Research, 62(6), [1700616]. https://doi.org/10.1002/mnfr.201700616

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abstract = "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.",

keywords = "3T3-L1, adipocytes, Allyl isothiocyanate, galectin-12, obesity",

author = "Lo, {Chia Wen} and Chen, {Chih Sheng} and Chen, {Ying Chi} and Hsu, {Yu An} and Huang, {Chi Chun} and Chang, {Ching Yao} and Lin, {Chao Jen} and Lin, {Cheng Wen} and Lin, {Hui Ju} and Fu-Tong Liu and Lei Wan",

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AU - Hsu, Yu An

AU - Huang, Chi Chun

AU - Chang, Ching Yao

AU - Lin, Chao Jen

AU - Lin, Cheng Wen

AU - Lin, Hui Ju

AU - Liu, Fu-Tong

AU - Wan, Lei

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N2 - 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.

AB - 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.

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KW - Allyl isothiocyanate

KW - galectin-12

KW - obesity

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10.1002/mnfr.201700616