Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2012) 29 P1226

ICEECE2012 Poster Presentations Obesity (114 abstracts)

Curcumin inhibits the upregulation of cathepsin L by palmitate in fat

J. Yoo 1, , Y. Lee 2 , J. Kim 2 , S. Kang 2 , J. Nam 1 , J. Park 2 , C. Ahn 2 , Y. Song 1 & K. Kim 2

1NHIC Ilsan Hospital, Goyang-si, Republic of Korea; 2College of Medicine, Yonsei University, Seoul, Republic of Korea.

Objective: Cathepsin L can control adipogenesis and relate to acute coronary syndrome. However, it is not clear whether cathepsin L can be affected by saturated fatty acid and decrease by curcumin. We examined the hypothesis that palmitate upregulates cathepsin L expression in adipose tissue and curcumin can be block that effect.

Methods: 3T3-L1 cells were fully differentiated for 8 to 10 days and treated with palmitate, LPS, IL6, TNF-α, IL6 neutralizing Ab, curcumin. Six-week-old C3H/HeN with normal TLR4 and C3H/HeJ with TLR4 mutation got LPS injection ip (1 mg/kg) or were fed with high fat diet for 13 weeks and sacrifice to harvest epididymal fat.

Results: Real-time PCR revealed that cathepsin L expression was upregulated by palmitate. But there was no additional effect when we use palmitate-treated RAW264.7 cells’ media instead of direct treatment to 3T3-L1 cells. Cathepsin L was upregulated after treatment of TNF-α or IL6 like palmitate. IL6 neutralizing Ab and curcumin attenuated this effect of palmitate. Cathepsin L increased in both kinds of mice fed high fat diet compared with chow diet. But we cannot find similar pattern at mice which got LPS ip injection.

Conclusions: We concluded that cathepsin L expression in fat are upregulated by palmitate via inflammatory cytokines, not TLR4, thereby might have a critical role in developing acute coronary syndrome of metabolic syndrome and there are no additional effects of infiltrating macrophages. In addition, curcumin can be a candidate of drug which can amilorate the metabolic syndrome.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

Volume 29

15th International & 14th European Congress of Endocrinology

European Society of Endocrinology 

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