Invention Grant
US08552069B2 Method for treatment of obesity, dyslipidemia, fatty liver or insulin resistance syndrome comprising camphene as active ingredient
有权
用于治疗肥胖,血脂异常,脂肪肝或胰岛素抵抗综合征的方法,其包含camp烯作为活性成分
- Patent Title: Method for treatment of obesity, dyslipidemia, fatty liver or insulin resistance syndrome comprising camphene as active ingredient
- Patent Title (中): 用于治疗肥胖,血脂异常,脂肪肝或胰岛素抵抗综合征的方法,其包含camp烯作为活性成分
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Application No.: US13256461Application Date: 2009-12-29
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Publication No.: US08552069B2Publication Date: 2013-10-08
- Inventor: Tae Sun Park
- Applicant: Tae Sun Park
- Applicant Address: KR Seoul
- Assignee: Industry-Academic Cooperation Foundation, Yonsei University
- Current Assignee: Industry-Academic Cooperation Foundation, Yonsei University
- Current Assignee Address: KR Seoul
- Agency: Clark & Elbing LLP
- Priority: KR10-2009-0022937 20090318
- International Application: PCT/KR2009/007905 WO 20091229
- International Announcement: WO2010/107177 WO 20100923
- Main IPC: A61K31/125
- IPC: A61K31/125 ; A61K36/00

Abstract:
Disclosed is a composition including camphene as an active ingredient for preventing or treating obesity, dyslipidemia, fatty liver or insulin resistance syndrome. The composition of the present disclosure including camphene as an active ingredient suppresses differentiation of adipocytes, reduces body fat, reduces visceral fat, reduces total cholesterol level, reduces serum triglyceride level and reduces liver tissue triglyceride level, and thus exhibits preventive or therapeutic activity for obesity, hyperlipidemia or fatty liver. Furthermore, the composition of the present disclosure exhibits the effect of improving type 2 diabetes or insulin resistance and related metabolic disease by significantly reducing fasting blood sugar level and blood insulin level. Also, the composition of the present disclosure exhibits the effect of reducing visceral fat by significantly reducing the expression of nuclear transcription factors (C/EBPα and PPARγ2) playing key roles in adipogenesis or their target gene (aP2), the effect of improving chronically activated inflammation in the visceral fat tissue induced by obesity by significantly reducing the expression of cytokines (TNF-α or IL-6) activating inflammation, and the effect of improving suppressed heat generation in the visceral fat tissue induced by obesity by significantly increasing the expression of UCP (UCP1 or UCP3) genes regulating body heat production.
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