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人参茎叶皂苷通过调节高脂饮食诱导的肥胖C57BL/6小鼠的产热、脂肪生成和脂肪分解来预防肥胖。

Saponins from stems and leaves of Panax ginseng prevent obesity via regulating thermogenesis, lipogenesis and lipolysis in high-fat diet-induced obese C57BL/6 mice.

作者信息

Chen Guilin, Li Haijun, Zhao Yan, Zhu Hongyan, Cai Enbo, Gao Yugang, Liu Shuangli, Yang He, Zhang Lianxue

机构信息

College of Chinese Medicinal Materials, Jilin Agriculture University, Changchun, China.

Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.

出版信息

Food Chem Toxicol. 2017 Aug;106(Pt A):393-403. doi: 10.1016/j.fct.2017.06.012. Epub 2017 Jun 7.

Abstract

In this study, high-fat diet (HFD)-induced obesity in mouse model was used to evaluate the dietary effect of saponins from stems and leaves of Panax ginseng (SLG), and to explore its mechanism of action in producing anti-obesity effects. The results indicate that SLG showed significant anti-obesity effects in diet-induced obese mice, represented by decreased serum levels of free fatty acids (FFA), total cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL)-cholesterol, glucose, leptin and insulin, as well as a reduction in overall body and liver weight, epididymal adipose tissue weight, and food efficiency, and inhibition of abnormal increases in acyl carnitine levels normally caused by an HFD. Additionally, the down-regulated expression of PPARγ, FAS, CD36, FATP2 and up-regulated expression of CPT-1, UCP-2, PPARα, HSL, and ATGL in liver tissue was induced by SLG. In addition, the SLG groups showed decreased PPARγ, aP2 and leptin mRNA levels and increased expression of PPARα, PGC-1α, UCP-1 and UCP-3 genes in adipose tissues, compared with the HFD group. In short, SLG may play a key role in producing anti-obesity effects in mice fed an HFD, and its mechanism may be related to regulation of thermogenesis, lipogenesis and lipolysis.

摘要

在本研究中,采用高脂饮食(HFD)诱导的小鼠肥胖模型来评估人参茎叶皂苷(SLG)的饮食效果,并探讨其产生抗肥胖作用的作用机制。结果表明,SLG在饮食诱导的肥胖小鼠中显示出显著的抗肥胖作用,表现为血清游离脂肪酸(FFA)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)胆固醇、葡萄糖、瘦素和胰岛素水平降低,以及总体重、肝脏重量、附睾脂肪组织重量和食物利用率降低,并抑制了高脂饮食通常引起的酰基肉碱水平异常升高。此外,SLG诱导肝脏组织中PPARγ、FAS、CD36、FATP2的表达下调以及CPT-1、UCP-2、PPARα、HSL和ATGL的表达上调。此外,与高脂饮食组相比,SLG组脂肪组织中PPARγ、aP2和瘦素mRNA水平降低,PPARα、PGC-1α、UCP-1和UCP-3基因表达增加。简而言之,SLG可能在高脂饮食喂养的小鼠产生抗肥胖作用中起关键作用,其机制可能与产热、脂肪生成和脂肪分解的调节有关。

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