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高脂饮食诱导肥胖小鼠中环烯醚萜苷富集提取物的抗肥胖作用的生化机制。

48Biochemical mechanisms of the anti-obesity effect of a triterpenoid-enriched extract of Cynomorium songaricum in mice with high-fat-diet-induced obesity.

机构信息

School of Life and Health Science, The Chinese University of Hong Kong, Shenzhen, Guangdong, 518172, China.

Division of Life Science, The Hong Kong University of Science & Technology, Clear Water Bay, Hong Kong SAR, China.

出版信息

Phytomedicine. 2020 Jul 15;73:153038. doi: 10.1016/j.phymed.2019.153038. Epub 2019 Jul 20.

Abstract

BACKGROUND

HCY2, a triterpenoid-enriched extract of Cynomorii Herba, has been shown to reduce body weight and adiposity and attenuate manifestations of the associated metabolic syndrome in high-fat-diet (HFD)-fed mice.

PURPOSE

The current study aimed to investigate the biochemical mechanism underlying the anti-obesity effect produced by HCY2.

STUDY DESIGN

An HCY2-containing extract was examined for its effects on the regulation of adenosine monophosphate-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma co-activator-1 (PGC1) pathways and the protein expression related to mitochondrial uncoupling and biogenesis in skeletal muscle using an HFD-induced obese mouse model.

METHODS

The obese mouse model was produced by providing HFD (60% kcal from fat) ad libitum. The effects and signaling mechanisms of HCY2 were examined using analytical procedures which included enzyme-linked immunosorbent assay kits, Western blot analysis, and the use of a Clark-type oxygen electrode.

RESULTS

The current study revealed that the weight reduction produced by HCY2 is associated with the activation of the AMPK signaling pathway, with resultant increases in mitochondrial biogenesis and expression of uncoupling protein 3 in skeletal muscle in vivo. The use of a recoupler, ketocholestanol, delineated the precise role of mitochondrial uncoupling in the anti-obesity effect afforded by HCY2 in obese mice.

CONCLUSION

Our experimental findings offer a promising prospect for the use of HCY2 in the management of obesity through the regulation of AMPK/PGC1 pathways.

摘要

背景

HCY2 是肉苁蓉草的一种三萜类化合物提取物,已被证明可减轻体重和脂肪含量,并减轻高脂肪饮食(HFD)喂养的小鼠中相关代谢综合征的表现。

目的

本研究旨在探讨 HCY2 产生抗肥胖作用的生化机制。

研究设计

使用高脂肪饮食诱导肥胖的小鼠模型,检查含有 HCY2 的提取物对腺苷单磷酸激活蛋白激酶(AMPK)/过氧化物酶体增殖物激活受体γ共激活因子 1(PGC1)途径的调节以及骨骼肌中线粒体解偶联和生物发生相关蛋白表达的影响。

方法

肥胖小鼠模型通过提供自由摄取高脂肪饮食(60%来自脂肪)来制备。使用酶联免疫吸附试剂盒、Western blot 分析和 Clark 型氧电极等分析程序检查 HCY2 的作用和信号机制。

结果

本研究表明,HCY2 减轻体重与 AMPK 信号通路的激活有关,导致体内骨骼肌中线粒体生物发生和解偶联蛋白 3 的表达增加。使用再偶联剂酮胆甾醇可阐明线粒体解偶联在 HCY2 对肥胖小鼠的抗肥胖作用中的精确作用。

结论

我们的实验结果为通过调节 AMPK/PGC1 途径将 HCY2 用于肥胖症的管理提供了有希望的前景。

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