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[普尼卡拉金通过AMPK/ACC途径抑制肥胖小鼠的肝脂沉积]

Re-Na Jiensi¹, Zhan-Ying Chang², Ruo-Hui Niu³

¹School of Pharmacy, Xinjiang Medical University Urumuqi 830011, China.

Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica

|June 7, 2023

概括

榴中的多素Punicalagin (PU) 有效地降低了肥胖小鼠的体重和食物摄入量. 它改善脂质和葡萄糖代谢,通过激活AMPK/ACC通路来减少肝脏脂肪沉积.

科学领域:

生物化学生物化学
药理学药理学是指药理学的学科.
肥胖问题研究研究

背景情况:

肝脂沉积是肥胖的一个关键指标.
药理干预对于控制肥胖至关重要.
榴皮中的聚烯,尼卡拉 (PU) 显示出抗肥胖的潜力.

研究的目的:

在小鼠模型中研究Punicalagin (PU) 的抗肥胖作用.
评估PU对脂质代谢,葡萄糖耐受性和胰岛素敏感性的影响.
阐明PU对肝脂沉积作用的分子机制.

主要方法:

在C57BL/6J小鼠中使用高脂肪饮食诱导肥胖.
小鼠接受了不同剂量的PU或orlistat治疗.
测量包括体重,食物摄入量,血清脂质谱,耐葡萄糖,胰岛素敏感性和组织学分析.
关键代谢调节者的基因和蛋白质表达 (PPARγ,C/EBPα,AMPK,ACC,CPT1A) 通过Q-PCR和西方布洛特分析.

主要成果:

肥胖小鼠的体重,李指数和血清脂质 (TG,TC,LDL-C) 显著增加,HDL-C降低.
在肥胖小鼠中观察到肝脂肪沉积,以及PPARγ和C/EBPα的mRNA水平增加,以及ACC的蛋白质水平.
相反,肥胖小鼠显示CPT1A和AMPK的mRNA和蛋白质水平降低.
PU治疗逆转了这些不良影响,改善了代谢参数,并减少了肝硬化.
PU治疗上调AMPK和下调ACC,表明AMPK/ACC通路的激活.

结论:

普尼卡拉 (PU) 有效地降低肥胖小鼠的体重和食物摄入量.
PU的使用改善了脂质和葡萄糖代谢,并显著减轻了肝脏脂肪沉积.
该机制涉及通过AMPK/ACC通路的激活来下调脂质合成和上调脂解.

关键词:

在AMPK/ACC信号通路中,肝脏脂质沉积肝脏脂质沉积脂质新陈代谢脂质新陈代谢肥胖症肥胖症肥胖症肥胖症这种疾病是Punicalagin.

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