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高脂肪饮食在小鼠中诱导对格林和LEAP2类型的抗性

L Holá¹, T Tureckiuová, J Kuneš

¹Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences, Praha 6, Czech Republic. maletin@uochb.cas.cz.

Physiological research

|November 28, 2023

概括

高脂肪饮食会诱导小鼠的肥胖和 ghrelin 耐药性,通过切换到标准饮食可以部分逆转. 肝脏表达的抗微生物2 (LEAP2) 也表现出耐药性,这表明在食欲调节方面存在复杂的相互作用.

科学领域:

代谢和内分泌学
肥胖问题研究研究
体信号传递体信号传递

背景情况:

格林和肝脏表达的抗微生物2 (LEAP2) 是食物摄入的关键调节剂.
肥胖通常与循环格林的减少有关,但对格林的反应受损.
在饮食诱导的肥胖中,格林和LEAP2之间的相互作用尚未得到充分理解.

研究的目的:

为了研究高脂肪 (HF) 饮食诱导的肥胖症在小鼠中的格林和LEAP2之间的相互作用.
检查饮食转换对格林和LEAP2水平和信号的影响.
评估肥胖症中对格林和LEAP2类型的耐药性的发展.

主要方法:

给小鼠食HF饮食以诱导肥胖,在不同时间点进行分析.
测量了等离子激素 (活性和总量),素和肝脏LEAP2 mRNA.
对格林和LEAP2类型的敏感性在肥胖期间和切换到标准饮食后进行了测试.

主要成果:

在HF饮食养中,血格林降低,肝脏LEAP2 mRNA增加,以及葡萄糖不耐受.
切换到标准饮食正常化了肝脏LEAP2 mRNA和活性 ghrelin,但不是总 ghrelin.
HF饮食诱导的对格林模拟物的耐药性在饮食转换后是可逆的,随后是对LEAP2模拟物的耐药性.

结论:

高脂肪饮食引起的肥胖会改变格林和LEAP2的动态和信号.
饮食干预可以部分逆转这些的与肥胖有关的变化.
需要对LEAP2对肥胖和格林抵抗的类似物进行进一步的研究.

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