Diet-Induced Obesity Attenuates Fasting-Induced Hyperphagia
Diet-Induced Obesity Attenuates Fasting-Induced Hyperphagia
复制标题
DOI：
10.1111/j.1365-2826.2011.02148.x
复制
发表时间：
2011-07-01
影响因子：
3.2
通讯作者：
Andrews, Z. B.
中科院分区：
文献类型：
--
作者：
Briggs, D. I.;Lemus, M. B.;Andrews, Z. B.
肥胖损害弓状（ARC）神经肽Y（NPY）/刺鼠肽（AgRP）神经元功能，并使这些稳态神经元对食欲激素生长素没有反应。在本研究中，我们研究了饮食诱导的肥胖（DIO）对摄食行为，ARC神经元激活和mRNA表达的影响，另一个食欲刺激，过夜快。我们发现，9周的高脂肪喂养通过抑制ARC神经元激活和下丘脑NPY/AgRP mRNA表达来减弱禁食诱导的摄食过多。因此，DIO小鼠对禁食缺乏适当的进食反应是由ARC神经元识别和/或响应食欲线索的失败引起的。我们认为，禁食诱导的暴食症是调节不通过稳态控制DIO小鼠的食欲，而是通过奖励电路的变化。
Obesity impairs arcuate (ARC) neuropeptide Y (NPY)/agouti-releated peptide (AgRP) neuronal function and renders these homeostatic neurones unresponsive to the orexigenic hormone ghrelin. In the present study, we investigated the effect of diet-induced obesity (DIO) on feeding behaviour, ARC neuronal activation and mRNA expression following another orexigenic stimulus, an overnight fast. We show that 9 weeks of high-fat feeding attenuates fasting-induced hyperphagia by suppressing ARC neuronal activation and hypothalamic NPY/AgRP mRNA expression. Thus, the lack of appropriate feeding responses in DIO mice to a fast is caused by failure ARC neurones to recognise and/or respond to orexigenic cues. We propose that fasting-induced hyperphagia is regulated not by homeostatic control of appetite in DIO mice, but rather by changes in the reward circuitry.