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首页> 外文期刊>Nature >UCP2 mediates ghrelin's action on NPY/ AgRP neurons by lowering free radicals
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UCP2 mediates ghrelin's action on NPY/ AgRP neurons by lowering free radicals

机译：UCP2通过降低自由基来介导生长素释放肽对NPY / AgRP神经元的作用

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摘要

The gut-derived hormone ghrelin exerts its effect on the brain by regulating neuronal activity. Ghrelin-induced feeding behaviour is controlled by arcuate nucleus neurons that co-express neuropeptide Y and agouti-related protein (NPY/AgRP neurons). However, the intracellular mechanisms triggered by ghrelin to alter NPY/AgRP neuronal activity are poorly understood. Here we show that ghrelin initiates robust changes in hypothalamic mitochondrial respiration in mice that are dependent on uncoupling protein 2 (UCP2). Activation of this mitochondrial mechanism is critical for ghrelin-induced mitochondrial proliferation and electric activation of NPY/AgRP neurons, for ghrelin-triggered synaptic plasticity of pro-opiomelanocortin-expressing neurons, and for ghrelin-induced food intake. The UCP2-dependent action of ghrelin on NPY/AgRP neurons is driven by a hypothalamic fatty acid oxidation pathway involving AMPK, CPT1 and free radicals that are scavenged by UCP2. These results reveal a signalling modality connecting mitochondria-mediated effects of G-protein-coupled receptors on neuronal function and associated behaviour.
机译：肠源性生长激素释放素通过调节神经元活动对大脑发挥作用。 Ghrelin诱导的进食行为由共同表达神经肽Y和刺古蛋白相关蛋白（NPY / AgRP神经元）的弓形核神经元控制。然而，由生长素释放肽触发的改变NPY / AgRP神经元活性的细胞内机制知之甚少。在这里，我们显示生长素释放肽在依赖解偶联蛋白2（UCP2）的小鼠中引发下丘脑线粒体呼吸的强大变化。线粒体机制的激活对于生长素释放肽诱导的线粒体增殖和NPY / AgRP神经元的电激活，生长素释放肽促促表达表达促黑素皮质激素的神经元的突触可塑性以及生长素释放肽诱导的食物摄入至关重要。 ghrelin对NPY / AgRP神经元的UCP2依赖性作用是由下丘脑脂肪酸氧化途径驱动的，该途径涉及AMPK，CPT1和被UCP2清除的自由基。这些结果揭示了连接线粒体介导的G蛋白偶联受体对神经元功能和相关行为的信号传导方式。

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