Roles of autonomic nervous system in inter-organ metabolic communication.

肥胖的发病率正以流行病的比例上升。非自愿过度喂养后体重正常化的几个机制被证明；然而，同样多的能量摄入导致的过度喂养并不会引起同样程度的体重增加。我们发现了一种新的通过神经元途径的器官间通讯，它抑制了过度营养状态下的能量消耗。通过对小鼠模型的研究，我们发现肝脏葡萄糖激酶的表达先于高脂肪喂养导致的体重增加，并表明腺病毒介导的肝脏葡萄糖激酶的表达抑制了能量消耗，导致体重增加。这些反应是由连接肝脏、传入迷走神经、白质中隔神经、传出交感神经和棕色脂肪组织的神经元通路介导的。此外，主要在营养过剩状态下观察到的瘦素诱导的能量消耗被该途径抑制。

The incidence of obesity is rising at epidemic proportions. Several mechanisms underlying the normalization of body weight following involuntary overfeeding are demonstrated ; however, the same excess amount of energy intake resulting from overfeeding does not evoke the same degree of body weight gain. We identified a novel inter-organ communication via neuronal pathway, which suppresses energy expenditure in over-nutritious state. By studying a mouse model, we found out that hepatic glucokinase expression precedes body weight gain due to high fat feeding, and showed that adenovirus-mediated expression of glucokinase in the liver suppressed energy expenditure, resulting in body weight gain. These responses are mediated by a neuronal pathway linking liver, afferent vagus, raphe palllidus, efferent sympathetic nerve, and finally brown adipose tissue, in this order. Furthermore, leptin-induced energy expenditure, primarily observed in overnutritious state, was suppressed by this pathway.