Neuronal pathway from the liver modulates energy expenditure and systemic insulin sensitivity
Neuronal pathway from the liver modulates energy expenditure and systemic insulin sensitivity
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DOI：
10.1126/science.1126010
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发表时间：
2006-06-16
期刊：
影响因子：
56.9
通讯作者：
Oka, Yoshitomo
中科院分区：
文献类型：
--
作者：
Uno, Kenji;Katagiri, Hideki;Oka, Yoshitomo
能量代谢和葡萄糖稳态的协调控制需要器官和组织之间的通信。我们确定了一个参与肝脏和脂肪组织之间串扰的神经元通路。通过研究小鼠模型，我们发现，腺病毒介导的过氧化物酶体增殖物激活受体（PPAR）-γ 2在肝脏中的表达诱导急性肝脂肪变性，同时显着降低外周肥胖。这些变化伴随着能量消耗增加和全身胰岛素敏感性改善。肝迷走神经切断术和选择性肝迷走神经传入阻滞显示，对周围组织的影响涉及迷走神经传入。此外，一种抗糖尿病的噻唑烷二酮（一种PPAR γ激动剂）增强了这一途径。这种来自肝脏的神经元通路可能起保护作用，以防止过度能量储存引起的代谢紊乱。
Coordinated control of energy metabolism and glucose homeostasis requires communication between organs and tissues. We identified a neuronal pathway that participates in the cross talk between the liver and adipose tissue. By studying a mouse model, we showed that adenovirus-mediated expression of peroxisome proliferator - activated receptor ( PPAR) - gamma 2 in the liver induces acute hepatic steatosis while markedly decreasing peripheral adiposity. These changes were accompanied by increased energy expenditure and improved systemic insulin sensitivity. Hepatic vagotomy and selective afferent blockage of the hepatic vagus revealed that the effects on peripheral tissues involve the afferent vagal nerve. Furthermore, an antidiabetic thiazolidinedione, a PPAR gamma agonist, enhanced this pathway. This neuronal pathway from the liver may function to protect against metabolic perturbation induced by excessive energy storage.