Identification of novel mechanisms in obesity development.

尽管肥胖研究在过去十年中取得了显著的进步，但肥胖背后的机制仍然没有完全被理解。在这项研究中，我们发现了一个来自肝脏的新的器官间神经网络。在能量摄入超过生理需要的状态下，肝脏中的葡萄糖代谢会随着迷走神经诱导的神经元信号传递而发生变化。这些信号被大脑接收，导致棕色脂肪组织(BAT)的交感神经支配失活。这会抑制蝙蝠的产热作用，从而有利于肥胖的发展。在食物并不总是充足的时期，这一制度对生存有利。然而，在当前这个物质丰富的时代，它被认为是一种将代谢转换为肥胖的机制。此外，不同品系的小鼠之间肝脏与蝙蝠相互作用的效果不同，这些差异可能有助于确定肥胖的易感性。

Despite remarkable advancements in obesity research over the past decade, the mechanisms underlying obesity are still not fully understood. In this study, we discovered a new inter-organ neural network from the liver. In states of energy intake beyond physiological requirements, glucose metabolism changes in the liver with the induction of neuronal signal transmissions via the vagal nerve. These signals, received by the brain, result in the inactivation of sympathetic innervation of brown adipose tissue (BAT). This leads to suppression of thermogenesis in BAT and thereby favors obesity development. During periods when sufficient food was not always available, this system worked in favor of survival. However, in the current age of plenty, it is assumed to work as a mechanism flipping a metabolic switch toward obesity. Furthermore, the efficacy of the liver-to-BAT interaction differs among mouse strains and these differences may contribute to determining the obesity predispositions.