Identification of novel mechanisms in obesity development.

尽管在过去的十年里，肥胖研究取得了显著的进步，但肥胖的潜在机制仍然没有被完全理解。在这项研究中，我们从肝脏中发现了一个新的器官间神经网络。在能量摄入超出生理需要的状态下，肝脏中的葡萄糖代谢随着迷走神经信号传递的诱导而发生变化。这些信号被大脑接收，导致棕色脂肪组织（BAT）交感神经的失活。这导致BAT中的产热作用受到抑制，从而有利于肥胖的发展。在食物不充足的时期，这个系统有利于生存。然而，在当今这个食物充足的时代，它被认为是一种机制，将新陈代谢转换为肥胖。此外，肝脏与bat相互作用的功效在小鼠品系之间存在差异，这些差异可能有助于确定肥胖倾向。

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.