北京大学杨竞研究组发现，代谢应激可导致肝脏内的交感神经病变。相关论文于2021年2月4日在线发表于国际学术期刊《细胞—代谢》。

研究人员使用先进的3D成像技术测试了小鼠、非人类灵长类动物和人类肝脏中的神经分布。研究人员观察到肝脏内的神经支配主要是交感神经输入，而不是副交感神经输入。而且，研究人员发现了新陈代谢过程中这种交感神经的大量、可逆丧失。肝交感神经病变是由高脂饮食（HFD）条件下源自CD11b⁺F4/80⁺免疫细胞的TNFα引起的。

研究人员进一步证明了Sarm1缺失可减轻HFD攻击小鼠的肝交感神经病变，并改善了代谢参数。从机理上讲，交感神经递质去甲肾上腺素减弱了免疫细胞的炎症，否则会触发肝细胞对胰岛素的不敏感性。这些结果共同揭示了肝脏中先前未发现的代谢相关神经病变事件。 

据了解，神经系统指示人体的新陈代谢，包括肝脏中的新陈代谢。然而，在正常或代谢应激条件下肝脏的神经解剖学仍有待明确评估。

附：英文原文

Title: Metabolic stress drives sympathetic neuropathy within the liver

Author: Kaili Liu, Lu Yang, Gang Wang, Jiaqi Liu, Xuan Zhao, Yi Wang, Jiali Li, Jing Yang

Issue&Volume: 2021-02-04

Abstract: The nervous system instructs the body’s metabolism, including that in the liver. However,the neural anatomy of the liver under either normal or metabolically stressed conditionsremains to be unequivocally assessed. Here, we examined neural distributions in themouse, nonhuman primate, and human livers with advanced 3D imaging. We observed thatneural innervations within the liver are predominantly sympathetic, but not parasympathetic,inputs. Moreover, we discovered the profound and reversible loss of such sympatheticinnervations during metabolic challenges. This hepatic sympathetic neuropathy wascaused by TNFα derived from CD11b+ F4/80+ immune cells under high-fat-diet (HFD) condition. We further demonstrated that theSarm1 deletion mitigated the hepatic sympathetic neuropathy and improved metabolic parametersin HFD-challenged mice. Mechanistically, the sympathetic neurotransmitter norepinephrineattenuated the immune-cell inflammation that would otherwise trigger the insulin insensitivityof hepatocytes. These results together reveal the previously unrecognized neuropathicevent in the liver with metabolic relevance.

DOI: 10.1016/j.cmet.2021.01.012

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(21)00012-7