中国科学技术大学薛天研究组发现，光通过视网膜-下丘脑-棕色脂肪组织轴调节葡萄糖代谢。相关论文于2023年1月19日发表于国际学术期刊《细胞》。

研究团队发现光可以通过激活支配下丘脑视上核（SON）的内在光敏性视网膜神经节细胞（ipRGC）急剧降低小鼠的葡萄糖耐量（GT）。SON中的血管加压素经元投射到室旁核，然后投射到孤束核中的GAB能神经元，最后投射到棕色脂肪组织（BAT）。该神经回路的光激活直接阻断了BAT中的自适应产热，从而降低了GT。在人类中，光也在BAT活跃的温度下调节GT。这项工作揭示了视网膜-SON-SON轴，它介导光对葡萄糖代谢的影响，这可能解释了人工光和代谢失调之间的联系，并为管理葡萄糖代谢障碍提供了一种潜在的预防和治疗策略。

据悉，公共卫生研究表明，人造光是代谢紊乱的高风险因素。然而，光调节代谢的神经机制仍不清楚。

附：英文原文

Title: Light modulates glucose metabolism by a retina-hypothalamus-brown adipose tissue axis

Author: Jian-Jun Meng, Jia-Wei Shen, Guang Li, Chang-Jie Ouyang, Jia-Xi Hu, Zi-Shuo Li, Hang Zhao, Yi-Ming Shi, Mei Zhang, Rong Liu, Ju-Tao Chen, Yu-Qian Ma, Huan Zhao, Tian Xue

Issue&Volume: 2023/01/19

Abstract: Public health studies indicate that artificial light is a high-risk factor for metabolic disorders. However, the neural mechanism underlying metabolic modulation by light remains elusive. Here, we found that light can acutely decrease glucose tolerance (GT) in mice by activation of intrinsically photosensitive retinal ganglion cells (ipRGCs) innervating the hypothalamic supraoptic nucleus (SON). Vasopressin neurons in the SON project to the paraventricular nucleus, then to the GABAergic neurons in the solitary tract nucleus, and eventually to brown adipose tissue (BAT). Light activation of this neural circuit directly blocks adaptive thermogenesis in BAT, thereby decreasing GT. In humans, light also modulates GT at the temperature where BAT is active. Thus, our work unveils a retina-SON-BAT axis that mediates the effect of light on glucose metabolism, which may explain the connection between artificial light and metabolic dysregulation, suggesting a potential prevention and treatment strategy for managing glucose metabolic disorders.

DOI: 10.1016/j.cell.2022.12.024

Source: https://www.cell.com/cell/fulltext/S0092-8674(22)01537-9