夜晚光線透過視黑質影響腸道菌相以及身體代謝

Abstract

環境光線可以透過自主感光視神經細胞 (intrinsically photosensitive retina ganglion cells) 傳遞光線訊息來影響哺乳動物的生理功能。電燈的發明不只影響了人類的生活作息，它更影響了人類的健康狀態。夜晚光線的照射增加了肥胖以及相關代謝疾病的風險。然而，我們對於光線如何引發這些症狀仍的機制仍然不是非常了解。故我們想要利用不同自主感光視神經細胞操弄的小鼠模型搭配上總體基因體學 (metagenomics) 的研究來回答這個問題。我們的研究發現，夜晚光線可以透過視黑質 (melanopsin) 以及自主感光視神經細胞與交感神經之間的迴路來造成老鼠的肥胖、血糖耐受性降低的症狀。同時，也改變了腸道菌的菌落組成、數量以及節律。我們的研究也指出控制腸道節律最重要的原因不是宿主本身的生理時鐘，而是由自主感光視神經細胞所傳遞的光線訊息。綜上所述，本研究顯示光線能夠改變腸道菌的組成，並為夜晚光線如何調控身體代謝提供了一個新的解釋觀點。

Ambient light signal could influence physiological function of mammals through intrinsically photosensitive retina ganglion cells (ipRGCs). The invention of artificial light source not only changes the living style of human but causes serious health problem. Aberrant light information, such as dim light at night (dLAN), enhance the risk of obesity and related metabolic disorders. However, the detailed mechanism of dLAN induced metabolic disorders remains poorly understood. Here, in combination of different ipRGC manipulation mice models and metagenomic analysis, we show that dLAN can induce obesity, hyperglycemia, as well as shift in microbial composition, abundance and oscillations through melanopsin and ipRGC-sympathetic nerve circuit. Furthermore, our data suggest that the zeitgeber information that influence microbial rhythmicity is the photic input from ipRGC but not the circadian rhythm of the host. Together, our results suggest that light could shape the architecture of gut microbiota, which provides a novel mechanism for dLAN-induced metabolic disorders.