The daily light–dark cycle is a key zeitgeber (time cue) for entraining an organism’s biological clock, whereby light sensing by retinal photoreceptors, particularly intrinsically photosensitive retinal ganglion cells, stimulates the suprachiasmatic nucleus of the hypothalamus, a central pacemaker that in turn orchestrates the rhythm of peripheral metabolic activities. Non-rhythmic effects of light on metabolism have also been long known, and their transduction mechanisms are only beginning to unfold. Here, we summarize emerging evidence that, in mammals, light exposure or deprivation profoundly affects glucose homeostasis, thermogenesis and other metabolic activities in a clock-independent manner. Such light regulation could involve melanopsin-based, intrinsically photosensitive retinal ganglion cell-initiated brain circuits via the suprachiasmatic nucleus of the hypothalamus and other nuclei, or direct stimulation of opsins expressed in the hypothalamus, adipose tissue, blood vessels and skin to regulate sympathetic tone, lipolysis, glucose uptake, mitochondrial activation, thermogenesis, food intake, blood pressure and melanogenesis. These photic signalling events may coordinate with circadian-based mechanisms to maintain metabolic homeostasis, with dysregulation of this system underlying metabolic diseases caused by aberrant light exposure, such as environmental night light and shift work.

每日的明暗周期是生物钟的关键时间线索，视网膜光感受器（尤其是本质上感光的视网膜神经节细胞）对光的感知会刺激下丘脑的视交叉上核，而视交叉上核是一个中央起搏器，反过来协调协调外周代谢活动的节律。光对新陈代谢的非节律效应也早已为人所知，而且它们的转导机制才刚刚开始揭示。在这里，我们总结了新的证据，表明在哺乳动物中，光照或剥夺会以与时钟无关的方式深刻影响葡萄糖稳态、产热和其他代谢活动。这种光调节可能涉及基于黑视蛋白的、本质上光敏的视网膜神经节细胞通过下丘脑的视交叉上核和其他核团启动的脑回路，或直接刺激下丘脑、脂肪组织、血管和皮肤中表达的视蛋白以调节交感神经张力、脂肪分解、葡萄糖摄取、线粒体激活、产热、食物摄入、血压和黑素生成。这些光信号事件可能与基于昼夜节律的机制相协调，以维持代谢稳态，该系统的失调是由异常光暴露（例如环境夜光和轮班工作）引起的代谢疾病的基础。