Abstract：
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.
摘要：
每天的明暗循环是一个关键的zeitgeber（时间线索），用于夹带生物体的生物钟，通过视网膜光感受器感知光，特别是内在光敏的视网膜神经节细胞，刺激下丘脑的视交叉上核，中央起搏器，反过来协调周围代谢活动的节奏。光对新陈代谢的非节律影响也早已为人所知，它们的转导机制才刚刚开始展开。这里,我们总结了新出现的证据，在哺乳动物中，光照或剥夺会严重影响葡萄糖稳态，产热和其他代谢活动以与时钟无关的方式进行。这种光调节可能涉及基于黑视蛋白的，通过下丘脑视交叉上核和其他核的内在光敏性视网膜神经节细胞启动的脑回路，或直接刺激下丘脑中表达的视蛋白，脂肪组织,血管和皮肤来调节交感神经紧张，脂解,葡萄糖摄取，线粒体激活，产热,食物摄入量,血压和黑色素生成。这些光信号事件可能与基于昼夜节律的机制协调以维持代谢稳态，与异常光照射引起的代谢疾病相关的系统失调，如环境夜灯和倒班工作。
