Department of Biochemistry, University of Washington, Seattle, United States.
Department of Ophthalmology, University of Washington, Seattle, United States.
Elife. 2017 Sep 13;6:e28899. doi: 10.7554/eLife.28899.
Here we report multiple lines of evidence for a comprehensive model of energy metabolism in the vertebrate eye. Metabolic flux, locations of key enzymes, and our finding that glucose enters mouse and zebrafish retinas mostly through photoreceptors support a conceptually new model for retinal metabolism. In this model, glucose from the choroidal blood passes through the retinal pigment epithelium to the retina where photoreceptors convert it to lactate. Photoreceptors then export the lactate as fuel for the retinal pigment epithelium and for neighboring Müller glial cells. We used human retinal epithelial cells to show that lactate can suppress consumption of glucose by the retinal pigment epithelium. Suppression of glucose consumption in the retinal pigment epithelium can increase the amount of glucose that reaches the retina. This framework for understanding metabolic relationships in the vertebrate retina provides new insights into the underlying causes of retinal disease and age-related vision loss.
在这里，我们报告了多种证据，证明了脊椎动物眼睛中能量代谢的综合模型。代谢通量、关键酶的位置，以及我们发现葡萄糖主要通过光感受器进入小鼠和斑马鱼的视网膜，支持了一种新的视网膜代谢概念模型。在这个模型中，脉络膜血液中的葡萄糖通过视网膜色素上皮进入视网膜，在那里光感受器将其转化为乳酸。然后，光感受器将乳酸输出作为视网膜色素上皮和相邻的 Muller 胶质细胞的燃料。我们使用人视网膜上皮细胞表明，乳酸可以抑制视网膜色素上皮对葡萄糖的消耗。抑制视网膜色素上皮对葡萄糖的消耗可以增加到达视网膜的葡萄糖量。这个理解脊椎动物视网膜代谢关系的框架为视网膜疾病和与年龄相关的视力丧失的根本原因提供了新的见解。
