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，我们报告了脊椎动物眼中能量代谢的综合模型的多条证据。代谢通量，关键酶的位置以及我们的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，这为视网膜代谢概念上的新模型提供了支持。在该模型中，脉络膜血液中的葡萄糖穿过视网膜色素上皮到达视网膜，在视网膜中感光细胞将其转化为乳酸。然后感光细胞将乳酸盐作为视网膜色素上皮和邻近的Müller神经胶质细胞的燃料输出。我们使用人类视网膜上皮细胞来证明乳酸可以抑制视网膜色素上皮对葡萄糖的消耗。视网膜色素上皮中葡萄糖消耗的抑制可增加到达视网膜的葡萄糖量。