Illumination of the retina is a major determinant of energy expenditure by its neurons. However, it remains unclear whether light exposure significantly contributes to the pathophysiology of common retinal disease. Driven by the premise that light exposure reduces the metabolic demand of the retina, recent clinical trials failed to demonstrate a benefit for constant illumination in the treatment of diabetic retinopathy. Here, we instead ask whether light deprivation or blockade of visual transduction could modulate the severity of this common cause of blindness. We randomized adult mice with two different models of diabetic retinopathy to 1-3 months of complete dark housing. Unexpectedly, we find that diabetic mice exposed to short or prolonged light deprivation have reduced diabetes-induced retinal pathology, using measures of visual function, compared to control animals in standard lighting conditions. To corroborate these results, we performed assays of retinal vascular health in diabetic Gnat1-/- and Rpe65-/- mice, which lack phototransduction. Both mutants displayed less diabetes-associated retinal vascular disease compared to respective wild-type controls. Collectively, these results suggest that light-induced visual transduction promotes the development of diabetic retinopathy and implicate photoreceptors as an early source of visual pathology in diabetes.

中文翻译：

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轻度剥夺可减轻实验性糖尿病视网膜病变的严重程度。

视网膜的照明是其神经元能量消耗的主要决定因素。然而，目前尚不清楚曝光是否对常见视网膜疾病的病理生理有重大贡献。在曝光减少视网膜的代谢需求的前提下，最近的临床试验未能证明在糖尿病性视网膜病的治疗中持续照射有益。在这里，我们改为问光剥夺或视觉传导障碍是否可以调节这种常见失明原因的严重性。我们将具有两种不同模型的糖尿病性视网膜病变的成年小鼠随机分为1-3个月的完全黑暗的外壳。出乎意料的是，我们发现使用短时或长时光剥夺的糖尿病小鼠使用视觉功能的测量方法，可以减少糖尿病引起的视网膜病变，与标准光照条件下的对照动物相比。为了证实这些结果，我们对缺乏光转导的糖尿病Gnat1-/-和Rpe65-/-小鼠进行了视网膜血管健康测定。与相应的野生型对照相比，两个突变体均显示出较少的糖尿病相关性视网膜血管疾病。总体而言，这些结果表明，光诱导的视觉转导促进了糖尿病性视网膜病的发展，并暗示了感光细胞是糖尿病患者视觉病理的早期来源。