Diabetic retinopathy is a major complication of chronic hyperglycemia and a leading cause of blindness in developed countries. In the present study the interaction between diabetes and retinal clocks was investigated in mice. It was seen that in the db/db mouse – a widely used animal model of diabetic retinopathy – clock function and circadian regulation of gene expression was disturbed in the retina. Remarkably, elimination of clock function by Bmal1-deficiency mitigates the progression of pathophysiology of the diabetic retina. Thus high-fat diet was seen to induce histopathology and molecular markers associated with diabetic retinopathy in wild type but not in Bmal1-deficient mice. The data of the present study suggest that Bmal1/the retinal clock system is both, a target and an effector of diabetes mellitus in the retina and hence represents a putative therapeutic target in the pathogenesis of diabetic retinopathy.

糖尿病视网膜病变是慢性高血糖的主要并发症，也是发达国家失明的主要原因。在本研究中，在小鼠中研究了糖尿病和视网膜生物钟之间的相互作用。可以看出，在db/db小鼠（一种广泛使用的糖尿病视网膜病变动物模型）中，视网膜中的时钟功能和基因表达的昼夜节律调节受到干扰。值得注意的是，Bmal1 缺陷对时钟功能的消除减缓了糖尿病视网膜病理生理学的进展。因此，高脂肪饮食被视为在野生型中诱导与糖尿病视网膜病变相关的组织病理学和分子标记，但在Bmal1缺陷小鼠中则不然。本研究的数据表明Bmal1视网膜生物钟系统既是视网膜中糖尿病的靶点又是效应器，因此代表了糖尿病视网膜病变发病机制中的推定治疗靶点。