Department of Anatomy, Histology and Embryology, Semmelweis University, Budapest, H-1085, Hungary.
Department of Ophthalmology, Semmelweis University, Budapest, H-1085, Hungary.
Sci Rep. 2017 Aug 21;7(1):8891. doi: 10.1038/s41598-017-09068-6.
In diabetes, retinal dysfunctions exist prior to clinically detectable vasculopathy, however the pathology behind these functional deficits is still not fully established. Previously, our group published a detailed study on the retinal histopathology of type 1 diabetic (T1D) rat model, where specific alterations were detected. Although the majority of human diabetic patients have type 2 diabetes (T2D), similar studies on T2D models are practically absent. To fill this gap, we examined Zucker Diabetic Fatty (ZDF) rats - a model for T2D - by immunohistochemistry at the age of 32 weeks. Glial reactivity was observed in all diabetic specimens, accompanied by an increase in the number of microglia cells. Prominent outer segment degeneration was detectable with changes in cone opsin expression pattern, without a decrease in the number of labelled elements. The immunoreactivity of AII amacrine cells was markedly decreased and changes were detectable in the number and staining of some other amacrine cell subtypes, while most other cells examined did not show any major alterations. Overall, the retinal histology of ZDF rats shows a surprising similarity to T1D rats indicating that despite the different evolution of the disease, the neuroretinal cells affected are the same in both subtypes of diabetes.
在糖尿病中，视网膜功能障碍存在于临床可检测到的血管病变之前，然而这些功能缺陷背后的病理学仍未完全确定。此前，我们的研究小组发表了一项关于 1 型糖尿病（T1D）大鼠模型的视网膜组织病理学的详细研究，其中检测到了特定的改变。尽管大多数糖尿病患者为 2 型糖尿病（T2D），但实际上几乎没有针对 T2D 模型的类似研究。为了填补这一空白，我们通过免疫组织化学方法在 32 周龄时检查了 Zucker 糖尿病肥胖（ZDF）大鼠 - T2D 的模型。在所有糖尿病标本中均观察到神经胶质反应，同时小胶质细胞数量增加。可见外节明显退化，伴有视锥蛋白表达模式的改变，而标记物数量没有减少。AII 无长突细胞的免疫反应明显降低，一些其他无长突细胞亚型的数量和染色也发生了变化，而检查的大多数其他细胞没有显示出任何重大变化。总的来说，ZDF 大鼠的视网膜组织学显示出与 T1D 大鼠惊人的相似性，表明尽管疾病的发展不同，但在两种类型的糖尿病中，受影响的神经视网膜细胞是相同的。
