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代谢综合征大鼠模型中糖耐量受损型肥胖对视网膜变性的影响

Impact of obesity with impaired glucose tolerance on retinal degeneration in a rat model of metabolic syndrome.

作者信息

Godisela Kishore Kumar, Reddy Singareddy Sreenivasa, Kumar Chekkilla Uday, Saravanan Natarajan, Reddy Paduru Yadagiri, Jablonski Monica M, Ayyagari Radha, Reddy Geereddy Bhanuprakash

机构信息

National Institute of Nutrition, Hyderabad, India.

University of Tennessee, Memphis, TN.

出版信息

Mol Vis. 2017 Apr 14;23:263-274. eCollection 2017.

PMID:28465658
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5398884/
Abstract

PURPOSE

Metabolic syndrome (MetS) is associated with several degenerative diseases, including retinal degeneration. Previously, we reported on progressive retinal degeneration in a spontaneous obese rat (WNIN/Ob) model. In this study, we investigated the additional effect of impaired glucose tolerance (IGT), an essential component of MetS, on retinal degeneration using the WNIN/GR-Ob rat model.

METHODS

The retinal morphology and ultrastructure of WNIN/GR-Ob and age-matched littermate lean rats were studied by microscopy and immunohistochemistry. The retinal transcriptome of WNIN/GR-Ob was compared with the respective lean controls and with the WNIN/Ob model using microarray analysis. Expression of selected retinal marker genes was studied via real-time PCR.

RESULTS

Progressive loss of photoreceptor cells was observed in WNIN/GR-Ob rats with an onset as early as 3 months. Similarly, thinning of the inner nuclear layer was observed from 6 months in these rats. Immunohistochemical analysis showed decreased levels of rhodopsin and postsynaptic density protein-95 (PSD-95) proteins and increased levels of glial fibrillary acidic protein (GFAP), vascular endothelial growth factor (VEGF), and calretinin in WNIN/GR-Ob rats compared with the age-matched lean controls, further supporting cellular stress/damage and retinal degeneration. The retinal transcriptome analysis indicated altered expression profiles in both the WNIN/GR-Ob and WNIN/Ob rat models compared to their respective lean controls; these pathways are associated with activation of pathways like cellular oxidative stress response, inflammation, apoptosis, and phototransduction, although the changes were more prominent in WNIN/GR-Ob than in WNIN/Ob animals.

CONCLUSIONS

WNIN/GR-Ob rats with added glucose intolerance developed retinal degeneration similar to the parent line WNIN/Ob. The severity of retinal degeneration was greater in WNIN/GR-Ob rats compared to WNIN/Ob, suggesting a possible role for IGT in this model. Hence, the WNIN/GR-Ob model could be a valuable tool for investigating the impact of MetS on retinal degeneration pathology.

摘要

目的

代谢综合征（MetS）与多种退行性疾病相关，包括视网膜变性。此前，我们报道了一种自发性肥胖大鼠（WNIN/Ob）模型中的进行性视网膜变性。在本研究中，我们使用WNIN/GR-Ob大鼠模型研究了代谢综合征的一个关键组成部分——糖耐量受损（IGT）对视网膜变性的额外影响。

方法

通过显微镜检查和免疫组织化学研究WNIN/GR-Ob大鼠以及年龄匹配的同窝瘦大鼠的视网膜形态和超微结构。使用微阵列分析将WNIN/GR-Ob大鼠的视网膜转录组与其各自的瘦对照以及WNIN/Ob模型进行比较。通过实时PCR研究选定的视网膜标记基因的表达。

结果

在WNIN/GR-Ob大鼠中观察到光感受器细胞的进行性丧失，最早在3个月时出现。同样，从6个月起在这些大鼠中观察到内核层变薄。免疫组织化学分析显示，与年龄匹配的瘦对照相比，WNIN/GR-Ob大鼠中视紫红质和突触后密度蛋白95（PSD-95）蛋白水平降低，而胶质纤维酸性蛋白（GFAP）、血管内皮生长因子（VEGF）和钙视网膜蛋白水平升高，进一步支持细胞应激/损伤和视网膜变性。视网膜转录组分析表明，与各自的瘦对照相比，WNIN/GR-Ob和WNIN/Ob大鼠模型中的表达谱均发生改变；这些途径与细胞氧化应激反应、炎症、细胞凋亡和光转导等途径的激活有关，尽管WNIN/GR-Ob中的变化比WNIN/Ob动物中更显著。

结论

伴有糖耐量受损的WNIN/GR-Ob大鼠发生了与亲本系WNIN/Ob相似的视网膜变性。与WNIN/Ob相比，WNIN/GR-Ob大鼠的视网膜变性更严重，表明IGT在该模型中可能起作用。因此，WNIN/GR-Ob模型可能是研究代谢综合征对视网膜变性病理学影响的有价值工具。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be3c/5398884/24587f894021/mv-v23-263-f8.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be3c/5398884/24587f894021/mv-v23-263-f8.jpg
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