Hammoum Imane, Mbarek Sihem, Dellaa Ahmed, Dubus Elisabeth, Baccouche Basma, Azaiz Rached, Charfeddine Ridha, Picaud Serge, Ben Chaouacha-Chekir Rafika
UR Ecophysiologie et Procédés Agroalimentaires, Institut Supérieur de Biotechnologie, Sidi Thabet 2020 Ariana, Université de la Manouba, Tunisia; Faculté des Sciences de Tunis, Université de Tunis El-manar, Tunis, Tunisia.
UR Ecophysiologie et Procédés Agroalimentaires, Institut Supérieur de Biotechnologie, Sidi Thabet 2020 Ariana, Université de la Manouba, Tunisia.
Acta Histochem. 2017 Jan;119(1):1-9. doi: 10.1016/j.acthis.2016.05.005. Epub 2016 Jun 2.
Diabetic retinopathy is a common complication of type 2 diabetes and the leading cause of blindness in adults of working age. The aim of this work was to study the repercussions of high fat diet (HFD) induced diabetes on the retina of Meriones shawi (M.sh). Two groups of six M.sh each was studied. Group I was a normal control, fed with standard laboratory granules. In Group II, rodents received a HFD of enriched laboratory granules, for a period of 3 months. Body weight and plasma glucose were determined in the two groups. Retinal sections of the two groups were stained with the Hematoxylin-Eosin. Photoreceptors were identified by immunolabeling for rhodopsin (rods) and PNA (cones). Gliosis and microglial activation were identified by immunolabeling for GFAP and Iba-1. Labeling of calretinin and parvalbumin were also carried out to study the AII amacrine cells. Retinal layers thicknesses, gliosis, and specific neural cell populations were quantified by microscopy. The body weight (+77%) and plasma glucose (+108%) were significantly greater in the HFD rodents. Three months of HFD induced a significant loss of 38.77% of cone photoreceptors, as well as gliosis and an increase of 70.67% of microglial cells. Calcium homeostatic enzymes were depleted. This work shows that HFD in Meriones shawi induces a type II diabetes-like condition that causes loss of retinal neurons and photoreceptors, as well as gliosis. Meriones shawi could be a useful experimental animal model for this physiopathology particularly in the study of retinal neuro-glial alterations in Type II diabetes.
糖尿病视网膜病变是2型糖尿病的常见并发症，也是工作年龄成年人失明的主要原因。本研究的目的是探讨高脂饮食（HFD）诱导的糖尿病对肖氏子午沙鼠（M.sh）视网膜的影响。研究了两组，每组6只M.sh。第一组为正常对照组，喂食标准实验室颗粒饲料。第二组的啮齿动物接受富含实验室颗粒的高脂饮食，为期3个月。测定两组动物的体重和血糖。两组的视网膜切片用苏木精-伊红染色。通过视紫红质（视杆细胞）和PNA（视锥细胞）免疫标记鉴定光感受器。通过GFAP和Iba-1免疫标记鉴定神经胶质增生和小胶质细胞活化。还进行了钙视网膜蛋白和小白蛋白的标记，以研究AII无长突细胞。通过显微镜对视网膜层厚度、神经胶质增生和特定神经细胞群进行定量分析。高脂饮食组的啮齿动物体重（增加77%）和血糖（增加108%）显著更高。3个月的高脂饮食导致视锥光感受器显著损失38.77%，以及神经胶质增生和小胶质细胞增加70.67%。钙稳态酶减少。这项研究表明，肖氏子午沙鼠的高脂饮食会诱发类似II型糖尿病的状况，导致视网膜神经元和光感受器丧失，以及神经胶质增生。肖氏子午沙鼠可能是这种病理生理学的有用实验动物模型，特别是在研究II型糖尿病视网膜神经胶质改变方面。
