Study of retinal alterations in a high fat diet-induced type ii diabetes rodent: Meriones shawi

详细信息    查看全文

• 作者：Imane Hammoum^a ; ^b ; Sihem Mbarek^a ; Ahmed Dellaa^a ; Elisabeth Dubus^c ; Basma Baccouche^a ; Rached Azaiz^d ; Ridha Charfeddine^d ; Serge Picaud^c ; Rafika Ben Chaouacha-Chekir^a ; ^{raf_chekir@yahoo.fr} ; ^{rafika.chekir@gmail.com}
• 关键词：Diabetic retinopathy ; High fat diet ; Meriones shawi ; Cone photoreceptors loss ; Immunohistochemistry
• 刊名：Acta Histochemica
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：119
• 期：1
• 页码：1-9
• 全文大小：2871 K
• 卷排序：119

文摘

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.