May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Is Spontaneously Diabetic Torii Rat a Model for Human Diabetic Retinopathy
Author Affiliations & Notes
  • H. Yamada
    Ophthalmology, Kansai Medical University, Moriguchi, Japan
  • E. Yamada
    Ophthalmology, Kansai Medical University, Moriguchi, Japan
    Yamada Eye Clinic, Sakai,Osaka, Japan
  • A. Higuchi
    Ophthalmology, Kansai Medical University, Moriguchi, Japan
  • M. Matsumura
    Ophthalmology, Kansai Medical University, Moriguchi, Japan
  • Footnotes
    Commercial Relationships  H. Yamada, None; E. Yamada, None; A. Higuchi, None; M. Matsumura, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 438. doi:
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      H. Yamada, E. Yamada, A. Higuchi, M. Matsumura; Is Spontaneously Diabetic Torii Rat a Model for Human Diabetic Retinopathy . Invest. Ophthalmol. Vis. Sci. 2005;46(13):438.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: The Spontaneous Diabetes Torii (SDT) rat established recently as a model of type II human diabetes mellitus. Male SDT rats develop severe diabetic ocular complications, which are similar to the one in human. In this study, we investigated if SDT rat is a suitable animal model for human proliferative diabetic retinopathy. Methods: Fifty–weeks–old male SDT rat were kept for 8 months. Under deep anesthesia, one eye of each animal was enucleated after perfused with fluorescein dextran and retinal flat mount was made to study vascular structure. The other eye was enucleated and investigated histologically with Hematoxylin–Eosin (HE) and Azan staining and immunohistochemically using antibodies of vascular endothelium (i.e. Griffonia Simpliciforia Isolectin B4, GSA) and vascular endothelial growth factor (VEGF). Results: From vascular structure study, 17 out of 32 (53%) showed proliferative retinopathy without vascular non–perfusion. Histological study revealed that there were traction retinal folds in SDT rat with proliferative retinopathy (SDT–PR). In Azan staining, there were some proliferative matrix observed in SDT rat with non–proliferative retinopathy (SDT–NPR) and SDT–PR compared to SDT normoglycemic control (SDT–control). GSA staining showed no particular vascular change among SDT–control, SDT–NPR and SDT–PR. VEGF staining revealed low immunireactivity in SDT–control retina. There was higher immunoreactivity in SDT–NPR and SDT–PR compared to those of SDT–control. Conclusions: SDT rat is apparently different model for diabetic retinopathy from human proliferative diabetic retinopathy because it develops retinal neovascularization without retinal ischemia. This is a very unique model for ocular neovascularization may be due to high expression of VEGF.

Keywords: neovascularization • diabetic retinopathy 

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