title: Absence of clinical correlates of diabetic retinopathy in the Ins2Akita retina.
abstract: BACKGROUND
  The Ins2(Akita) mouse has been reported to display retinal pathology degeneration associated with advanced diabetic retinopathy. In the present study, we monitored retinal changes in these mice to establish if this model displays clinical features associated with advanced diabetic retinopathy in human patients.
  
  
  METHODS
  Ins2(Akita) mice (n = 55) on a C57Bl/6J background were monitored clinically from 9 to 25 weeks of age using a combination of scanning laser ophthalmoscopy, fluorescein angiography and optical coherence tomography. After clinical imaging, eyes were processed for immunostaining to examine microglial, astroglial and Muller glial responses to hyperglycaemia. To complement our optical coherence tomography imaging, retinal morphology and thicknesses were examined in high-quality semi-thin sections.
  
  
  RESULTS
  No retinal thinning or disruption of retinal architecture was observed by optical coherence tomography or resin histology in Ins2(Akita) mice up to 6 months of age. In addition, no vascular changes were detected by fluorescein angiography or by scanning laser ophthalmoscopy. With the exception of microglial activation, reduced glial fibrillary acid protein expression in astrocytes and an increase in glial fibrillary acid protein expression by Muller cells, no other changes were observed in the Ins2(Akita) retina.
  
  
  CONCLUSIONS
  Our results indicate that the classical clinical correlates of human diabetic retinopathy are absent in Ins2(Akita) mice up to 6 months of age suggesting that either the histopathological processes underlying the development of diabetic retinopathy in this model require longer than 5 months of hyperglycaemia to result in disruption of retinal architecture or that advanced diabetic retinopathy is not a feature of the Ins2(Akita) diabetic mouse.
authors: Centre for Ophthalmology and Visual Science, The University of Western Australia, Perth, Western Australia, Australia.
authors: Samuel
authors: S
authors: McLenachan
authors: Xiangting
authors: X
authors: Chen
authors: Paul G
authors: PG
authors: McMenamin
authors: Elizabeth P
authors: EP
authors: Rakoczy
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000175:diagnosis* / Q000235:genetics / Q000378:metabolism; D003930:Diabetic Retinopathy / Q000175:diagnosis* / Q000235:genetics / Q000378:metabolism; D005451:Fluorescein Angiography; D019084:Fluorescent Antibody Technique, Indirect; D005629:Frozen Sections; D005838:Genotype; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006442:Glycated Hemoglobin / Q000378:metabolism; D007328:Insulin / Q000235:genetics*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009419:Nerve Tissue Proteins / Q000235:genetics; D009457:Neuroglia / Q000378:metabolism; D009887:Ophthalmoscopy; D017354:Point Mutation; D016133:Polymerase Chain Reaction; D012171:Retinal Vessels / Q000473:pathology*; D041623:Tomography, Optical Coherence
chemical_list: D001786:Blood Glucose; D005904:Glial Fibrillary Acidic Protein; D006442:Glycated Hemoglobin; D007328:Insulin; D009419:Nerve Tissue Proteins; C453730:Crb1 protein, mouse; C561967:Ins2 protein, mouse
keywords: Ins2Akita; diabetes; retinopathy