PurposeMice homozygous for Ins2Akita develop type 1 diabetes mellitus. These animals die by 12 weeks old age due to rapid and severe hyperglycemia, which leaves the mice with a short window period to manifest diabetic retinopathy (DR). Here we report the rare development of DR in a 22 week‐old male Akita mouse.MethodsElectroretinography (ERG) and spatial‐domain optical coherence tomography (SD‐OCT) imaging as a measure of visual function, which was coupled to fluorescein angiography (FA) and trypsin digestion (TD).ResultsThe homozygous mouse exhibited hyperglycemia and retinal complications including early signs of vascular damage consistent with DR. TD demonstrated the presence of pericyte ghosts, whereas FA exhibited the manifestation of retinal neovascularization, vascular leakage and microaneurysm formation. ERG recording and OCT imaging were sensitive in detecting the degree of retinal degeneration and RPE tear as compared to the wildtype control. The RPE tear created an area where photoreceptors have no RPE support. Scotopic ERG analysis exhibited significantly faster b‐wave responses as compared to wildtype control. Further analysis using b/a‐wave ratio revealed a strikingly disproportionate reduction in the b‐ and a‐wave amplitudes. SD‐OCT demonstrated a reduction in the overall retinal thickness (OS‐NFL) of homozygous Ins2Akita mouse but not age‐matched control.ConclusionsOur study reports and for the first time the rare development of full‐blown clinical expression of diabetic retinopathy in a 22‐week old homozygous Akita.