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Nasal to fovea, some areas had neurons in the inner nuclear layer appearing normal in number, even though viable retinal vasculature was not present in the area (Figs. In sections through the macular region, two patterns of neuronal loss were apparent (Figs. Two of the four animals with this pattern of vascular loss had apparent cilioretinal vascular systems that were still viable ( Fig. In these most severe cases, the central half of fovea was nonperfused, whereas the temporal fovea had viable blood vessels (Fig. In three of these animals, the area of dropout included most of the vasculature between optic disc and fovea. In four of the severely diabetic monkeys, large areas of capillary loss were apparent (Fig. 5 6 One benefit of galactose feeding is that the animals are more easily maintained and have a longer lifespan. However, elevations in dietary galactose in dogs, rats, or mice produce retinal changes similar to those observed after destruction of β-cells. These models of type 1 diabetes have elevated plasma glucose. 4 Although microaneurysms and intraretinal microvascular abnormalities (IRMAs), which some interpret to be intraretinal neovascularization, occur in cats and some rats, preretinal neovascularization has never been observed in an animal model of diabetes. When pancreatectomy is performed on cats, thickened vascular basement membranes develop with loss of pericytes and retinal capillary segments, which eventually results in a large area of vascular nonperfusion temporal to the optic disk. They lose retinal pericytes and capillaries, have thickened vascular basement membranes, and have increased vascular permeability in the retina. 3 The life of these rodents is greatly shortened. 2 Mice or rats given streptozotocin (STZ) or alloxan lose β-cells and become insulin dependent. Most models of diabetes mimic type 1 diabetes, which is caused by destruction of the β-cells in pancreatic islets. Hypertension correlates with the severity of the diabetic retinopathy.
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Monkeys with type 2 diabetes have many of the angiopathic changes associated with human diabetic retinopathy. This is the first detailed analysis of retinopathy in a colony of spontaneous type 2 diabetic monkeys.
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In elastase-digested retinas, the ratio of pericytes to endothelial cells was 0.66:1 in diabetic and 0.64:1 in nondiabetic ( P = 0.75) retinas.Ĭonclusions. There was a significant correlation between the occurrence of retinopathy and hypertension ( P = 0.037 for systolic pressure P = 0.019 for diastolic pressure). There were apparent fluid-filled spaces in the outer plexiform layer in three of these maculas, suggesting macular edema. Formation of small intraretinal microvascular abnormalities (IRMAs) and microaneurysms were associated with the areas of nonperfusion. Large nonperfused areas extending from optic disc to midfovea were observed in four diabetic monkeys. Dot/blot hemorrhages, cotton-wool spots, and small nonperfused areas were the earliest histologically documented changes in the retinas. Cotton-wool spots, intraretinal hemorrhages, and hard exudates in the macula were observed by ophthalmoscopy in some diabetic monkeys. Tissue sections were cut through areas of interest. Retinas from 16 diabetic monkeys and 6 nondiabetic monkeys were incubated postmortem for adenosine diphosphatase (ADPase) activity (labels viable retinal blood vessels) and flat-embedded in JB-4. Ophthalmoscopic examinations were performed on aged normal and diabetic monkeys.
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The purpose of this study was to investigate clinically and histopathologically the ocular changes in these monkeys. Type 2 diabetes occurs spontaneously in rhesus monkeys and shows an extraordinary similarity to human diabetes in clinical features and relative time course.