Pathological Features of Diabetic Retinopathy in Spontaneously Diabetic Torii Fatty Rats

Cataract and retinopathy remain the preventable cause of blindness worldwide, and many pharmacological strategies have been proposed for the treatment of these eye diseases. Animal models play an important role in understanding the pathophysiological features of eye disease and developing for a new therapy. In this study, we investigated the development of cataract and retinal lesion with diabetes using an obese type 2 diabetic models SDT fatty rat. Macroscopic analysis in eyes was performed from 16 to 24 weeks of age and histological analysis was performed at 24 weeks of age. As a result, the lens cloudiness was observed from 19 weeks of age and the degree of the cloudiness was more progressed until 24 weeks of age. Histopathological findings, such as degeneration of lens fiber and shortening and irregular arrangement of cone and rod in retinal tissue, were observed at 24 weeks of age. In conclusion, SDT fatty rats may be useful to understand the pathological features in diabetic cataract and retinopathy develop a new therapy for the disease.

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“…Retinal folds in SDT fatty rats develop at an early age and peak at 24 weeks of age [26]. No obvious retinal folds were observed in this study.…”

Section: Resultscontrasting

confidence: 50%

Ocular changes –cataract and retinal lesion- in Spontaneously Diabetic Torii (SDT) fatty rats, an obese type 2 diabetic model

Maekawa

Nakamura²,

Miyajima

et al. 2021

JSMARTech

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“…Using a long-term low dose of glibenclamide, retinal thickness was reduced, as observed with short-term local treatment [ 21 ], although the retina remained thicker than in non-diabetic Wistar rats and no thinning was observed. Depending on the model and the studied time points, various retinal morphological changes were reported in vivo using OCT. Whilst retina thinning was observed in 20-week-old db/+ mice [ 38 ], retina thickening was noted in 40 week-old diabetic Torii fatty and non-fatty rats [ 39 ], showing that in the long term, loss of visual neurons can be measured.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Oral Treatment with Non-Hypoglycemic Dose of Glibenclamide Reduces Diabetic Retinopathy Damage in the Goto-KakizakiRat Model

et al. 2021

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Diabetic retinopathy (DR) remains a major cause of vision loss, due to macular edema, retinal ischemia and death of retinal neurons. We previously demonstrated that acute administration of glibenclamide into the vitreous, or given orally at a non-hypoglycemic dose, protected the structure and the function of the retina in three animal models that each mimic aspects of diabetic retinopathy in humans. In this pilot study, we investigated whether one year of chronic oral glibenclamide, in a non-hypoglycemic regimen (Amglidia®, 0.4 mg/kg, Ammtek/Nordic Pharma, 5 d/week), could alleviate the retinopathy that develops in the Goto-Kakizaki (GK) rat. In vivo, retinal function was assessed by electroretinography (ERG), retinal thickness by optical coherence tomography (OCT) and retinal perfusion by fluorescein and indocyanin green angiographies. The integrity of the retinal pigment epithelium (RPE) that constitutes the outer retinal barrier was evaluated by quantitative analysis of the RPE morphology on flat-mounted fundus ex vivo. Oral glibenclamide did not significantly reduce the Hb1Ac levels but still improved retinal function, as witnessed by the reduction in scotopic implicit times, limited diabetes-induced neuroretinal thickening and the extension of ischemic areas, and it improved the capillary coverage. These results indicate that low doses of oral glibenclamide could still be beneficial for the prevention of type 2 diabetic retinopathy. Whether the retinas ofpatients treated specifically with glibenclamideare less at risk of developing diabetic complications remains to be demonstrated.

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“…Following inherited or acquired retinal pathology, GFAP is expressed also in Muller cells [19,20]. GFAP expression in Muller cells has been widely used as a cellular marker for retinal pathology [21][22][23][24][25]. Hypoxia-inducible factor 1 alpha (HIF-1α) is known to be a key regulator of a tissue's response to hypoxia [26] and plays a role in obesity-induced metabolic syndrome.…”

Section: Introductionmentioning

confidence: 99%

Characterizing the Retinal Phenotype in the High-Fat Diet and Western Diet Mouse Models of Prediabetes

Asare-Bediako

Noothi

Calzi

et al. 2020

Cells

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We sought to delineate the retinal features associated with the high-fat diet (HFD) mouse, a widely used model of obesity. C57BL/6 mice were fed either a high-fat (60% fat; HFD) or low-fat (10% fat; LFD) diet for up to 12 months. The effect of HFD on body weight and insulin resistance were measured. The retina was assessed by electroretinogram (ERG), fundus photography, permeability studies, and trypsin digests for enumeration of acellular capillaries. The HFD cohort experienced hypercholesterolemia when compared to the LFD cohort, but not hyperglycemia. HFD mice developed a higher body weight (60.33 g vs. 30.17g, p < 0.0001) as well as a reduced insulin sensitivity index (9.418 vs. 62.01, p = 0.0002) compared to LFD controls. At 6 months, retinal functional testing demonstrated a reduction in a-wave and b-wave amplitudes. At 12 months, mice on HFD showed evidence of increased retinal nerve infarcts and vascular leakage, reduced vascular density, but no increase in number of acellular capillaries compared to LFD mice. In conclusion, the HFD mouse is a useful model for examining the effect of prediabetes and hypercholesterolemia on the retina. The HFD-induced changes appear to occur slower than those observed in type 2 diabetes (T2D) models but are consistent with other retinopathy models, showing neural damage prior to vascular changes.

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Pathological Features of Diabetic Retinopathy in Spontaneously Diabetic Torii Fatty Rats

Cited by 12 publications

References 24 publications

Ocular changes –cataract and retinal lesion- in Spontaneously Diabetic Torii (SDT) fatty rats, an obese type 2 diabetic model

Ocular changes –cataract and retinal lesion- in Spontaneously Diabetic Torii (SDT) fatty rats, an obese type 2 diabetic model

Long-Term Oral Treatment with Non-Hypoglycemic Dose of Glibenclamide Reduces Diabetic Retinopathy Damage in the Goto-KakizakiRat Model

Characterizing the Retinal Phenotype in the High-Fat Diet and Western Diet Mouse Models of Prediabetes

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