Benefits of early glycemic control by insulin on sensory neuropathy and cataract in diabetic rats.

While there is an emphasis on the early glycemic control for its long-term benefits in preventing microvascular complications of diabetes, the biochemical mechanisms responsible for the long-lasting effects are not clearly understood. Therefore the impact of early insulin (EI) versus late insulin (LI) treatment on diabetic sensory neuropathy and cataract in streptozotocin-induced diabetic Wistar male rats were evaluated. EI group received insulin (2.5 IU/animal, once daily) treatment from day 1 to 90 while LI group received insulin from day 60 to 90. Early insulin treatment significantly reduced the biochemical markers like glucose, triglyceride, glycated hemoglobin, thiobarbituric acid reactive substances, advanced glycation end products and ratio of reduced glutathione and oxidized glutathione in diabetic rats. The late insulin treatment failed to resist the biochemical changes in diabetic rats. Diabetic rats developed sensory neuropathy as evidenced by mechanical and thermal hyperalgesia and showed a higher incidence and severity of cataract as revealed by slit lamp examination. Early insulin treatment protected the rats from the development of neuropathy and cataract, but late insulin administration failed to do so. The results demonstrate the benefits of early glycemic control in preventing neuropathy and cataract development in diabetic rats.

Visual outcomes of pan-retinal photocoagulation in diabetic retinopathy at one-year follow-up and associated risk factors.

PURPOSE: To assess the visual outcomes at one-year follow-up after pan-retinal photocoagulation (PRP) in type 2 diabetes mellitus subjects with proliferative diabetic retinopathy (PDR) and associated risk factors. MATERIALS AND METHODS: A retrospective study, using data from medical records of 5000 Type 2 diabetic patients who underwent a retinal examination between 1995 and 1999 at a diabetic centre. Ocular, clinical and biochemical parameters were assessed at baseline and at one-year follow-up after PRP. Diabetic retinopathy (DR) was documented by colour photography and PRP was performed according to the ETDRS criteria. RESULTS: PRP was done in 413 eyes, of which 261 eyes of 160 subjects were eligible for the study. One hundred and forty eyes (73%) of 191 eyes with good visual acuity (6/9) at baseline maintained the same vision at one-year follow-up. Of the 53 eyes with visual acuity of 6/12-6/36 at baseline, 58.5% (31 eyes) maintained same vision and 18.9% (10 eyes) improved their vision at one-year follow-up. Of the 17 eyes with visual acuity < or =6/60 at baseline, 12 maintained the same vision and the remaining 5 improved their vision. The causes of visual loss included vitreous haemorrhage in 20 subjects (31.7%), progression of cataract in 19 (30%), chronic macular oedema in 15 (23.8%), pre-retinal haemorrhage in the macula in 6 (9.5%) and pre-retinal fibrosis in the macula in 3 (4.7%) subjects. On multiple logistic regression analysis, diastolic blood pressure (P =0.03), duration of diabetes (P =0.006), fasting blood glucose (P =0.02) and nephropathy (P =0.01) were associated with decreased vision after PRP. Glycated haemoglobin (HbA1c) (P < 0.001), serum creatinine (P =0.03), HDL cholesterol (P =0.05), diabetic neuropathy (P < 0.001), hypertension (P =0.01) and diabetic nephropathy (P < 0.001) showed a significant association with PDR. CONCLUSION: Visual acuity at baseline, the duration of diabetes and proteinuria played a significant role in determining the post-PRP visual acuity.

Genes and diabetic retinopathy.

Several recent studies have provided evidence that good diabetes control is important to prevent diabetic retinopathy. However, some groups of patients develop diabetic retinopathy despite good control and others escape retinopathy despite poor control. This suggests the role of genetic factors in susceptibility to retinopathy. This article reviews the role of genetic factors in determining diabetic retinopathy.