Role of Advanced Gglycation End Products (AGEs) and Obesity in Diabetic Cataract Rats

摘要

Background: obese subjects have a more elevated degree of oxidative stress than normal asincreased body fat stimu lates excessive reactive oxygen species (ROS) production. Also, obesity is associatedwith serious morbidities including a high incidence of type 2 diabetes and cataractogenesis. Methods: in thepresent study the body mass index (BMI) was evaluated. Fasting blood glucose (FBG), glycosylatedhemoglobin (HbA1c), Malondialdehyde (MDA), Antioxidant markers (Total antioxidant capacity (TAC), reducedglutathione (GSH). Superoxide dismutase (SOD) and Advanced glycation end products (AGEs) were assayed.Also, determination of total protein and electrophoretic analysis of lens proteins were estimated in 40 ratsdivided into four groups of 10 animals each: control (group I); diabetic (group II) injected with a dose of 40mg/kg by streptozotosin; high fat diet (Group III) were access to high fat diet and (Group IV) were access toa high fat diet and injected with a dose of 40 mg/kg by streptozotosin. Results: there was a statistical significantincrease in FBG, HbA1c, MDA and AGEs levels in diabetic and HFD groups compared to control group.Meanwhile, there were statistical significant decrease in GSH and SOD activities in both diabetic and HFDgroups compared to control group. On the other hand, there were statistical significant decrease in TAC leveland total lens proteins in diabetic groups compared to control group. Sodium dodecyl sulfate (SDS)electrophoresis showed aggregation of lens proteins in the diabetic groups compared to HFD and controlgroups. Conclusion: this study clarifies increased accumulation of AGEs and increased lipid peroxidationproducts along with impaired antioxidant status in obesity and at accelerated rate in diabetics. Proper controlof hyperglycemia, blocking of AGEs pathways by AGEs-inhibitors and low fat diet may be beneficial to delaydiabetic cataractogensis.