Abstract
The aim of this study was to estimate the effects of oral supplementation of alpha-lipoic acid (ALA) on contrast sensitivity (CS) in patients with type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). The study included 12 patients with T1DM aged 43±12 years, 48 patients with T2DM aged 59±10 years, and 20 control subjects aged 33±8 years. Patients from each studied group, including the control group, were randomly assigned to receive 300 mg of ALA orally once daily for 3 months. CS was evaluated with the Functional Acuity Contrast Test (FACT, Stereo Optical). In the group of patients with T1DM receiving ALA for 3 months CS remained stable and improved in those with T2DM. Reduction of CS in both T1DM and T2DM patients without alpha-lipoic acid supplementation was observed. In the control group on alpha-lipoic acid supplementation, CS improvement was noticed at one spatial frequency. Changes in the CS were observed, despite stable visual acuity and eye fundus image in all studied subjects. Our study demonstrated that oral administration of alpha-lipoic acid had influence on CS in both T1DM and T2DM patients.
Highlights
Diabetic retinopathy (DR) is a chronic and potentially sightthreatening disease resulting from microvascular damage to the retina
There has been little research that would evaluate the effects of oral treatment of patients with alpha-lipoic acid (ALA) for the help on contrast sensitivity (CS) in patients with type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM)
The aim of this study was to estimate the effect of oral supplementation with ALA on CS in patients with T1DM and T2DM
Summary
Diabetic retinopathy (DR) is a chronic and potentially sightthreatening disease resulting from microvascular damage to the retina. Chronic hyperglycemia, which initiates the development of DR [3, 4], generates reactive oxygen species (ROS) in the retinal tissue, characterized by high oxygen partial pressure of oxygen. ROS, mainly superoxide, inactivate glyceraldehyde3-phosphate dehydrogenase (GADPH), an enzyme crucial in the process of glycolysis [5, 6]. This metabolic block directs substrate flux into biochemical pathways leading to endothelial cell damage. This process constitutes the unifying mechanism of hyperglycemia induced cellular damage [7]
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