Serum levels of advanced glycation end products negatively correlates with activity of Paraoxonase1 and Lecithin-Cholesterol Acyltransferase in diabetic retinopathy; A cross-sectional case-control study

Abstract

Background: Development of diabetic retinopathy (DR) is closely linked to oxidative stress triggered by various metabolic pathways. Paraoxonase 1 (PON1) and Lecithin-Cholesterol Acyltransferase (LCAT) have protective roles in DR that remain poorly understood. Higher AGEs levels and its role in vascular complications of type 2 diabetes has been shown in previous studies. This case-control study aimed to assess LCAT and PON1 activity and their correlation with advanced glycation end products (AGEs) in patients with diabetes with or without retinopathy.

Method: 45 healthy individuals and 88 diabetic patients were enrolled, categorized as No Diabetic Retinopathy (NDR), Non-Proliferative Diabetic Retinopathy (NPDR), and Proliferative Diabetic Retinopathy (PDR).

Results: PON1 and LCAT activity conversely correlated with serum levels of advanced glycation end products in patients with diabetic retinopathy. There was not such a correlation in patients without DR nor in controls. The correlation was stronger between PON1 and AGEs in comparison to LCAT. PON1 activity was significantly lower in type 2 diabetes patients compared to healthy controls (45.39 ± 16.48 and 203.75 ± 8.92, respectively, P < 0.001). Activity further decreased in NPDR and PDR compared to NDR (23.99 ± 9.79 and 21.28 ± 8.22, respectively, P < 0.001). LCAT activity was significantly lower in diabetic patients compared to controls (33.16 ± 5.98 and 44.35 ± 2.26, respectively, P < 0.001). However, LCAT activity was not lower in diabetic retinopathy compared to NDR (P > 0.05).

Conclusion: Serum PON1 activity negatively correlated with AGEs levels in patients with diabetes but not in controls. The LCAT-AGEs correlation however was only significant in PDR patients. These findings emphasize the potential importance of AGES and PON1 in diabetic retinopathy development and progression.

Keywords: Advanced glycation end products; Diabetic retinopathy; LCAT; Oxidative stress; PON1.