Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

The Modification of Detrimental Biochemical Anomalies May Reduce the Rate of Development of Diabetic Retinopathy in Type 2 Diabetes Mellitus

Version 1 : Received: 7 June 2022 / Approved: 8 June 2022 / Online: 8 June 2022 (12:40:07 CEST)

How to cite: Pramanik, S.; Banerjee, K.; Mondal, L.K. The Modification of Detrimental Biochemical Anomalies May Reduce the Rate of Development of Diabetic Retinopathy in Type 2 Diabetes Mellitus. Preprints 2022, 2022060129 (doi: 10.20944/preprints202206.0129.v1). Pramanik, S.; Banerjee, K.; Mondal, L.K. The Modification of Detrimental Biochemical Anomalies May Reduce the Rate of Development of Diabetic Retinopathy in Type 2 Diabetes Mellitus. Preprints 2022, 2022060129 (doi: 10.20944/preprints202206.0129.v1).

Abstract

Excessive intracellular glucose in insulin independent tissues including nerve, nephron, lens and retina invites mishandling of metabolism of glucose resulting in a background of increased oxidative stress, advanced glycation end products (AGE) formation, lipid peroxidation and failure of antioxidant defense systems in type 2 diabetes mellitus (T2DM). All these detrimental biochemical anomalies ultimately attack biological membranes and especially capillary beds of retina and glomerulus of kidney, resulting in break-down of inner blood-retinal i.e. initiation of diabetic retinopathy (DR). If these disarrays are corrected to a large extent, development of DR can be avoided or delayed. In this prospective clinical trial, 185 patients with T2DM who received B-vitamins, vitamin-C, and E along with anti-diabetic medication for five years, demonstrated a slower rate of the development of DR and reduced abnormal biochemical mediators like reactive oxygen species (ROS), malondialdehyde (MDA), AGE, and vascular endothelial growth factor (VEGF) compared to 175 T2DM individuals who were treated with only anti-hyperglycemic drugs.

Keywords

Diabetic retinopathy; Oxidative stress; Advanced glycation end products (AGEs); Antioxidant enzymes; Vascular endothelial growth factor; B-vitamins; Vitamin-C; Vitamin- E

Subject

LIFE SCIENCES, Endocrinology & Metabolomics

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