Abstract
Aims/Purpose: Diabetic retinopathy (DR) is a common, sight‐threatening microvascular complication of diabetes. The end‐stage form of the disease, proliferative DR (PDR), is characterized by ischemia and inflammation‐induced pathological neovascularization at the vitreoretinal interface, often accompanied by vitreous hemorrhage and tractional retinal detachment (TRD). The mechanisms behind the progression of PDR, and the effect of different treatments on these processes, are not fully understood. As the number of diabetics is on the rise, and current treatment options are invasive and limited in their efficacy, the search for novel targets for treatment and prevention of PDR progression is crucial.The aim of our study is to reveal differences between vitreous metabolite profiles of non‐PDR and PDR disease states, and the effect of treatment on those profiles. We aim to better understand the progression of the disease and to identify potential target metabolites and pathways.Methods: We analyzed metabolites in vitreous samples from type II diabetic patients with different stages of DR (non‐PDR patients, PDR patients, and PDR patients with TRD) via targeted LC‐MS metabolomics. Pathway enrichment analyses were performed using MetaboAnalyst 5.0.Results: We identified various significantly altered metabolites such as deoxycarnitine, indole‐3‐acetic acid and glycine between non‐PDR and PDR patients. Metabolite enrichment analyses revealed strong associations with, for example, tryptophan and glycine metabolism.Conclusions: We identified metabolites, processes and metabolic pathways of interest in PDR progression in type II diabetic patients, some of which could be potentially useful for development of novel treatment options. Furthermore, this metabolic information provides new insight into pathogenetic mechanisms behind PDR progression.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have