Abstract
BackgroundOne of the most prevalent microvascular complications for patients with diabetes is diabetic retinopathy (DR) associated with increased retinal endothelial blood vessel formation. Treatments to reduce vascularisation in the retinal endothelium are linked to improved sight in patients with DR. Recently, we have demonstrated the novel protective role of the artificial sweetener, sucralose, and the sweet taste receptor, T1R3, in the pulmonary endothelium to reduce vascular leak. In the present study, we examined the role of sucralose and sweet taste receptors on vasculogenic processes (proliferation, migration, adhesion and tube formation) in a cell model of the retinal endothelium.MethodsWe exposed human retinal microvascular endothelial cells (RMVEC) to VEGF as an in vitro model of DR in the presence and absence of T1R3 agonist sucralose.ResultsIn RMVEC, we observed increased VEGF-induced cell proliferation, migration, adhesion and tube formation, which was significantly attenuated by exposure to the artificial sweetener sucralose. Following siRNA knockdown of the sweet taste receptor, T1R3, but not T1R2, the protective effect of sucralose on VEGF-induced RMVEC vasculogenic processes was blocked. We further demonstrate that sucralose attenuates VEGF-induced Akt phosphorylation to protect the retinal microvasculature.ConclusionThese studies are the first to demonstrate a protective effect of an artificial sweetener, through the sweet taste receptor T1R3, on VEGF-induced vasculogenesis in a retinal microvascular endothelial cell line.
Highlights
Worldwide, there are currently 425 million people estimated to suffer from type 1 and 2 diabetes, which results in a yearly healthcare expenditure of 727 billion USD
We further demonstrate that vascular endothelial growth factor (VEGF) mediates excessive cell migration, adhesion, proliferation and tube formation in a retinal microvascular endothelial cell line which is blocked by sucralose
Our studies show that sweet taste sensing through T1R3 plays a significant role in aberrant vascularisation processes which are seen in diabetes and highlights a potential anti-VEGF therapeutic agent for patients with diabetic retinopathy (DR)
Summary
There are currently 425 million people estimated to suffer from type 1 and 2 diabetes, which results in a yearly healthcare expenditure of 727 billion USD. Disease associated with diabetic retinopathy (DR), diabetic macular edema and glaucoma [1]. Hyperglycaemia increases metabolic disruption, inflammation and hypoxia in patients with diabetes, associated with the pathophysiology of DR [2]. One of the most prevalent microvascular complications for patients with diabetes is diabetic retinopathy (DR) associated with increased retinal endothelial blood vessel formation. Treatments to reduce vascularisation in the retinal endothelium are linked to improved sight in patients with DR. We have demonstrated the novel protective role of the artificial sweetener, sucralose, and the sweet taste receptor, T1R3, in the pulmonary endothelium to reduce vascular leak. We examined the role of sucralose and sweet taste receptors on vasculogenic processes (proliferation, migration, adhesion and tube formation) in a cell model of the retinal endothelium
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