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Research has shown that increased levels of retinol binding protein 3 (RBP3) may protect and treat diabetic retinopathy

Researchers at the Joslin Diabetes Centre, Boston have identified that a protein can protect against diabetic retinopathy (DR) and potentially reverse the effects of complications in mouse models of diabetes.  The level of retinol binding protein 3 (RBP3) expressed in both the vitreous and retina appears to be higher in people who don’t progress to diabetic eye disease.  The researchers indicate that 35% of type 1 diabetes patients exhibit either none or mild diabetic retinopathy, independent of glycemic control.  This suggests that a natural variant has endogenous protective factors against diabetic retinopathy, which could help to develop multiple strategies to ameliorate the pathology.  The results of the research conclude that scientists “found that preservation of RBP3, through either supplementation or increased expression from the photoreceptors, can protect neuroretina and vascular retina from diabetes-induced retinal dysfunction and pathology. This protective activity is partially mediated by RBP3 binding to GLUT1 and inhibition of glucose uptake in retinal cells, with subsequent decreased expression of VEGF and inflammatory cytokines”.


The patient cohort for the research was developed by the Joslin Medalist Study, based at the Joslin Diabetes Centre in Boston, and recruited from across 50 states in the United States between 2004 and 2019.  The study is aimed to identify factors in the retina or vitreous that are associated with resistance to the initiation or progression of retinopathy in the presence of hyperglycemia.   In the study candidate proteins were up-regulated in the retina and vitreous of Medalist patients with no-mild NPDR and RBP3 was then selected for further study.  The protein was also selected because the expression of RBP3 has reported to decrease in DR in independent research.


RBP3 is a large 135-kDa secreted protein produced mainly in the photoreceptors and works for binding and transporting cis/trans retinols between photoreceptors and RPE.  The findings of the research showed that there was an estimated 5-fold decrease in RBP3 expression in the retina and vitreous in patients with severe DR, compared to non-diabetic mellitus eyes.  In essence, the level of RBP3 in the vitreous and retina in a sup-population of patients are higher in those who do no progress to DR.  A range of potential strategies could be used to improve DR using, for example, small molecules, supplementation, gene therapy approaches and many others.  One of the main authors, Dr. George King, stated that “if we could find out what’s causing the decrease of RBP3 in the retina in the first place, we could design some kind of treatment to maintain its production, allowing all diabetic patients to have an endogenous protection against eye disease”.