Abstract
Diabetic retinopathy and age-related macular degeneration are the leading causes of blindness in Western populations. Although it is a matter of controversy, large-scale population-based studies have reported increased prevalence of age-related macular degeneration in patients with diabetes or diabetic retinopathy. We hypothesized that metabolic syndrome, one of the major risk factors for type 2 diabetes, would represent a favorable environment for the development of choroidal neovascularization, the main complication of age-related macular degeneration. The fructose-fed rat was used as a model for metabolic syndrome in which choroidal neovascularization was induced by laser photocoagulation. Male Brown Norway rats were fed for 1, 3, and 6 months with a standard equilibrated chow diet or a 60%-rich fructose diet (n = 24 per time point). The animals expectedly developed significant body adiposity (+17%), liver steatosis at 3 and 6 months, hyperleptinemia at 1 and 3 months (two-fold increase) and hyperinsulinemia at 3 and 6 months (up to two-fold increase), but remained normoglycemic and normolipemic. The fructose-fed animals exhibited partial loss of rod sensitivity to light stimulus and reduced amplitude of oscillatory potentials at 6 months. Fructose-fed rats developed significantly more choroidal neovascularization at 14 and 21 days post-laser photocoagulation after 1 and 3 months of diet compared to animals fed the control diet. These results were consistent with infiltration/activation of phagocytic cells and up-regulation of pro-angiogenic gene expression such as Vegf and Leptin in the retina. Our data therefore suggested that metabolic syndrome would exacerbate the development of choroidal neovascularization in our experimental model.
Highlights
Diabetic retinopathy (DR) and age-related macular degeneration (AMD) are the leading causes of visual loss in Western populations before and after the age of 50 years, respectively [1]
Fructose diet triggered metabolic syndrome in the rat The fructose diet did not affect body weight, but significantly increased body fat by 17% compared to rats of the control group at the corresponding ages (Figure 2)
Choroidal neovascularization (CNV) significantly enhanced CD68 immunostaining in fructose-fed rats, suggesting massive infiltration of circulating macrophages and/or activation of resident microglia
Summary
Diabetic retinopathy (DR) and age-related macular degeneration (AMD) are the leading causes of visual loss in Western populations before and after the age of 50 years, respectively [1]. High-fructose diets have been associated with metabolic changes and excess weight gain that are typical of MetS and may predispose to T2D [14,16,17,18]. This concern was supported mainly by observations in high-fructose-fed rodents that reported hyperinsulinemia, increase of body fat, and hepatomegaly associated with accumulation of lipids in the liver [19,20]. We sought first to characterize the functional and gene expression changes in the retina of fructose-fed rats, and second to evaluate whether fructose-fed rats would be more prone to developing CNV than control animals
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
