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Magalie THIERRY, Bruno Pasquis, Niyazi Acar, Stéphane Grégoire, Valérie Febvret, Ségolène Gambert-Nicot, Alain Bron, Catherine Garcher, Lionel Bretillon; Metabolic syndrome triggered by fructose feeding exacerbated laser-induced choroidal neovascularization in the rat. Invest. Ophthalmol. Vis. Sci. 2013;54(15):325.
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Metabolic syndrome (MS) encompasses several clinical characteristics including insulin resistance, glucose intolerance or abdominal adiposity. MS remains a major risk factor for development of type II diabetes. Beyond diabetes, the microvascular complications of the disease are of major importance, especially for the retina. It is still unclear whether retinal neovascularization may be promoted at the stage of MS. Rodents administered a fructose rich diet develop most of the features of MS. Our purpose was to evaluate the consequences of a long term high fructose diet in the rat on the development of retinal neovascularization, using a model of laser-induced choroidal neovascularization.
Male Brown Norway rats (6 weeks of age) were fed for 3 months either a regular chow diet or a 60%-rich fructose diet (n=16 in each group). Choroidal neovascularization was induced by laser rupture of Bruch's membrane (five 532nn-laser burns 300mW, 50ms, 75µm per eye). The fate of retinal neovascularization evolution was followed once a week during the following three weeks using fluorescein and indocyanin green angiography. Quantification of neovascularization was obtained by 2 independent investigators by assessing the ratio of the fluorescent area to the optical nerve head area using Image J software. Body fat was assessed by EchoMRI in the living rats. At the time of euthanasia, plasma lipids (triglycerides, cholesterol, LDL, HDL) were measured as well as plasma glucose, fructosamine, leptin and insulin.
Expectedly, rats fed the fructose diet had elevated circulating glucose, insulin (+32%) and leptin (+119%) levels, and exhibited steatosis, compared to rats fed the control diet. EchoMRI data highlighted an increase of bady fat (+17%) in frructose fed rats. Our data showed a significant 20%-increase of choroidal neovascularization in the rats fed the fructose diet two and three weeks after laser-induction of neovascularization, compared to rats fed the control diet (p<0.05).
The fructose diet consistently triggered MS in the rat. Despite the model of laser-induced neovascularization does not account for the microvascular complications seen in diabetes, our findings strongly support the notion that MS would be a promoting factor for the development of neovascularization. Based on its pro-angiogenic properties, leptin may likely be involved in this process.
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