Please use this identifier to cite or link to this item: http://hdl.handle.net/2067/43380
Title: Retinal damage in a new model of hyperglycemia induced by high-sucrose diets
Authors: Catalani, Elisabetta
Silvestri, Federica
Bongiorni, Silvia
Taddei, Anna Rita
Fanelli, Giuseppina
Rinalducci, Sara 
De Palma, Clara
Perrotta, Cristiana
Prantera, Giorgio 
Cervia, Davide 
Journal: PHARMACOLOGICAL RESEARCH 
Issue Date: 2021
Abstract: 
Loss of retinal neurons may precede clinical signs of diabetic retinopathy (DR). We studied for the first time the effects of hyperglycemia on the visual system of the fruit fly Drosophila melanogaster to characterize a model for glucose-induced retinal neurodegeneration, thus complementing more traditional vertebrate systems. Adult flies were fed with increased high-sucrose regimens which did not modify the locomotion ability, muscle phenotype and mobility after 10 days. The increased availability of dietary sucrose induced hyperglycemia and phosphorylation of Akt in fat tissue, without significant effects on adult growth and viability, consistent with the early phase of insulin signaling and a low impact on the overall metabolic profile of flies at short term. Noteworthy, high-sucrose diets significantly decreased Drosophila responsiveness to the light as a consequence of vision defects. Hyperglycemia did not alter the gross anatomical architecture of the external eye phenotype although a progressive damage of photosensitive units was observed. Appreciable levels of cleaved caspase 3 and nitrotyrosine were detected in the internal retina network as well as punctate staining of Light-Chain 3 and p62, and accumulated autophagosomes, indicating apoptotic features, peroxynitrite formation and autophagy turnover defects. In summary, our results in Drosophila support the view that hyperglycemia induced by high-sucrose diets lead to eye defects, apoptosis/autophagy dysregulation, oxidative stress, and visual dysfunctions which are evolutionarily conserved, thus offering a meaningful opportunity of using a simple in vivo model to study the pathophysiology of neuroretinal alterations that develop in patients at the early stages of DR.
URI: http://hdl.handle.net/2067/43380
ISSN: 1043-6618
DOI: 10.1016/j.phrs.2021.105488
Rights: Attribution-NonCommercial-NoDerivs 3.0 United States
Appears in Collections:A1. Articolo in rivista

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