Histological Evaluation of Diabetic Neurodegeneration in the Retina of Zucker Diabetic Fatty (ZDF) Rats

Abstract In diabetes, retinal dysfunctions exist prior to clinically detectable vasculopathy, however the pathology behind these functional deficits is still not fully established. Previously, our group published a detailed study on the retinal histopathology of type 1 diabetic (T1D) rat model, wher...

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Main Authors: Klaudia Szabó, Anna Énzsöly, Bulcsú Dékány, Arnold Szabó, Rozina I. Hajdú, Tamás Radovits, Csaba Mátyás, Attila Oláh, Lenke K. Laurik, Gábor M. Somfai, Béla Merkely, Ágoston Szél, Ákos Lukáts
Format: Article
Language:English
Published: Nature Portfolio 2017-08-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-017-09068-6
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author Klaudia Szabó
Anna Énzsöly
Bulcsú Dékány
Arnold Szabó
Rozina I. Hajdú
Tamás Radovits
Csaba Mátyás
Attila Oláh
Lenke K. Laurik
Gábor M. Somfai
Béla Merkely
Ágoston Szél
Ákos Lukáts
author_facet Klaudia Szabó
Anna Énzsöly
Bulcsú Dékány
Arnold Szabó
Rozina I. Hajdú
Tamás Radovits
Csaba Mátyás
Attila Oláh
Lenke K. Laurik
Gábor M. Somfai
Béla Merkely
Ágoston Szél
Ákos Lukáts
author_sort Klaudia Szabó
collection DOAJ
description Abstract In diabetes, retinal dysfunctions exist prior to clinically detectable vasculopathy, however the pathology behind these functional deficits is still not fully established. Previously, our group published a detailed study on the retinal histopathology of type 1 diabetic (T1D) rat model, where specific alterations were detected. Although the majority of human diabetic patients have type 2 diabetes (T2D), similar studies on T2D models are practically absent. To fill this gap, we examined Zucker Diabetic Fatty (ZDF) rats - a model for T2D - by immunohistochemistry at the age of 32 weeks. Glial reactivity was observed in all diabetic specimens, accompanied by an increase in the number of microglia cells. Prominent outer segment degeneration was detectable with changes in cone opsin expression pattern, without a decrease in the number of labelled elements. The immunoreactivity of AII amacrine cells was markedly decreased and changes were detectable in the number and staining of some other amacrine cell subtypes, while most other cells examined did not show any major alterations. Overall, the retinal histology of ZDF rats shows a surprising similarity to T1D rats indicating that despite the different evolution of the disease, the neuroretinal cells affected are the same in both subtypes of diabetes.
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spelling doaj.art-57d0d283bf724bdb8426c37685ee16e62022-12-21T22:56:09ZengNature PortfolioScientific Reports2045-23222017-08-017111710.1038/s41598-017-09068-6Histological Evaluation of Diabetic Neurodegeneration in the Retina of Zucker Diabetic Fatty (ZDF) RatsKlaudia Szabó0Anna Énzsöly1Bulcsú Dékány2Arnold Szabó3Rozina I. Hajdú4Tamás Radovits5Csaba Mátyás6Attila Oláh7Lenke K. Laurik8Gábor M. Somfai9Béla Merkely10Ágoston Szél11Ákos Lukáts12Department of Anatomy, Histology and Embryology, Semmelweis UniversityDepartment of Anatomy, Histology and Embryology, Semmelweis UniversityDepartment of Anatomy, Histology and Embryology, Semmelweis UniversityDepartment of Anatomy, Histology and Embryology, Semmelweis UniversityDepartment of Anatomy, Histology and Embryology, Semmelweis UniversityHeart and Vascular Center, Semmelweis UniversityHeart and Vascular Center, Semmelweis UniversityHeart and Vascular Center, Semmelweis UniversityDepartment of Ophthalmology, Semmelweis UniversityDepartment of Ophthalmology, Semmelweis UniversityHeart and Vascular Center, Semmelweis UniversityDepartment of Anatomy, Histology and Embryology, Semmelweis UniversityDepartment of Anatomy, Histology and Embryology, Semmelweis UniversityAbstract In diabetes, retinal dysfunctions exist prior to clinically detectable vasculopathy, however the pathology behind these functional deficits is still not fully established. Previously, our group published a detailed study on the retinal histopathology of type 1 diabetic (T1D) rat model, where specific alterations were detected. Although the majority of human diabetic patients have type 2 diabetes (T2D), similar studies on T2D models are practically absent. To fill this gap, we examined Zucker Diabetic Fatty (ZDF) rats - a model for T2D - by immunohistochemistry at the age of 32 weeks. Glial reactivity was observed in all diabetic specimens, accompanied by an increase in the number of microglia cells. Prominent outer segment degeneration was detectable with changes in cone opsin expression pattern, without a decrease in the number of labelled elements. The immunoreactivity of AII amacrine cells was markedly decreased and changes were detectable in the number and staining of some other amacrine cell subtypes, while most other cells examined did not show any major alterations. Overall, the retinal histology of ZDF rats shows a surprising similarity to T1D rats indicating that despite the different evolution of the disease, the neuroretinal cells affected are the same in both subtypes of diabetes.https://doi.org/10.1038/s41598-017-09068-6
spellingShingle Klaudia Szabó
Anna Énzsöly
Bulcsú Dékány
Arnold Szabó
Rozina I. Hajdú
Tamás Radovits
Csaba Mátyás
Attila Oláh
Lenke K. Laurik
Gábor M. Somfai
Béla Merkely
Ágoston Szél
Ákos Lukáts
Histological Evaluation of Diabetic Neurodegeneration in the Retina of Zucker Diabetic Fatty (ZDF) Rats
Scientific Reports
title Histological Evaluation of Diabetic Neurodegeneration in the Retina of Zucker Diabetic Fatty (ZDF) Rats
title_full Histological Evaluation of Diabetic Neurodegeneration in the Retina of Zucker Diabetic Fatty (ZDF) Rats
title_fullStr Histological Evaluation of Diabetic Neurodegeneration in the Retina of Zucker Diabetic Fatty (ZDF) Rats
title_full_unstemmed Histological Evaluation of Diabetic Neurodegeneration in the Retina of Zucker Diabetic Fatty (ZDF) Rats
title_short Histological Evaluation of Diabetic Neurodegeneration in the Retina of Zucker Diabetic Fatty (ZDF) Rats
title_sort histological evaluation of diabetic neurodegeneration in the retina of zucker diabetic fatty zdf rats
url https://doi.org/10.1038/s41598-017-09068-6
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