Metabolism in the Zebrafish Retina
Retinal photoreceptors are amongst the most metabolically active cells in the body, consuming more glucose as a metabolic substrate than even the brain. This ensures that there is sufficient energy to establish and maintain photoreceptor functions during and after their differentiation. Such high de...
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Format: | Article |
Language: | English |
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MDPI AG
2021-03-01
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Series: | Journal of Developmental Biology |
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Online Access: | https://www.mdpi.com/2221-3759/9/1/10 |
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author | Natalia Jaroszynska Philippa Harding Mariya Moosajee |
author_facet | Natalia Jaroszynska Philippa Harding Mariya Moosajee |
author_sort | Natalia Jaroszynska |
collection | DOAJ |
description | Retinal photoreceptors are amongst the most metabolically active cells in the body, consuming more glucose as a metabolic substrate than even the brain. This ensures that there is sufficient energy to establish and maintain photoreceptor functions during and after their differentiation. Such high dependence on glucose metabolism is conserved across vertebrates, including zebrafish from early larval through to adult retinal stages. As the zebrafish retina develops rapidly, reaching an adult-like structure by 72 hours post fertilisation, zebrafish larvae can be used to study metabolism not only during retinogenesis, but also in functionally mature retinae. The interplay between rod and cone photoreceptors and the neighbouring retinal pigment epithelium (RPE) cells establishes a metabolic ecosystem that provides essential control of their individual functions, overall maintaining healthy vision. The RPE facilitates efficient supply of glucose from the choroidal vasculature to the photoreceptors, which produce metabolic products that in turn fuel RPE metabolism. Many inherited retinal diseases (IRDs) result in photoreceptor degeneration, either directly arising from photoreceptor-specific mutations or secondary to RPE loss, leading to sight loss. Evidence from a number of vertebrate studies suggests that the imbalance of the metabolic ecosystem in the outer retina contributes to metabolic failure and disease pathogenesis. The use of larval zebrafish mutants with disease-specific mutations that mirror those seen in human patients allows us to uncover mechanisms of such dysregulation and disease pathology with progression from embryonic to adult stages, as well as providing a means of testing novel therapeutic approaches. |
first_indexed | 2024-03-10T13:13:56Z |
format | Article |
id | doaj.art-deddc6427fa948ada8b3ee450b87f93e |
institution | Directory Open Access Journal |
issn | 2221-3759 |
language | English |
last_indexed | 2024-03-10T13:13:56Z |
publishDate | 2021-03-01 |
publisher | MDPI AG |
record_format | Article |
series | Journal of Developmental Biology |
spelling | doaj.art-deddc6427fa948ada8b3ee450b87f93e2023-11-21T10:35:52ZengMDPI AGJournal of Developmental Biology2221-37592021-03-01911010.3390/jdb9010010Metabolism in the Zebrafish RetinaNatalia Jaroszynska0Philippa Harding1Mariya Moosajee2Institute of Ophthalmology, University College London, London EC1V 9EL, UKInstitute of Ophthalmology, University College London, London EC1V 9EL, UKInstitute of Ophthalmology, University College London, London EC1V 9EL, UKRetinal photoreceptors are amongst the most metabolically active cells in the body, consuming more glucose as a metabolic substrate than even the brain. This ensures that there is sufficient energy to establish and maintain photoreceptor functions during and after their differentiation. Such high dependence on glucose metabolism is conserved across vertebrates, including zebrafish from early larval through to adult retinal stages. As the zebrafish retina develops rapidly, reaching an adult-like structure by 72 hours post fertilisation, zebrafish larvae can be used to study metabolism not only during retinogenesis, but also in functionally mature retinae. The interplay between rod and cone photoreceptors and the neighbouring retinal pigment epithelium (RPE) cells establishes a metabolic ecosystem that provides essential control of their individual functions, overall maintaining healthy vision. The RPE facilitates efficient supply of glucose from the choroidal vasculature to the photoreceptors, which produce metabolic products that in turn fuel RPE metabolism. Many inherited retinal diseases (IRDs) result in photoreceptor degeneration, either directly arising from photoreceptor-specific mutations or secondary to RPE loss, leading to sight loss. Evidence from a number of vertebrate studies suggests that the imbalance of the metabolic ecosystem in the outer retina contributes to metabolic failure and disease pathogenesis. The use of larval zebrafish mutants with disease-specific mutations that mirror those seen in human patients allows us to uncover mechanisms of such dysregulation and disease pathology with progression from embryonic to adult stages, as well as providing a means of testing novel therapeutic approaches.https://www.mdpi.com/2221-3759/9/1/10metabolismglucoseretinaphotoreceptorsRPEzebrafish |
spellingShingle | Natalia Jaroszynska Philippa Harding Mariya Moosajee Metabolism in the Zebrafish Retina Journal of Developmental Biology metabolism glucose retina photoreceptors RPE zebrafish |
title | Metabolism in the Zebrafish Retina |
title_full | Metabolism in the Zebrafish Retina |
title_fullStr | Metabolism in the Zebrafish Retina |
title_full_unstemmed | Metabolism in the Zebrafish Retina |
title_short | Metabolism in the Zebrafish Retina |
title_sort | metabolism in the zebrafish retina |
topic | metabolism glucose retina photoreceptors RPE zebrafish |
url | https://www.mdpi.com/2221-3759/9/1/10 |
work_keys_str_mv | AT nataliajaroszynska metabolisminthezebrafishretina AT philippaharding metabolisminthezebrafishretina AT mariyamoosajee metabolisminthezebrafishretina |