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...

Full description

Bibliographic Details
Main Authors: Natalia Jaroszynska, Philippa Harding, Mariya Moosajee
Format: Article
Language:English
Published: MDPI AG 2021-03-01
Series:Journal of Developmental Biology
Subjects:
Online Access:https://www.mdpi.com/2221-3759/9/1/10
_version_ 1797541296742596608
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