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Lack of Melanopsin Is Associated with Extreme Weight Loss in Mice upon Dietary Challenge
Metabolic disorders have been established as major risk factors for ocular complications and poor vision. However, little is known about the inverse possibility that ocular disease may cause metabolic dysfunction. To test this hypothesis, we assessed the metabolic consequences of a robust dietary ch...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4444252/ https://www.ncbi.nlm.nih.gov/pubmed/26011287 http://dx.doi.org/10.1371/journal.pone.0127031 |
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author | Aytürk, Didem Göz Castrucci, Ana Maria Carr, David E. Keller, Susanna R. Provencio, Ignacio |
author_facet | Aytürk, Didem Göz Castrucci, Ana Maria Carr, David E. Keller, Susanna R. Provencio, Ignacio |
author_sort | Aytürk, Didem Göz |
collection | PubMed |
description | Metabolic disorders have been established as major risk factors for ocular complications and poor vision. However, little is known about the inverse possibility that ocular disease may cause metabolic dysfunction. To test this hypothesis, we assessed the metabolic consequences of a robust dietary challenge in several mouse models suffering from retinal mutations. To this end, mice null for melanopsin (Opn4(-/-)), the photopigment of intrinsically photosensitive retinal ganglion cells (ipRGCs), were subjected to five weeks of a ketogenic diet. These mice lost significantly more weight than wild-type controls or mice lacking rod and cone photoreceptors (Pde6b(rd1/rd1)). Although ipRGCs are critical for proper circadian entrainment, and circadian misalignment has been implicated in metabolic pathology, we observed no differences in entrainment between Opn4(-/-) and control mice. Additionally, we observed no differences in any tested metabolic parameter between these mouse strains. Further studies are required to establish the mechanism giving rise to this dramatic phenotype observed in melanopsin-null mice. We conclude that the causality between ocular disease and metabolic disorders merits further investigation due to the popularity of diets that rely on the induction of a ketogenic state. Our study is a first step toward understanding retinal pathology as a potential cause of metabolic dysfunction. |
format | Online Article Text |
id | pubmed-4444252 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-44442522015-06-16 Lack of Melanopsin Is Associated with Extreme Weight Loss in Mice upon Dietary Challenge Aytürk, Didem Göz Castrucci, Ana Maria Carr, David E. Keller, Susanna R. Provencio, Ignacio PLoS One Research Article Metabolic disorders have been established as major risk factors for ocular complications and poor vision. However, little is known about the inverse possibility that ocular disease may cause metabolic dysfunction. To test this hypothesis, we assessed the metabolic consequences of a robust dietary challenge in several mouse models suffering from retinal mutations. To this end, mice null for melanopsin (Opn4(-/-)), the photopigment of intrinsically photosensitive retinal ganglion cells (ipRGCs), were subjected to five weeks of a ketogenic diet. These mice lost significantly more weight than wild-type controls or mice lacking rod and cone photoreceptors (Pde6b(rd1/rd1)). Although ipRGCs are critical for proper circadian entrainment, and circadian misalignment has been implicated in metabolic pathology, we observed no differences in entrainment between Opn4(-/-) and control mice. Additionally, we observed no differences in any tested metabolic parameter between these mouse strains. Further studies are required to establish the mechanism giving rise to this dramatic phenotype observed in melanopsin-null mice. We conclude that the causality between ocular disease and metabolic disorders merits further investigation due to the popularity of diets that rely on the induction of a ketogenic state. Our study is a first step toward understanding retinal pathology as a potential cause of metabolic dysfunction. Public Library of Science 2015-05-26 /pmc/articles/PMC4444252/ /pubmed/26011287 http://dx.doi.org/10.1371/journal.pone.0127031 Text en © 2015 Aytürk et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Aytürk, Didem Göz Castrucci, Ana Maria Carr, David E. Keller, Susanna R. Provencio, Ignacio Lack of Melanopsin Is Associated with Extreme Weight Loss in Mice upon Dietary Challenge |
title | Lack of Melanopsin Is Associated with Extreme Weight Loss in Mice upon Dietary Challenge |
title_full | Lack of Melanopsin Is Associated with Extreme Weight Loss in Mice upon Dietary Challenge |
title_fullStr | Lack of Melanopsin Is Associated with Extreme Weight Loss in Mice upon Dietary Challenge |
title_full_unstemmed | Lack of Melanopsin Is Associated with Extreme Weight Loss in Mice upon Dietary Challenge |
title_short | Lack of Melanopsin Is Associated with Extreme Weight Loss in Mice upon Dietary Challenge |
title_sort | lack of melanopsin is associated with extreme weight loss in mice upon dietary challenge |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4444252/ https://www.ncbi.nlm.nih.gov/pubmed/26011287 http://dx.doi.org/10.1371/journal.pone.0127031 |
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