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Glial cells in anorexia

Anorexia is a loss of appetite or an inability to eat and is often associated with eating disorders. However, animal anorexia is physiologically regulated as a part of the life cycle; for instance, during hibernation, migration or incubation. Anorexia nervosa (AN), on the other hand, is a common eat...

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Autor principal: Reyes-Haro, Daniel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9394595/
https://www.ncbi.nlm.nih.gov/pubmed/36003140
http://dx.doi.org/10.3389/fncel.2022.983577
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author Reyes-Haro, Daniel
author_facet Reyes-Haro, Daniel
author_sort Reyes-Haro, Daniel
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description Anorexia is a loss of appetite or an inability to eat and is often associated with eating disorders. However, animal anorexia is physiologically regulated as a part of the life cycle; for instance, during hibernation, migration or incubation. Anorexia nervosa (AN), on the other hand, is a common eating disorder among adolescent females that experience an intense fear of gaining weight due to body image distortion that results in voluntary avoidance of food intake and, thus, severe weight loss. It has been shown that the neurobiology of feeding extends beyond the hypothalamus. The prefrontal cortex (PFC) is involved in food choice and body image perception, both relevant in AN. However, little is known about the neurobiology of AN, and the lack of effective treatments justifies the use of animal models. Glial cells, the dominant population of nerve cells in the central nervous system, are key in maintaining brain homeostasis. Accordingly, recent studies suggest that glial function may be compromised by anorexia. In this review, we summarize recent findings about anorexia and glial cells.
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spelling pubmed-93945952022-08-23 Glial cells in anorexia Reyes-Haro, Daniel Front Cell Neurosci Neuroscience Anorexia is a loss of appetite or an inability to eat and is often associated with eating disorders. However, animal anorexia is physiologically regulated as a part of the life cycle; for instance, during hibernation, migration or incubation. Anorexia nervosa (AN), on the other hand, is a common eating disorder among adolescent females that experience an intense fear of gaining weight due to body image distortion that results in voluntary avoidance of food intake and, thus, severe weight loss. It has been shown that the neurobiology of feeding extends beyond the hypothalamus. The prefrontal cortex (PFC) is involved in food choice and body image perception, both relevant in AN. However, little is known about the neurobiology of AN, and the lack of effective treatments justifies the use of animal models. Glial cells, the dominant population of nerve cells in the central nervous system, are key in maintaining brain homeostasis. Accordingly, recent studies suggest that glial function may be compromised by anorexia. In this review, we summarize recent findings about anorexia and glial cells. Frontiers Media S.A. 2022-08-08 /pmc/articles/PMC9394595/ /pubmed/36003140 http://dx.doi.org/10.3389/fncel.2022.983577 Text en Copyright © 2022 Reyes-Haro. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Reyes-Haro, Daniel
Glial cells in anorexia
title Glial cells in anorexia
title_full Glial cells in anorexia
title_fullStr Glial cells in anorexia
title_full_unstemmed Glial cells in anorexia
title_short Glial cells in anorexia
title_sort glial cells in anorexia
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9394595/
https://www.ncbi.nlm.nih.gov/pubmed/36003140
http://dx.doi.org/10.3389/fncel.2022.983577
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