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Neuronal primary cilia integrate peripheral signals with metabolic drives

Neuronal primary cilia have recently emerged as important contributors to the central regulation of energy homeostasis. As non-motile, microtubule-based organelles, primary cilia serve as signaling antennae for metabolic status. The impairment of ciliary structure or function can produce ciliopathie...

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Autores principales: DeMars, Kelly M., Ross, Madeleine R., Starr, Alana, McIntyre, Jeremy C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10090425/
https://www.ncbi.nlm.nih.gov/pubmed/37064917
http://dx.doi.org/10.3389/fphys.2023.1150232
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author DeMars, Kelly M.
Ross, Madeleine R.
Starr, Alana
McIntyre, Jeremy C.
author_facet DeMars, Kelly M.
Ross, Madeleine R.
Starr, Alana
McIntyre, Jeremy C.
author_sort DeMars, Kelly M.
collection PubMed
description Neuronal primary cilia have recently emerged as important contributors to the central regulation of energy homeostasis. As non-motile, microtubule-based organelles, primary cilia serve as signaling antennae for metabolic status. The impairment of ciliary structure or function can produce ciliopathies for which obesity is a hallmark phenotype and global ablation of cilia induces non-syndromic adiposity in mouse models. This organelle is not only a hub for metabolic signaling, but also for catecholamine neuromodulation that shapes neuronal circuitry in response to sensory input. The objective of this review is to highlight current research investigating the mechanisms of primary cilium-regulated metabolic drives for maintaining energy homeostasis.
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spelling pubmed-100904252023-04-13 Neuronal primary cilia integrate peripheral signals with metabolic drives DeMars, Kelly M. Ross, Madeleine R. Starr, Alana McIntyre, Jeremy C. Front Physiol Physiology Neuronal primary cilia have recently emerged as important contributors to the central regulation of energy homeostasis. As non-motile, microtubule-based organelles, primary cilia serve as signaling antennae for metabolic status. The impairment of ciliary structure or function can produce ciliopathies for which obesity is a hallmark phenotype and global ablation of cilia induces non-syndromic adiposity in mouse models. This organelle is not only a hub for metabolic signaling, but also for catecholamine neuromodulation that shapes neuronal circuitry in response to sensory input. The objective of this review is to highlight current research investigating the mechanisms of primary cilium-regulated metabolic drives for maintaining energy homeostasis. Frontiers Media S.A. 2023-03-29 /pmc/articles/PMC10090425/ /pubmed/37064917 http://dx.doi.org/10.3389/fphys.2023.1150232 Text en Copyright © 2023 DeMars, Ross, Starr and McIntyre. 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 Physiology
DeMars, Kelly M.
Ross, Madeleine R.
Starr, Alana
McIntyre, Jeremy C.
Neuronal primary cilia integrate peripheral signals with metabolic drives
title Neuronal primary cilia integrate peripheral signals with metabolic drives
title_full Neuronal primary cilia integrate peripheral signals with metabolic drives
title_fullStr Neuronal primary cilia integrate peripheral signals with metabolic drives
title_full_unstemmed Neuronal primary cilia integrate peripheral signals with metabolic drives
title_short Neuronal primary cilia integrate peripheral signals with metabolic drives
title_sort neuronal primary cilia integrate peripheral signals with metabolic drives
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10090425/
https://www.ncbi.nlm.nih.gov/pubmed/37064917
http://dx.doi.org/10.3389/fphys.2023.1150232
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