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Potential Roles of O-GlcNAcylation in Primary Cilia- Mediated Energy Metabolism

The primary cilium, an antenna-like structure on most eukaryotic cells, functions in transducing extracellular signals into intracellular responses via the receptors and ion channels distributed along it membrane. Dysfunction of this organelle causes an array of human diseases, known as ciliopathies...

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Autores principales: Tian, Jie L., Gomeshtapeh, Farzad Islami
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7693894/
https://www.ncbi.nlm.nih.gov/pubmed/33139642
http://dx.doi.org/10.3390/biom10111504
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author Tian, Jie L.
Gomeshtapeh, Farzad Islami
author_facet Tian, Jie L.
Gomeshtapeh, Farzad Islami
author_sort Tian, Jie L.
collection PubMed
description The primary cilium, an antenna-like structure on most eukaryotic cells, functions in transducing extracellular signals into intracellular responses via the receptors and ion channels distributed along it membrane. Dysfunction of this organelle causes an array of human diseases, known as ciliopathies, that often feature obesity and diabetes; this indicates the primary cilia’s active role in energy metabolism, which it controls mainly through hypothalamic neurons, preadipocytes, and pancreatic β-cells. The nutrient sensor, O-GlcNAc, is widely involved in the regulation of energy homeostasis. Not only does O-GlcNAc regulate ciliary length, but it also modifies many components of cilia-mediated metabolic signaling pathways. Therefore, it is likely that O-GlcNAcylation (OGN) plays an important role in regulating energy homeostasis in primary cilia. Abnormal OGN, as seen in cases of obesity and diabetes, may play an important role in primary cilia dysfunction mediated by these pathologies.
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spelling pubmed-76938942020-11-28 Potential Roles of O-GlcNAcylation in Primary Cilia- Mediated Energy Metabolism Tian, Jie L. Gomeshtapeh, Farzad Islami Biomolecules Review The primary cilium, an antenna-like structure on most eukaryotic cells, functions in transducing extracellular signals into intracellular responses via the receptors and ion channels distributed along it membrane. Dysfunction of this organelle causes an array of human diseases, known as ciliopathies, that often feature obesity and diabetes; this indicates the primary cilia’s active role in energy metabolism, which it controls mainly through hypothalamic neurons, preadipocytes, and pancreatic β-cells. The nutrient sensor, O-GlcNAc, is widely involved in the regulation of energy homeostasis. Not only does O-GlcNAc regulate ciliary length, but it also modifies many components of cilia-mediated metabolic signaling pathways. Therefore, it is likely that O-GlcNAcylation (OGN) plays an important role in regulating energy homeostasis in primary cilia. Abnormal OGN, as seen in cases of obesity and diabetes, may play an important role in primary cilia dysfunction mediated by these pathologies. MDPI 2020-11-01 /pmc/articles/PMC7693894/ /pubmed/33139642 http://dx.doi.org/10.3390/biom10111504 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Tian, Jie L.
Gomeshtapeh, Farzad Islami
Potential Roles of O-GlcNAcylation in Primary Cilia- Mediated Energy Metabolism
title Potential Roles of O-GlcNAcylation in Primary Cilia- Mediated Energy Metabolism
title_full Potential Roles of O-GlcNAcylation in Primary Cilia- Mediated Energy Metabolism
title_fullStr Potential Roles of O-GlcNAcylation in Primary Cilia- Mediated Energy Metabolism
title_full_unstemmed Potential Roles of O-GlcNAcylation in Primary Cilia- Mediated Energy Metabolism
title_short Potential Roles of O-GlcNAcylation in Primary Cilia- Mediated Energy Metabolism
title_sort potential roles of o-glcnacylation in primary cilia- mediated energy metabolism
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7693894/
https://www.ncbi.nlm.nih.gov/pubmed/33139642
http://dx.doi.org/10.3390/biom10111504
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