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Transcriptional coordination of hepatic autophagy by nutrient-sensing nuclear receptor PPARα and FXR

Nuclear receptors are in general ligand-dependent transcription factors that control a variety of mammalian physiologies including development, differentiation, proliferation, and homeostasis. Recent studies have found that two nutrient-sensing nuclear receptors, peroxisome proliferator-activated re...

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Autor principal: Lee, Jae Man
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Pediatric Endocrinology 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290173/
https://www.ncbi.nlm.nih.gov/pubmed/28164071
http://dx.doi.org/10.6065/apem.2016.21.4.193
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author Lee, Jae Man
author_facet Lee, Jae Man
author_sort Lee, Jae Man
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description Nuclear receptors are in general ligand-dependent transcription factors that control a variety of mammalian physiologies including development, differentiation, proliferation, and homeostasis. Recent studies have found that two nutrient-sensing nuclear receptors, peroxisome proliferator-activated receptor α and farnesoid x receptor, responding to fasting or feeding state, respectively are able to regulate autophagy, an evolutionarily conserved catabolic process involved in lysosomal degradation. In this review, we discuss the role of these nutrient-sensing nuclear receptors in an aspect of transcriptional regulation of autophagy, and how these nuclear receptor-driven transcriptional programs integrate lipophagy, a lipid autophagy with fatty acid oxidation to coordinate hepatic lipid metabolism in the fasted state of the liver.
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spelling pubmed-52901732017-02-03 Transcriptional coordination of hepatic autophagy by nutrient-sensing nuclear receptor PPARα and FXR Lee, Jae Man Ann Pediatr Endocrinol Metab Review Article Nuclear receptors are in general ligand-dependent transcription factors that control a variety of mammalian physiologies including development, differentiation, proliferation, and homeostasis. Recent studies have found that two nutrient-sensing nuclear receptors, peroxisome proliferator-activated receptor α and farnesoid x receptor, responding to fasting or feeding state, respectively are able to regulate autophagy, an evolutionarily conserved catabolic process involved in lysosomal degradation. In this review, we discuss the role of these nutrient-sensing nuclear receptors in an aspect of transcriptional regulation of autophagy, and how these nuclear receptor-driven transcriptional programs integrate lipophagy, a lipid autophagy with fatty acid oxidation to coordinate hepatic lipid metabolism in the fasted state of the liver. The Korean Society of Pediatric Endocrinology 2016-12 2016-12-31 /pmc/articles/PMC5290173/ /pubmed/28164071 http://dx.doi.org/10.6065/apem.2016.21.4.193 Text en © 2016 Annals of Pediatric Endocrinology & Metabolism http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Lee, Jae Man
Transcriptional coordination of hepatic autophagy by nutrient-sensing nuclear receptor PPARα and FXR
title Transcriptional coordination of hepatic autophagy by nutrient-sensing nuclear receptor PPARα and FXR
title_full Transcriptional coordination of hepatic autophagy by nutrient-sensing nuclear receptor PPARα and FXR
title_fullStr Transcriptional coordination of hepatic autophagy by nutrient-sensing nuclear receptor PPARα and FXR
title_full_unstemmed Transcriptional coordination of hepatic autophagy by nutrient-sensing nuclear receptor PPARα and FXR
title_short Transcriptional coordination of hepatic autophagy by nutrient-sensing nuclear receptor PPARα and FXR
title_sort transcriptional coordination of hepatic autophagy by nutrient-sensing nuclear receptor pparα and fxr
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290173/
https://www.ncbi.nlm.nih.gov/pubmed/28164071
http://dx.doi.org/10.6065/apem.2016.21.4.193
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