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Autophagy Dysregulation and Obesity-Associated Pathologies

Autophagy is one of the major degradative mechanisms that can eliminate excessive nutrients, toxic protein aggregates, damaged organelles and invading microorganisms. In response to obesity and obesity-associated lipotoxic, proteotoxic and oxidative stresses, autophagy plays an essential role in mai...

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Detalles Bibliográficos
Autores principales: Namkoong, Sim, Cho, Chun-Seok, Semple, Ian, Lee, Jun Hee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Society for Molecular and Cellular Biology 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5792710/
https://www.ncbi.nlm.nih.gov/pubmed/29370691
http://dx.doi.org/10.14348/molcells.2018.2213
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author Namkoong, Sim
Cho, Chun-Seok
Semple, Ian
Lee, Jun Hee
author_facet Namkoong, Sim
Cho, Chun-Seok
Semple, Ian
Lee, Jun Hee
author_sort Namkoong, Sim
collection PubMed
description Autophagy is one of the major degradative mechanisms that can eliminate excessive nutrients, toxic protein aggregates, damaged organelles and invading microorganisms. In response to obesity and obesity-associated lipotoxic, proteotoxic and oxidative stresses, autophagy plays an essential role in maintaining physiological homeostasis. However, obesity and its associated stress insults can often interfere with the autophagic process through various mechanisms, which result in further aggravation of obesity-related metabolic pathologies in multiple metabolic organs. Paradoxically, inhibition of autophagy, within specific contexts, indirectly produces beneficial effects that can alleviate several detrimental consequences of obesity. In this minireview, we will provide a brief discussion about our current understanding of the impact of obesity on autophagy and the role of autophagy dysregulation in modulating obesity-associated pathological outcomes.
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spelling pubmed-57927102018-02-14 Autophagy Dysregulation and Obesity-Associated Pathologies Namkoong, Sim Cho, Chun-Seok Semple, Ian Lee, Jun Hee Mol Cells Minireview Autophagy is one of the major degradative mechanisms that can eliminate excessive nutrients, toxic protein aggregates, damaged organelles and invading microorganisms. In response to obesity and obesity-associated lipotoxic, proteotoxic and oxidative stresses, autophagy plays an essential role in maintaining physiological homeostasis. However, obesity and its associated stress insults can often interfere with the autophagic process through various mechanisms, which result in further aggravation of obesity-related metabolic pathologies in multiple metabolic organs. Paradoxically, inhibition of autophagy, within specific contexts, indirectly produces beneficial effects that can alleviate several detrimental consequences of obesity. In this minireview, we will provide a brief discussion about our current understanding of the impact of obesity on autophagy and the role of autophagy dysregulation in modulating obesity-associated pathological outcomes. Korean Society for Molecular and Cellular Biology 2018-01-31 2018-01-23 /pmc/articles/PMC5792710/ /pubmed/29370691 http://dx.doi.org/10.14348/molcells.2018.2213 Text en © The Korean Society for Molecular and Cellular Biology. All rights reserved. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/.
spellingShingle Minireview
Namkoong, Sim
Cho, Chun-Seok
Semple, Ian
Lee, Jun Hee
Autophagy Dysregulation and Obesity-Associated Pathologies
title Autophagy Dysregulation and Obesity-Associated Pathologies
title_full Autophagy Dysregulation and Obesity-Associated Pathologies
title_fullStr Autophagy Dysregulation and Obesity-Associated Pathologies
title_full_unstemmed Autophagy Dysregulation and Obesity-Associated Pathologies
title_short Autophagy Dysregulation and Obesity-Associated Pathologies
title_sort autophagy dysregulation and obesity-associated pathologies
topic Minireview
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5792710/
https://www.ncbi.nlm.nih.gov/pubmed/29370691
http://dx.doi.org/10.14348/molcells.2018.2213
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