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Hypothalamic lipophagy and energetic balance

Autophagy is a conserved cellular turnover process that degrades unwanted cytoplasmic material within lysosomes. Through “in bulk” degradation of cytoplasmic proteins and organelles, including lipid droplets, autophagy helps provide an alternative fuel source, in particular, when nutrients are scarc...

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Autor principal: Singh, Rajat
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229970/
https://www.ncbi.nlm.nih.gov/pubmed/22024462
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author Singh, Rajat
author_facet Singh, Rajat
author_sort Singh, Rajat
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description Autophagy is a conserved cellular turnover process that degrades unwanted cytoplasmic material within lysosomes. Through “in bulk” degradation of cytoplasmic proteins and organelles, including lipid droplets, autophagy helps provide an alternative fuel source, in particular, when nutrients are scarce. Recent work demonstrates a role for autophagy in hypothalamic agouti-related peptide (AgRP) neurons in regulation of food intake and energy balance. The induction of autophagy in hypothalamic neurons during starvation mobilizes neuronal neutral lipids to generate neuron-intrinsic free fatty acids that serve to upregulate fasting-induced AgRP levels. Blocking autophagy in AgRP neurons in mice reduces fasting-induced food intake, and increases constitutive levels of anorexigenic hypothalamic proopiomelanocortin and its cleavage product α-melanocyte stimulating hormone. The energetic consequences of these molecular events are decreased body weight and reduced adiposity. The present article discusses this recent finding, as well as considers possible future directions that may help better understand how neuronal autophagy, and its possible reduction during aging, may affect whole body energy balance.
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spelling pubmed-32299702011-12-05 Hypothalamic lipophagy and energetic balance Singh, Rajat Aging (Albany NY) Research Perspective Autophagy is a conserved cellular turnover process that degrades unwanted cytoplasmic material within lysosomes. Through “in bulk” degradation of cytoplasmic proteins and organelles, including lipid droplets, autophagy helps provide an alternative fuel source, in particular, when nutrients are scarce. Recent work demonstrates a role for autophagy in hypothalamic agouti-related peptide (AgRP) neurons in regulation of food intake and energy balance. The induction of autophagy in hypothalamic neurons during starvation mobilizes neuronal neutral lipids to generate neuron-intrinsic free fatty acids that serve to upregulate fasting-induced AgRP levels. Blocking autophagy in AgRP neurons in mice reduces fasting-induced food intake, and increases constitutive levels of anorexigenic hypothalamic proopiomelanocortin and its cleavage product α-melanocyte stimulating hormone. The energetic consequences of these molecular events are decreased body weight and reduced adiposity. The present article discusses this recent finding, as well as considers possible future directions that may help better understand how neuronal autophagy, and its possible reduction during aging, may affect whole body energy balance. Impact Journals LLC 2011-10-23 /pmc/articles/PMC3229970/ /pubmed/22024462 Text en Copyright: © 2011 Singh http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
spellingShingle Research Perspective
Singh, Rajat
Hypothalamic lipophagy and energetic balance
title Hypothalamic lipophagy and energetic balance
title_full Hypothalamic lipophagy and energetic balance
title_fullStr Hypothalamic lipophagy and energetic balance
title_full_unstemmed Hypothalamic lipophagy and energetic balance
title_short Hypothalamic lipophagy and energetic balance
title_sort hypothalamic lipophagy and energetic balance
topic Research Perspective
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229970/
https://www.ncbi.nlm.nih.gov/pubmed/22024462
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