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What induces watts in WAT?

Excess calories stored in white adipose tissue (WAT) could be reduced either through the activation of brown adipose tissue (BAT) or the development of brown-like cells (“beige” or “brite”) in WAT, a process named “browning.” Calorie dissipation in brown and beige adipocytes might rely on the induct...

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Autores principales: Forest, Claude, Joffin, Nolwenn, Jaubert, Anne-Marie, Noirez, Philippe
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916896/
https://www.ncbi.nlm.nih.gov/pubmed/27386158
http://dx.doi.org/10.1080/21623945.2016.1187345
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author Forest, Claude
Joffin, Nolwenn
Jaubert, Anne-Marie
Noirez, Philippe
author_facet Forest, Claude
Joffin, Nolwenn
Jaubert, Anne-Marie
Noirez, Philippe
author_sort Forest, Claude
collection PubMed
description Excess calories stored in white adipose tissue (WAT) could be reduced either through the activation of brown adipose tissue (BAT) or the development of brown-like cells (“beige” or “brite”) in WAT, a process named “browning.” Calorie dissipation in brown and beige adipocytes might rely on the induction of uncoupling protein 1 (UCP1), which is absent in white fat cells. Any increase in UCP1 is commonly considered as the trademark of energy expenditure. The intracellular events involved in the recruitment process of beige precursors were extensively studied lately, as were the effectors, hormones, cytokines, nutrients and drugs able to modulate the route of browning and theoretically affect fat mass in rodents and in humans. The aim of this review is to update the characterization of the extracellular effectors that induce UCP1 in WAT and potentially provoke calorie dissipation. The potential influence of metabolic cycling in energy expenditure is also questioned.
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spelling pubmed-49168962016-07-06 What induces watts in WAT? Forest, Claude Joffin, Nolwenn Jaubert, Anne-Marie Noirez, Philippe Adipocyte Review Excess calories stored in white adipose tissue (WAT) could be reduced either through the activation of brown adipose tissue (BAT) or the development of brown-like cells (“beige” or “brite”) in WAT, a process named “browning.” Calorie dissipation in brown and beige adipocytes might rely on the induction of uncoupling protein 1 (UCP1), which is absent in white fat cells. Any increase in UCP1 is commonly considered as the trademark of energy expenditure. The intracellular events involved in the recruitment process of beige precursors were extensively studied lately, as were the effectors, hormones, cytokines, nutrients and drugs able to modulate the route of browning and theoretically affect fat mass in rodents and in humans. The aim of this review is to update the characterization of the extracellular effectors that induce UCP1 in WAT and potentially provoke calorie dissipation. The potential influence of metabolic cycling in energy expenditure is also questioned. Taylor & Francis 2016-05-21 /pmc/articles/PMC4916896/ /pubmed/27386158 http://dx.doi.org/10.1080/21623945.2016.1187345 Text en © 2016 The Author(s). Published with license by Taylor & Francis Group, LLC http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.
spellingShingle Review
Forest, Claude
Joffin, Nolwenn
Jaubert, Anne-Marie
Noirez, Philippe
What induces watts in WAT?
title What induces watts in WAT?
title_full What induces watts in WAT?
title_fullStr What induces watts in WAT?
title_full_unstemmed What induces watts in WAT?
title_short What induces watts in WAT?
title_sort what induces watts in wat?
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916896/
https://www.ncbi.nlm.nih.gov/pubmed/27386158
http://dx.doi.org/10.1080/21623945.2016.1187345
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