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Wnt inhibition enhances browning of mouse primary white adipocytes

The global epidemic in obesity and metabolic syndrome requires novel approaches to tackle. White adipose tissue, traditionally seen as a passive energy-storage organ, can be induced to take on certain characteristics of brown fat in a process called browning. The “browned” white adipose tissue, or b...

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Autores principales: Lo, Kinyui Alice, Ng, Pei Yi, Kabiri, Zahra, Virshup, David, Sun, Lei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916886/
https://www.ncbi.nlm.nih.gov/pubmed/27386162
http://dx.doi.org/10.1080/21623945.2016.1148834
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author Lo, Kinyui Alice
Ng, Pei Yi
Kabiri, Zahra
Virshup, David
Sun, Lei
author_facet Lo, Kinyui Alice
Ng, Pei Yi
Kabiri, Zahra
Virshup, David
Sun, Lei
author_sort Lo, Kinyui Alice
collection PubMed
description The global epidemic in obesity and metabolic syndrome requires novel approaches to tackle. White adipose tissue, traditionally seen as a passive energy-storage organ, can be induced to take on certain characteristics of brown fat in a process called browning. The “browned” white adipose tissue, or beige fat, is a potential anti-obesity target. Various signaling pathways can enhance browning. Wnt is a key regulator of adipocyte biology, but its role in browning has not been explored. In this study, we found that in primary mouse adipocytes derived from the inguinal depot, Wnt inhibition by both chemical and genetic methods significantly enhanced browning. The effect of Wnt inhibition on browning most likely targets the beige precursor cells in selected adipose depots.
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spelling pubmed-49168862016-07-06 Wnt inhibition enhances browning of mouse primary white adipocytes Lo, Kinyui Alice Ng, Pei Yi Kabiri, Zahra Virshup, David Sun, Lei Adipocyte Brief Report The global epidemic in obesity and metabolic syndrome requires novel approaches to tackle. White adipose tissue, traditionally seen as a passive energy-storage organ, can be induced to take on certain characteristics of brown fat in a process called browning. The “browned” white adipose tissue, or beige fat, is a potential anti-obesity target. Various signaling pathways can enhance browning. Wnt is a key regulator of adipocyte biology, but its role in browning has not been explored. In this study, we found that in primary mouse adipocytes derived from the inguinal depot, Wnt inhibition by both chemical and genetic methods significantly enhanced browning. The effect of Wnt inhibition on browning most likely targets the beige precursor cells in selected adipose depots. Taylor & Francis 2016-03-22 /pmc/articles/PMC4916886/ /pubmed/27386162 http://dx.doi.org/10.1080/21623945.2016.1148834 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 Brief Report
Lo, Kinyui Alice
Ng, Pei Yi
Kabiri, Zahra
Virshup, David
Sun, Lei
Wnt inhibition enhances browning of mouse primary white adipocytes
title Wnt inhibition enhances browning of mouse primary white adipocytes
title_full Wnt inhibition enhances browning of mouse primary white adipocytes
title_fullStr Wnt inhibition enhances browning of mouse primary white adipocytes
title_full_unstemmed Wnt inhibition enhances browning of mouse primary white adipocytes
title_short Wnt inhibition enhances browning of mouse primary white adipocytes
title_sort wnt inhibition enhances browning of mouse primary white adipocytes
topic Brief Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916886/
https://www.ncbi.nlm.nih.gov/pubmed/27386162
http://dx.doi.org/10.1080/21623945.2016.1148834
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