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Adipose tissue macrophages: going off track during obesity

Inflammation originating from the adipose tissue is considered to be one of the main driving forces for the development of insulin resistance and type 2 diabetes in obese individuals. Although a plethora of different immune cells shapes adipose tissue inflammation, this review is specifically focuse...

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Detalles Bibliográficos
Autores principales: Boutens, Lily, Stienstra, Rinke
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4826424/
https://www.ncbi.nlm.nih.gov/pubmed/26940592
http://dx.doi.org/10.1007/s00125-016-3904-9
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author Boutens, Lily
Stienstra, Rinke
author_facet Boutens, Lily
Stienstra, Rinke
author_sort Boutens, Lily
collection PubMed
description Inflammation originating from the adipose tissue is considered to be one of the main driving forces for the development of insulin resistance and type 2 diabetes in obese individuals. Although a plethora of different immune cells shapes adipose tissue inflammation, this review is specifically focused on the contribution of macrophages that reside in adipose tissue in lean and obese conditions. Both conventional and tissue-specific functions of adipose tissue macrophages (ATMs) in lean and obese adipose tissue are discussed and linked with metabolic and inflammatory changes that occur during the development of obesity. Furthermore, we will address various circulating and adipose tissue-derived triggers that may be involved in shaping the ATM phenotype and underlie ATM function in lean and obese conditions. Finally, we will highlight how these changes affect adipose tissue inflammation and may be targeted for therapeutic interventions to improve insulin sensitivity in obese individuals.
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spelling pubmed-48264242016-04-20 Adipose tissue macrophages: going off track during obesity Boutens, Lily Stienstra, Rinke Diabetologia Review Inflammation originating from the adipose tissue is considered to be one of the main driving forces for the development of insulin resistance and type 2 diabetes in obese individuals. Although a plethora of different immune cells shapes adipose tissue inflammation, this review is specifically focused on the contribution of macrophages that reside in adipose tissue in lean and obese conditions. Both conventional and tissue-specific functions of adipose tissue macrophages (ATMs) in lean and obese adipose tissue are discussed and linked with metabolic and inflammatory changes that occur during the development of obesity. Furthermore, we will address various circulating and adipose tissue-derived triggers that may be involved in shaping the ATM phenotype and underlie ATM function in lean and obese conditions. Finally, we will highlight how these changes affect adipose tissue inflammation and may be targeted for therapeutic interventions to improve insulin sensitivity in obese individuals. Springer Berlin Heidelberg 2016-03-03 2016 /pmc/articles/PMC4826424/ /pubmed/26940592 http://dx.doi.org/10.1007/s00125-016-3904-9 Text en © The Author(s) 2016 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Review
Boutens, Lily
Stienstra, Rinke
Adipose tissue macrophages: going off track during obesity
title Adipose tissue macrophages: going off track during obesity
title_full Adipose tissue macrophages: going off track during obesity
title_fullStr Adipose tissue macrophages: going off track during obesity
title_full_unstemmed Adipose tissue macrophages: going off track during obesity
title_short Adipose tissue macrophages: going off track during obesity
title_sort adipose tissue macrophages: going off track during obesity
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4826424/
https://www.ncbi.nlm.nih.gov/pubmed/26940592
http://dx.doi.org/10.1007/s00125-016-3904-9
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