Cargando…
Negative legacy of obesity
Obesity promotes excessive inflammation, which is associated with senescence-like changes in visceral adipose tissue (VAT) and the development of type 2 diabetes (T2DM) and cardiovascular diseases. We have reported that a unique population of CD44(hi) CD62L(lo) CD4(+) T cells that constitutively exp...
Autores principales: | , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5657997/ https://www.ncbi.nlm.nih.gov/pubmed/29073165 http://dx.doi.org/10.1371/journal.pone.0186303 |
_version_ | 1783273921154383872 |
---|---|
author | Shirakawa, Kohsuke Endo, Jin Katsumata, Yoshinori Yamamoto, Tsunehisa Kataoka, Masaharu Isobe, Sarasa Yoshida, Naohiro Fukuda, Keiichi Sano, Motoaki |
author_facet | Shirakawa, Kohsuke Endo, Jin Katsumata, Yoshinori Yamamoto, Tsunehisa Kataoka, Masaharu Isobe, Sarasa Yoshida, Naohiro Fukuda, Keiichi Sano, Motoaki |
author_sort | Shirakawa, Kohsuke |
collection | PubMed |
description | Obesity promotes excessive inflammation, which is associated with senescence-like changes in visceral adipose tissue (VAT) and the development of type 2 diabetes (T2DM) and cardiovascular diseases. We have reported that a unique population of CD44(hi) CD62L(lo) CD4(+) T cells that constitutively express PD-1 and CD153 exhibit cellular senescence and cause VAT inflammation by producing large amounts of osteopontin. Weight loss improves glycemic control and reduces cardiovascular disease risk factors, but its long-term effects on cardiovascular events and longevity in obese individuals with T2DM are somewhat disappointing and not well understood. High-fat diet (HFD)-fed obese mice were subjected to weight reduction through a switch to a control diet. They lost body weight and visceral fat mass, reaching the same levels as lean mice fed a control diet. However, the VAT of weight reduction mice exhibited denser infiltration of macrophages, which formed more crown-like structures compared to the VAT of obese mice kept on the HFD. Mechanistically, CD153(+) PD-1(+) CD4(+) T cells are long-lived and not easily eliminated, even after weight reduction. Their continued presence maintains a self-sustaining chronic inflammatory loop via production of large amounts of osteopontin. Thus, we concluded that T-cell senescence is essentially a negative legacy effect of obesity. |
format | Online Article Text |
id | pubmed-5657997 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-56579972017-11-09 Negative legacy of obesity Shirakawa, Kohsuke Endo, Jin Katsumata, Yoshinori Yamamoto, Tsunehisa Kataoka, Masaharu Isobe, Sarasa Yoshida, Naohiro Fukuda, Keiichi Sano, Motoaki PLoS One Research Article Obesity promotes excessive inflammation, which is associated with senescence-like changes in visceral adipose tissue (VAT) and the development of type 2 diabetes (T2DM) and cardiovascular diseases. We have reported that a unique population of CD44(hi) CD62L(lo) CD4(+) T cells that constitutively express PD-1 and CD153 exhibit cellular senescence and cause VAT inflammation by producing large amounts of osteopontin. Weight loss improves glycemic control and reduces cardiovascular disease risk factors, but its long-term effects on cardiovascular events and longevity in obese individuals with T2DM are somewhat disappointing and not well understood. High-fat diet (HFD)-fed obese mice were subjected to weight reduction through a switch to a control diet. They lost body weight and visceral fat mass, reaching the same levels as lean mice fed a control diet. However, the VAT of weight reduction mice exhibited denser infiltration of macrophages, which formed more crown-like structures compared to the VAT of obese mice kept on the HFD. Mechanistically, CD153(+) PD-1(+) CD4(+) T cells are long-lived and not easily eliminated, even after weight reduction. Their continued presence maintains a self-sustaining chronic inflammatory loop via production of large amounts of osteopontin. Thus, we concluded that T-cell senescence is essentially a negative legacy effect of obesity. Public Library of Science 2017-10-26 /pmc/articles/PMC5657997/ /pubmed/29073165 http://dx.doi.org/10.1371/journal.pone.0186303 Text en © 2017 Shirakawa et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Shirakawa, Kohsuke Endo, Jin Katsumata, Yoshinori Yamamoto, Tsunehisa Kataoka, Masaharu Isobe, Sarasa Yoshida, Naohiro Fukuda, Keiichi Sano, Motoaki Negative legacy of obesity |
title | Negative legacy of obesity |
title_full | Negative legacy of obesity |
title_fullStr | Negative legacy of obesity |
title_full_unstemmed | Negative legacy of obesity |
title_short | Negative legacy of obesity |
title_sort | negative legacy of obesity |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5657997/ https://www.ncbi.nlm.nih.gov/pubmed/29073165 http://dx.doi.org/10.1371/journal.pone.0186303 |
work_keys_str_mv | AT shirakawakohsuke negativelegacyofobesity AT endojin negativelegacyofobesity AT katsumatayoshinori negativelegacyofobesity AT yamamototsunehisa negativelegacyofobesity AT kataokamasaharu negativelegacyofobesity AT isobesarasa negativelegacyofobesity AT yoshidanaohiro negativelegacyofobesity AT fukudakeiichi negativelegacyofobesity AT sanomotoaki negativelegacyofobesity |