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Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice
It has been shown that CD1d expression and glycolipid-reactive, CD1d-restricted NKT cells exacerbate the development of obesity and insulin resistance in mice. However, the relevant CD1d-expressing cells that influence the effects of NKT cells on the progression of obesity remain incompletely define...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916414/ https://www.ncbi.nlm.nih.gov/pubmed/27329323 http://dx.doi.org/10.1038/srep28473 |
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author | Satoh, Masashi Hoshino, Miyuki Fujita, Koki Iizuka, Misao Fujii, Satoshi Clingan, Christopher S. Van Kaer, Luc Iwabuchi, Kazuya |
author_facet | Satoh, Masashi Hoshino, Miyuki Fujita, Koki Iizuka, Misao Fujii, Satoshi Clingan, Christopher S. Van Kaer, Luc Iwabuchi, Kazuya |
author_sort | Satoh, Masashi |
collection | PubMed |
description | It has been shown that CD1d expression and glycolipid-reactive, CD1d-restricted NKT cells exacerbate the development of obesity and insulin resistance in mice. However, the relevant CD1d-expressing cells that influence the effects of NKT cells on the progression of obesity remain incompletely defined. In this study, we have demonstrated that 3T3-L1 adipocytes can present endogenous ligands to NKT cells, leading to IFN-γ production, which in turn, stimulated 3T3-L1 adipocytes to enhance expression of CD1d and CCL2, and decrease expression of adiponectin. Furthermore, adipocyte-specific CD1d deletion decreased the size of the visceral adipose tissue mass and enhanced insulin sensitivity in mice fed a high-fat diet (HFD). Accordingly, NKT cells were less activated, IFN-γ production was significantly reduced, and levels of adiponectin were increased in these animals as compared with control mice on HFD. Importantly, macrophage recruitment into the adipose tissue of adipocyte-specific CD1d-deficient mice was significantly blunted. These findings indicate that interactions between NKT cells and CD1d-expressing adipocytes producing endogenous NKT cell ligands play a critical role in the induction of inflammation and functional modulation of adipose tissue that leads to obesity. |
format | Online Article Text |
id | pubmed-4916414 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-49164142016-06-27 Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice Satoh, Masashi Hoshino, Miyuki Fujita, Koki Iizuka, Misao Fujii, Satoshi Clingan, Christopher S. Van Kaer, Luc Iwabuchi, Kazuya Sci Rep Article It has been shown that CD1d expression and glycolipid-reactive, CD1d-restricted NKT cells exacerbate the development of obesity and insulin resistance in mice. However, the relevant CD1d-expressing cells that influence the effects of NKT cells on the progression of obesity remain incompletely defined. In this study, we have demonstrated that 3T3-L1 adipocytes can present endogenous ligands to NKT cells, leading to IFN-γ production, which in turn, stimulated 3T3-L1 adipocytes to enhance expression of CD1d and CCL2, and decrease expression of adiponectin. Furthermore, adipocyte-specific CD1d deletion decreased the size of the visceral adipose tissue mass and enhanced insulin sensitivity in mice fed a high-fat diet (HFD). Accordingly, NKT cells were less activated, IFN-γ production was significantly reduced, and levels of adiponectin were increased in these animals as compared with control mice on HFD. Importantly, macrophage recruitment into the adipose tissue of adipocyte-specific CD1d-deficient mice was significantly blunted. These findings indicate that interactions between NKT cells and CD1d-expressing adipocytes producing endogenous NKT cell ligands play a critical role in the induction of inflammation and functional modulation of adipose tissue that leads to obesity. Nature Publishing Group 2016-06-22 /pmc/articles/PMC4916414/ /pubmed/27329323 http://dx.doi.org/10.1038/srep28473 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Satoh, Masashi Hoshino, Miyuki Fujita, Koki Iizuka, Misao Fujii, Satoshi Clingan, Christopher S. Van Kaer, Luc Iwabuchi, Kazuya Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice |
title | Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice |
title_full | Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice |
title_fullStr | Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice |
title_full_unstemmed | Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice |
title_short | Adipocyte-specific CD1d-deficiency mitigates diet-induced obesity and insulin resistance in mice |
title_sort | adipocyte-specific cd1d-deficiency mitigates diet-induced obesity and insulin resistance in mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916414/ https://www.ncbi.nlm.nih.gov/pubmed/27329323 http://dx.doi.org/10.1038/srep28473 |
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