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Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure
BACKGROUND: The chemokine receptor CCR7, expressed on various immune cells, is associated with cell migration and lympho-node homing. Mice lacking Ccr7 are protected from diet-induced obesity and subsequent insulin resistance. We evaluated the mechanism underlying these protective effects from the s...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6610939/ https://www.ncbi.nlm.nih.gov/pubmed/31312229 http://dx.doi.org/10.1186/s12986-019-0372-5 |
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author | Sano, Tomomi Sanada, Taiki Sotomaru, Yusuke Shinjo, Takanori Iwashita, Misaki Yamashita, Akiko Fukuda, Takao Sanui, Terukazu Asano, Tomoichiro Kanematsu, Takashi Nishimura, Fusanori |
author_facet | Sano, Tomomi Sanada, Taiki Sotomaru, Yusuke Shinjo, Takanori Iwashita, Misaki Yamashita, Akiko Fukuda, Takao Sanui, Terukazu Asano, Tomoichiro Kanematsu, Takashi Nishimura, Fusanori |
author_sort | Sano, Tomomi |
collection | PubMed |
description | BACKGROUND: The chemokine receptor CCR7, expressed on various immune cells, is associated with cell migration and lympho-node homing. Mice lacking Ccr7 are protected from diet-induced obesity and subsequent insulin resistance. We evaluated the mechanism underlying these protective effects from the standpoint of energy expenditure. METHODS: Wild-type and Ccr7 null mice were fed a high-fat diet, and the regulation of energy metabolism and energy metabolism-related molecules, e.g., Ucp1, Cidea, and Pgc1α, were evaluated. RESULTS: Food intake did not differ between groups. O(2) consumption and CO(2) production were higher in Ccr7 null mice than in wild-type mice, despite a similar respiratory quotient and glucose and lipid utilization, suggesting that energy expenditure increased in Ccr7 null mice via enhanced metabolism. In white adipose tissues of Ccr7 null mice, Prdm16, Cd137, Tmem26, Th, and Tbx1 expression increased. Similarly, in brown adipose tissues of Ccr7 null mice, Dio2, Pgc1α, Cidea, Sirt1, and Adiponectin expression increased. In both white and brown adipose tissues, Ucp1 gene and protein expression levels were higher in null mice than in wild-type mice. CONCLUSIONS: In Ccr7 null mice, browning of white adipocytes as well as the activation of brown adipocytes cause enhanced energy metabolism, resulting in protection against diet-induced obesity. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12986-019-0372-5) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6610939 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-66109392019-07-16 Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure Sano, Tomomi Sanada, Taiki Sotomaru, Yusuke Shinjo, Takanori Iwashita, Misaki Yamashita, Akiko Fukuda, Takao Sanui, Terukazu Asano, Tomoichiro Kanematsu, Takashi Nishimura, Fusanori Nutr Metab (Lond) Research BACKGROUND: The chemokine receptor CCR7, expressed on various immune cells, is associated with cell migration and lympho-node homing. Mice lacking Ccr7 are protected from diet-induced obesity and subsequent insulin resistance. We evaluated the mechanism underlying these protective effects from the standpoint of energy expenditure. METHODS: Wild-type and Ccr7 null mice were fed a high-fat diet, and the regulation of energy metabolism and energy metabolism-related molecules, e.g., Ucp1, Cidea, and Pgc1α, were evaluated. RESULTS: Food intake did not differ between groups. O(2) consumption and CO(2) production were higher in Ccr7 null mice than in wild-type mice, despite a similar respiratory quotient and glucose and lipid utilization, suggesting that energy expenditure increased in Ccr7 null mice via enhanced metabolism. In white adipose tissues of Ccr7 null mice, Prdm16, Cd137, Tmem26, Th, and Tbx1 expression increased. Similarly, in brown adipose tissues of Ccr7 null mice, Dio2, Pgc1α, Cidea, Sirt1, and Adiponectin expression increased. In both white and brown adipose tissues, Ucp1 gene and protein expression levels were higher in null mice than in wild-type mice. CONCLUSIONS: In Ccr7 null mice, browning of white adipocytes as well as the activation of brown adipocytes cause enhanced energy metabolism, resulting in protection against diet-induced obesity. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12986-019-0372-5) contains supplementary material, which is available to authorized users. BioMed Central 2019-07-04 /pmc/articles/PMC6610939/ /pubmed/31312229 http://dx.doi.org/10.1186/s12986-019-0372-5 Text en © The Author(s). 2019 Open AccessThis 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. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Sano, Tomomi Sanada, Taiki Sotomaru, Yusuke Shinjo, Takanori Iwashita, Misaki Yamashita, Akiko Fukuda, Takao Sanui, Terukazu Asano, Tomoichiro Kanematsu, Takashi Nishimura, Fusanori Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure |
title | Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure |
title_full | Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure |
title_fullStr | Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure |
title_full_unstemmed | Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure |
title_short | Ccr7 null mice are protected against diet-induced obesity via Ucp1 upregulation and enhanced energy expenditure |
title_sort | ccr7 null mice are protected against diet-induced obesity via ucp1 upregulation and enhanced energy expenditure |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6610939/ https://www.ncbi.nlm.nih.gov/pubmed/31312229 http://dx.doi.org/10.1186/s12986-019-0372-5 |
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