ID 112461
Author
Nawaz, Allah University of Toyama
Aminuddin, Aminuddin University of Toyama|University of Hasanuddin
Kado, Tomonobu University of Toyama
Takikawa, Akiko University of Toyama
Yamamoto, Seiji University of Toyama
Igarashi, Yoshiko University of Toyama
Ikutani, Masashi National Center for Global Health and Medicine
Nishida, Yasuhiro University of Toyama
Nagai, Yoshinori University of Toyama|JST
Takatsu, Kiyoshi University of Toyama|Toyama Prefectural Institute for Pharmaceutical Research
Imura, Johji University of Toyama
Sasahara, Masakiyo University of Toyama
Okazaki, Yukiko The University of Tokyo
Ueki, Kohjiro The University of Tokyo|National Center for Global Health and Medicine
Okamura, Tadashi National Center for Global Health and Medicine
Tokuyama, Kumpei University of Tsukuba
Ando, Akira University of Tsukuba
Matsumoto, Michihiro National Center for Global Health and Medicine
Mori, Hisashi University of Toyama
Nakagawa, Takashi University of Toyama
Kobayashi, Norihiko National Center for Global Health and Medicine
Saeki, Kumiko National Center for Global Health and Medicine
Usui, Isao University of Toyama
Fujisaka, Shiho University of Toyama
Tobe, Kazuyuki University of Toyama
Content Type
Journal Article
Description
Adipose tissue resident macrophages have important roles in the maintenance of tissue homeostasis and regulate insulin sensitivity for example by secreting pro-inflammatory or anti-inflammatory cytokines. Here, we show that M2-like macrophages in adipose tissue regulate systemic glucose homeostasis by inhibiting adipocyte progenitor proliferation via the CD206/TGFβ signaling pathway. We show that adipose tissue CD206+ cells are primarily M2-like macrophages, and ablation of CD206+ M2-like macrophages improves systemic insulin sensitivity, which was associated with an increased number of smaller adipocytes. Mice genetically engineered to have reduced numbers of CD206+ M2-like macrophages show a down-regulation of TGFβ signaling in adipose tissue, together with up-regulated proliferation and differentiation of adipocyte progenitors. Our findings indicate that CD206+ M2-like macrophages in adipose tissues create a microenvironment that inhibits growth and differentiation of adipocyte progenitors and, thereby, control adiposity and systemic insulin sensitivity.
Journal Title
Nature Communications
ISSN
20411723
NCID
AA12645905
Publisher
Springer Nature
Volume
8
Start Page
286
Published Date
2017-08-18
Remark
Peer Review File : ncomms_8_286_s1.pdf
Supplementary Information : ncomms_8_286_s2.pdf
Rights
This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Medical Sciences