CD206+ M2-like macrophages regulate systemic glucose metabolism by inhibiting proliferation of adipocyte progenitors

• Nawaz, Allah

• Aminuddin, Aminuddin

• Kado, Tomonobu

• Takikawa, Akiko

• Yamamoto, Seiji

• Tsuneyama, Koichi

• Igarashi, Yoshiko

• Ikutani, Masashi

• Nishida, Yasuhiro

• Nagai, Yoshinori

• Takatsu, Kiyoshi

• Imura, Johji

• Sasahara, Masakiyo

• Okazaki, Yukiko

• Ueki, Kohjiro

• Okamura, Tadashi

• Tokuyama, Kumpei

• Ando, Akira

• Matsumoto, Michihiro

• Mori, Hisashi

• Nakagawa, Takashi

• Kobayashi, Norihiko

• Saeki, Kumiko

• Usui, Isao

• Fujisaka, Shiho

• Tobe, Kazuyuki

Abstract

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

• Nature Communications

  Nature Communications 8 286-, 2017-08-18

  Springer Nature

Keywords

• General Physics and Astronomy
• General Biochemistry, Genetics and Molecular Biology
• General Chemistry
• Multidisciplinary

Details

• CRID: 1050001337802858496
• NII Article ID: 120006535075
• NII Book ID: AA12645905
• ISSN: 20411723
• DOI: 10.1038/s41467-017-00231-1
• Web Site: http://repo.lib.tokushima-u.ac.jp/112461
• Web Site: https://www.nature.com/articles/s41467-017-00231-1
• Web Site: https://www.nature.com/articles/s41467-017-00231-1.pdf
• Text Lang: en
• Article Type: journal article
• Data Source:
  • IRDB
  • Crossref
  • CiNii Articles
  • KAKEN