期刊
NATURE COMMUNICATIONS
卷 8, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-017-00231-1
关键词
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资金
- Ministry of Education, Science, Sports, and Culture, Japan [26461327, 22790853, 22590971]
- Novonordisc Insulin Foundation
- Lilly research grant
- grant for National Center for Global Health and Medicine [26A105]
- Grants-in-Aid for Scientific Research [22790853, 17K08653, 26461327, 22590971, 15K08527, 17H04062, 15H05789, 15H04851, 16K09777] Funding Source: KAKEN
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/TGF beta 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 TGF beta 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.
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