期刊
SCIENTIFIC REPORTS
卷 8, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-018-32803-6
关键词
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资金
- Ministry of Education, Science, Sports, and Culture, Japan [26461327, 17K09821]
- Japan Diabetes Foundation
- Bristol-Myers Squibb Research grant
- Kobayashi International Foundation
- Japan Agency for Medical Research and Development, AMED
- [18F18102]
- Grants-in-Aid for Scientific Research [26461327, 17K09821] Funding Source: KAKEN
Beige adipocytes are an inducible form of thermogenic adipocytes that become interspersed within white adipose tissue (WAT) depots in response to cold exposure. Previous studies have shown that type 2 cytokines and M2 macrophages induce cold-induced browning in inguinal WAT (ingWAT) by producing catecholamines. Exactly how the conditional and partial depletion of CD206(+) M2-like macrophages regulates the cold-induced browning of ingWAT, however, remains unknown. We examined the role of CD206(+) M2-like macrophages in the cold-induced browning of WAT using genetically engineered CD206DTR mice, in which CD206(+) M2-like macrophages were conditionally depleted. The partial depletion of CD206(+) M2-like enhanced UCP1 expression in ingWAT, as shown by immunostaining, and also upregulated the expression of Ucp1 and other browning-related marker genes in ingWAT after cold exposure. A flow cytometry analysis showed that the partial depletion of CD206(+) M2-like macrophages caused an increase in the number of beige progenitors in ingWAT in response to cold. Thus, we concluded that CD206(+) M2-like macrophages inhibit the proliferation of beige progenitors and that the partial depletion of CD206(+) M2-like macrophages releases this inhibition, thereby enhancing browning and insulin sensitivity.
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