| Reduced hepatic bradykinin degradation accounts for cold-induced BAT thermogenesis and WAT browning in male mice |
| 論文作者 |
Xiao, F; Jiang, HZ; Li, Z; Jiang, XX; Chen, SH; Niu, YG; Yin, HR; Shu, YS; Peng, B; Lu, W; Li, XY; Li, ZG; Lan, SJ; Xu, XY; Guo, FF |
| 期刊/會議名稱 |
NATURE COMMUNICATIONS |
| 論文年度 |
2023 |
| 論文類別 |
Article |
| 摘要 |
An important role for liver in the regulation of adipose tissue thermogenesis upon cold exposure has been suggested; however, the underlying mechanisms remain incompletely defined. Here, we identify elevated serum bradykinin levels in response to acute cold exposure in male mice. A bolus of anti-bradykinin antibodies reduces body temperature during acute cold exposure, whereas bradykinin has the opposite effect. We demonstrate that bradykinin induces brown adipose tissue thermogenesis and white adipose tissue browning, and bradykinin increases uncoupling protein 1 (UCP1) expression in adipose tissue. The bradykinin B2 receptor (B2R), adrenergic signaling and nitric oxide signaling are involved in regulating bradykinin-increased UCP1 expression. Moreover, acute cold exposure inhibits hepatic prolyl endopeptidase (PREP) activity, causing reduced liver bradykinin degradation and increased serum bradykinin levels. Finally, by blocking the breakdown of bradykinin, angiotensin-converting enzyme inhibitors (ACEIs) increase serum bradykinin levels and induce brown adipose tissue thermogenesis and white adipose tissue browning via B2R. Collectively, our data provide new insights into the mechanisms underlying organ crosstalk in whole-body physiology control during cold exposure and also suggest bradykinin as a possible anti-obesity target. Adipose tissue thermogenesis plays a role in appropriate response to cold exposure through incompletely understood mechanisms. Here the authors report that acute cold exposure increases the serum levels of bradykinin, which induces brown adipose tissue thermogenesis and white adipose tissue browning in male mice. |
| 期 |
1 |
| 卷 |
14 |
| 影響因子 |
16.6 |
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