Reduced hepatic bradykinin degradation accounts for cold-induced BAT thermogenesis and WAT browning in male mice

Fei Xiao, Haizhou Jiang, Zi Li, Xiaoxue Jiang, Shanghai Chen, Yuguo Niu, Hanrui Yin, Yousheng Shu, Bo Peng, Wei Lu, Xiaoying Li, Zhigang Li, Shujue Lan, Xiaoyan Xu and Feifan Guo ()
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Fei Xiao: MOE Frontiers Center for Brain Science, Fudan University
Haizhou Jiang: University of Chinese Academy of Sciences, Chinese Academy of Sciences
Zi Li: University of Chinese Academy of Sciences, Chinese Academy of Sciences
Xiaoxue Jiang: MOE Frontiers Center for Brain Science, Fudan University
Shanghai Chen: MOE Frontiers Center for Brain Science, Fudan University
Yuguo Niu: MOE Frontiers Center for Brain Science, Fudan University
Hanrui Yin: University of Chinese Academy of Sciences, Chinese Academy of Sciences
Yousheng Shu: MOE Frontiers Center for Brain Science, Fudan University
Bo Peng: MOE Frontiers Center for Brain Science, Fudan University
Wei Lu: MOE Frontiers Center for Brain Science, Fudan University
Xiaoying Li: MOE Frontiers Center for Brain Science, Fudan University
Zhigang Li: University of Chinese Academy of Sciences, Chinese Academy of Sciences
Shujue Lan: Chinese Academy of Sciences
Xiaoyan Xu: Chinese Academy of Sciences
Feifan Guo: MOE Frontiers Center for Brain Science, Fudan University

Nature Communications, 2023, vol. 14, issue 1, 1-17

Abstract: Abstract 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.

Date: 2023
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DOI: 10.1038/s41467-023-38141-0

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