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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2021.8
- 수록면
- 419 - 424 (6page)
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Cold-induced norepinephrine activates β3-adrenergic receptors(β3-AR) to stimulate the kinase cascade and cAMP-responseelement-binding protein, leading to the induction of thermogenicgene expression including uncoupling protein 1 (Ucp1). Here,we showed that stimulation of the β3-AR by its agonists isoproterenoland CL316,243 in adipocytes increased the expressionof Ucp1 and Heme Oxygenase 1 (Hmox1), the principal Nrf2target gene, suggesting the functional interaction of Nrf2 withβ3-AR signaling. The activation of Nrf2 by tert-butylhydroquinoneand reactive oxygen species (ROS) production by glucoseoxidase induced both Ucp1 and Hmox1 expression. The increasedexpression of Ucp1 and Hmox1 was significantly reduced inthe presence of a Nrf2 chemical inhibitor or in Nrf2-deleted(knockout) adipocytes. Furthermore, Nrf2 directly activated theUcp1 promoter, and this required DNA regions located at ?3.7 and ?2.0 kb of the transcription start site. The CL316,243-induced Ucp1 expression in adipocytes and oxygen consumptionin obese mice were partly compromised in the absence ofNrf2 expression. These data provide additional insight into therole of Nrf2 in β3-AR-mediated Ucp1 expression and energyexpenditure, further highlighting the utility of Nrf2-mediatedthermogenic stimulation as a therapeutic approach to diet-inducedobesity.
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