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Nrf2 induces Ucp1 expression in adipocytes in response to モ3-AR stimulation and enhances oxygen consumption in high-fat diet-fed obese mice
Seo-Hyuk Chang1 (Graduate student), Jae Yool Jang1 (Graduate student), Seungjun Oh1 (Graduate student), Jung-Hoon Yoon1 (Professor), Dong-Gyu Jo2 (Professor), Ui Jeong Yun1 (Post-doctoral researcher), Kye Won Park 1,* (Professor)
1Department of Food Science and Biotechnology and 2School of Pharmacy, Sungkyunkwan University
Abstract
Cold-induced norepinephrine activates モ3-adrenergic receptors (モ3-ARs) to stimulate the kinase cascade and cAMP-response element-binding protein, leading to the induction of thermogenic gene expression including uncoupling protein 1 (Ucp1). Here, we showed that stimulation of the モ3-AR by its agonists isoproterenol and CL316,243 in adipocytes increased the expression of Ucp1 and heme oxygenase 1 (Hmox1), the principal Nrf2 target gene, suggesting the functional interaction of Nrf2 with モ3-AR signaling. The activation of Nrf2 by tert-butylhydroquinone and reactive oxygen species (ROS) production by glucose oxidase induced both Ucp1 and Hmox1 expression. The increased expression of Ucp1 and Hmox1 was significantly reduced in the presence of an Nrf2 inhibitor or in Nrf2-deleted (knockout) adipocytes. Furthermore, Nrf2 directly activated the Ucp1 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 consumption in obese mice were partly compromised in the absence of Nrf2 expression. These data provide additional insight into the role of Nrf2 in モ3-AR-mediated Ucp1 expression and energy expenditure, further highlighting the utility of Nrf2-mediated thermogenic stimulation as a therapeutic approach to diet-induced obesity.
Abstract, Accepted Manuscript(in press) [Submitted on February 16, 2021, Accepted on March 9, 2021]
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