Nrf2 in adipocytes

White adipocytes play a key role in maintaining whole body energy homeostasis by forming white adipose tissue (WAT). The impairment of WAT formation or WAT dysfunction is clearly associated with severe metabolic disorders. Mature adipocytes are derived from differentiated preadipocytes and are pivot...

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Published inArchives of pharmacal research Vol. 43; no. 3; pp. 350 - 360
Main Authors Wang, Zhendi, Zuo, Zhuo, Li, Lu, Ren, Suping, Gao, Tianchang, Fu, Jingqi, Hou, Yongyong, Chen, Yanyan, Pi, Jingbo
Format Journal Article
LanguageEnglish
Published Seoul Pharmaceutical Society of Korea 01.03.2020
대한약학회
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Summary:White adipocytes play a key role in maintaining whole body energy homeostasis by forming white adipose tissue (WAT). The impairment of WAT formation or WAT dysfunction is clearly associated with severe metabolic disorders. Mature adipocytes are derived from differentiated preadipocytes and are pivotal in energy storage and metabolism. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a member of a family of CNC-bZIP proteins which exert their transcriptional control on genes harboring antioxidant response elements (ARE) in partnership with small musculoaponeurotic fibrosarcoma proteins. The activation of Nrf2-ARE coordinated by specific repressor Kelch-like ECH-associated protein 1 (Keap1) regulates networks of genes controlling diverse homeostatic processes involving adaptive antioxidant response and detoxification among many other adaptive responses. Interestingly, accumulating evidence indicates that Nrf2 may act as a transcription factor in regulating the formation and function of adipose tissues, including adipogenesis, lipid metabolism and insulin sensitivity. In this mini-review, an overview on the distinct roles of Nrf2 in adipocytes is provided. While highlighting the regulatory role of Nrf2 in adipogenesis, recent key findings on Nrf2 in insulin signal transduction and energy metabolism of adipocytes are also summarized.
Bibliography:https://doi.org/10.1007/s12272-020-01227-0
ISSN:0253-6269
1976-3786
DOI:10.1007/s12272-020-01227-0