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Negative regulation of adiponectin receptor 1 promoter by insulin via a repressive nuclear inhibitory protein element
Author(s) -
Sun Xiaolan,
He Jing,
Mao Chenqian,
Han Ruijun,
Wang Zhenzhen,
Liu Yong,
Chen Yan
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.08.037
Subject(s) - adiponectin , insulin , insulin receptor , medicine , adiponectin receptor 1 , endocrinology , pi3k/akt/mtor pathway , adipose tissue , receptor , chemistry , c2c12 , biology , microbiology and biotechnology , signal transduction , insulin resistance , myocyte , myogenesis
Adiponectin is an adipose‐derived hormone that has anti‐diabetic and anti‐atherogenic effects through interaction with adiponectin receptors AdipoR1 and AdipoR2. We analyzed the transcriptional regulation of AdipoR1 by insulin. Insulin repressed the promoter activity of AdipoR1 in C2C12 myoblasts via PI3K and Foxo1. Deletion studies demonstrated the presence of a putative insulin‐responsive region which is composed of a nuclear inhibitory protein (NIP) binding element. Mutation of the NIP element abrogated the negative regulation of AdipoR1 promoter by insulin. Insulin treatment could induce formation of a protein complex that bound the NIP element. Collectively, our data suggest that a repressive NIP element is involved in the negative regulation of AdipoR1 promoter by insulin.