Sun Xiaolan, He Jing, Mao Chenqian, Han Ruijun, Wang Zhenzhen, Liu Yong, Chen Yan
Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, 294 Taiyuan Road, Shanghai 200031, China.
FEBS Lett. 2008 Oct 15;582(23-24):3401-7. doi: 10.1016/j.febslet.2008.08.037. Epub 2008 Sep 19.
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.
脂联素是一种由脂肪组织分泌的激素，通过与脂联素受体AdipoR1和AdipoR2相互作用发挥抗糖尿病和抗动脉粥样硬化作用。我们分析了胰岛素对AdipoR1的转录调控。胰岛素通过PI3K和Foxo1抑制C2C12成肌细胞中AdipoR1的启动子活性。缺失研究表明存在一个由核抑制蛋白（NIP）结合元件组成的假定胰岛素反应区域。NIP元件的突变消除了胰岛素对AdipoR1启动子的负调控。胰岛素处理可诱导形成与NIP元件结合的蛋白复合物。总之，我们的数据表明，一个抑制性的NIP元件参与了胰岛素对AdipoR1启动子的负调控。
