应我校“青年学者论坛”邀请，国家杰出青年科学基金获得者、天津医科大学常永生教授来访我校，访问期间将举办学术报告进行交流，欢迎相关师生参加。
报告题目：甲状腺激素刺激脂肪产热分子机制
报告人：常永生教授
报告时间：10月28日上午9:00
报告地点：明德楼B305
主持人：陈政研究员
主办单位：人事处
承办单位：生命科学中心
报告人简介：
常永生，天津医科大学教授；国家杰出青年科学基金获得者（2018年），入选科技部中青年科技创新领军人才（2015年）；获得国务院特殊津贴。作为课题负责人获得国家自然科学基金重点项目，重大研发计划，面上项目，科技部863等项目的资助；迄今为止发表SCI论文20多篇。
报告摘要：
Thyroid thermogenesis phenomenon has been well known for more than one century. However, how thyroid hormones stimulate thermogenesis remains largely unclear. In the present study we show that fat Klf9 expression is markedly induced by T3. Moreover, Klf9 expression level in human WAT is inversely correlated to adiposity. Klf9 overexpression in primary fat cells stimulates cellular thermogenesis, which is UCP1-dependent. Fat-specific Klf9 transgenic mice gain less weight and have smaller fat pads due to increased thermogenesis of brown and beige fat. Klf9 transgene markedly promotes browning of white adipose tissue. Conversely, Klf9 mutation in brown adipocytes reduces expression of thermogenic genes, causing a reduction in cellular respiration. Global Klf9 mutant mice exhibited obesity and cold sensitivity due to the impaired thermogenic function of fat. Furthermore, fat-specific Klf9-deleted mice are prone to obesity on a high-fat diet. Finally, fat Klf9 deletion inhibits the T3-mediated induction of browning of WAT and thermogenesis of BAT. Mechanistically, T3/TRα complex directly bind to Klf9 gene promoter and activate its expression in fat, which in turn stimulates PGC1α, a master regulator of fat thermogenesis, subsequently promoting energy expenditure. The present study reveals a critical role for Klf9 in mediating thyroid thermogenesis. Targeting Klf9 in fat might be therapeutically exploited to treat obesity and metabolic diseases, while avoiding the side effects of thyroid hormones.
