1、职称职务：副教授，博士生导师
2、学科专业： 药理学
3、研究方向：
药理学（胎源性疾病发生机制及药物防治）
药物毒理学（药物发育毒理的基础与应用研究）
4、实验室位置：
1号楼发育源性疾病湖北省重点实验室、2号楼4楼药理学教研室
5、联系电话： 027-68758959 15972228956
6、Email： xuyidan70188@whu.edu.cn
7、学习经历：
2007/09 -2010/06，武汉大学，基础医学院药理学系，博士
2005/09-2007/06，武汉大学，基础医学院药理学系，硕士
2000/09-2005/06，武汉大学，医学院临床医学专业，学士
8、主要工作经历与任职
2013/01-至今，武汉大学，基础医学院药理学系，副教授
2011/01 -2012/12，武汉大学，基础医学院药理学系，讲师
2010/07 -2012/06，武汉大学，生命科学学院发育生物学，博士后
2010/07-2010/12，武汉大学，基础医学院药理学系，助教
- 9、目前主要科学研究领域和兴趣
主要从事外源物发育毒理和胎源性疾病发病机制研究。在前期研究中，系统证实了孕期外源物（咖啡因、尼古丁）暴露所致宫内发育迟缓（IUGR）子代成年下丘脑-垂体-肾上腺（HPA）轴相关疾病（如脂肪肝、抑郁症）易感的胎儿起源现象，创新性提出咖啡因、尼古丁所致胎HPA轴轴神经内分泌代谢编程改变是引起IUGR仔鼠成年HPA轴相关疾病易感的胎儿起源机制。
10、教学情况：
承担研究生、本科生、留学生（全英）的教学; 积极开展教学研究；发表教学论文1篇；参编教材1部。
11、近5年代表性论文（第一作者/通讯作者）
Lu J, Wen YX, Zhang L, Zhang C, Zhong WH, Zhang L, Yu Ying, Chen LB, Xu D*, Wang H*. Prenatal ethanol exposure induces an intrauterine programming of enhanced sensitivity of the hypothalamic-pituitary-adrenal axis in female offspring rats fed with post-weaning high-fat diet. Toxicol Res. 2015; 4(5): 1238-1249.
Xu D, Bai J, Zhang L, Shen L, Wang LL, Liu ZF, Xia LP, Wang H. Prenatal nicotine exposure-induced intrauterine programming alteration increases the susceptibility of high-fat diet-induced non-alcoholic simple fatty liver in female adult offspring rats. Toxicol Res. 2015; 4(1): 112-120.
Zhang C, Xu D (Co-first author), Luo HW, Lu J, Liu L, Ping J, Wang H. Prenatal xenobiotic exposure and intrauterine hypothalamus-pituitary-adrenal axis programming alteration. Toxicology. 2014. Accepted.
Xu D, Xia LP, Shen L, Lei YY, Liu L, Zhang L, Magdalou J, Wang H. Prenatal nicotine exposure enhances the susceptibility to metabolic syndrome in adult offspring rats fed high-fat diet via alteration of HPA axis-associated neuroendocrine metabolic programming. Acta Pharmacol Sin, 34(12), 1526-34, 2013.
Zhang L, Xu D (Co-first author), Zhang B, Liu Y, Chu F, Guo Y, Gong J, Zheng X, Chen L, Wang H. Prenatal food restriction induces a hypothalamic-pituitary-adrenocortical axis-associated neuroendocrine metabolic programmed alteration in adult offspring rats. Arch Med Res, 44(5), 335-45, 2013.
Xu D, Liang G, Yan YE, He WW, Liu YS, Chen LB, Magdalou J, Wang H. Nicotine-induced over-exposure to maternal glucocorticoid and activated glucocorticoid metabolism causes hypothalamic-pituitary-adrenal axis-associated neuroendocrine metabolic alterations in fetal rats. Toxicol Lett, 209(3), 282-90, 2012.
Xu D, Wu Y, Liu F, Liu YS, Shen L, Lei YY, Liu J, Ping J, Qin J, Zhang C, Chen LB, Magdalou J, Wang H. A hypothalamic–pituitary–adrenal axis-associated neuroendocrine metabolic programmed alteration in offspring rats of IUGR induced by prenatal caffeine ingestion. Toxicol Appl Pharmacol, 264(3), 395-403, 2012.
Xu D, Zhang BJ, Liang G, Ping J, Kou H, Li XJ, Xiong J, Chen LB, Magdalou J, Wang H. Caffeine-induced activated glucocorticoid metabolism in hippocampus causes hypothalamic-pituitary-adrenal axis inhibition in fetal rats. PLoS ONE, 7(9), e44497, 2012.
Liu YS, Xu D (Co-first author), Feng JH, Kou H, Liang G, Yu H, He XH, Zhang BF, Chen LB, Magdalou J, Wang H. Fetal rat metabonome alteration by prenatal caffeine ingestion probably due to the increased circulatory glucocorticoid level and altered peripheral glucose and lipid metabolic pathways. Toxicol Appl Pharmacol, 262(2), 205-16, 2012.
Xu D, Chen M, Pan XL, Xia LP, Wang H. Dexamethasone induces fetal developmental toxicity through affecting the placental glucocorticoid barrier and depressing fetal adrenal function. Environ Toxicol Pharmacol, 32(3), 356-63, 2011. 被国际生物和医学论文评价系统“Faculty of 1000”选为“推荐”论文（http://f1000.com/14264021）