常永生课题组在《J Biol Chem》 杂志发表研究论文“Forkhead Box P1 (FOXP1) Transcription Factor Regulates Hepatic Glucose Homeostasis （2015）”。

为研究FOXP1对肝脏糖代谢，中国医学科学院基础医学研究所，“医学分子生物学国家重点实验室”的常永生课题组发现FOXP1通过与FOXO1相互作用，抑制FOXO1糖异生作用，可达到降血糖作用。

【摘要】：Dysregulation of hepatic gluconeogenesis contributes to the pathogenesis of diabetes, yet the detailed molecular mechanisms remain to be fully elucidated. Here we show that FOXP1,a transcriptional repressor, plays a key role in the regulation of systemic glucose homeostasis. Hepatic expression levels of FOXP1 are decreased in diabetic mice. Modest hepatic overexpression of FOXP1 in mice inhibited the expression of gluconeogenic genes, such as peroxisome proliferators-activated receptor  coactivator-1  (PGC-1 ), phosphoenolpyruvate carboxykinase(PEPCK), and glucose-6-phosphatase (G6PC), leading to a decrease in hepatic glucose production and fasting bloodglucose levels in normal mice and different mouse models of diabetes, including db/db diabetic and high-fat diet-induced obese mice. FOXP1 physically interacted with FOXO1 in vivo and competed with FOXO1 for binding to the insulin response element in the promoter region of gluconeogenic genes, thereby interfering expression of these genes. These results identify a previously unrecognized role for FOXP1 in the transcriptional control of hepatic glucose homeostasis.

相关结果已发表于《J Biol Chem》 杂志（2015，290(51):30607-15.），其作者为常永生课题组博士研究生邹永康，重点室常永生研究员是本文的通讯作者。该研究工作得到了以下基金的支持：973，国自然。

医学分子生物学国家重点实验室