宫内发育迟缓胎鼠肝脏PGC-1和PEPCK基因的表达变化

目的宫内发育迟缓(IUGR)是胰岛素抵抗的独立危险因素,通过检测IUGR胎鼠肝脏糖代谢相关酶的表达,探讨IUGR个体发生胰岛素抵抗的分子机制。方法通过孕期蛋白质营养不良法建立大鼠IUGR模型,孕21天时剖宫产,测量胎鼠的体重和肝重,采用RT-PCR和蛋白印迹技术检测胎鼠肝脏PGC-1和PEPCK的mRNA及蛋白表达的变化。结果与正常对照相比,IUGR胎鼠肝脏PGC-1的mRNA和蛋白表达水平明显增高(P<0.01),肝中PEPCKmRNA的表达也明显增高(P<0.01)。结论IUGR胎鼠肝脏PGC-1表达增加诱导了糖异生关键酶PEPCK的表达,促进肝脏糖异生,这是IUGR鼠成年后发生胰岛素抵抗的原因之一。

Gene expression of PGC-1and PEPCK in the hepatic from IUGR fetal rats

Objective] To explore the molecular mechanism of insulin resistance in IUGR, and to analyze the expression of genes relevant to glucose metabolism in hepatic of fetal rats with IUGR. Methods] IUGR model were established by protein-malnutrition. On day 21 of gestation, the body weight and liver weight of fetal rats were measured. The mRNA and protein levels of PGC-1 and PEPCK were analyzed by RT-PCR and Western blot. Results] The levels of PGC-1 in the hepatics of fetal rats with IUGR were significantly higher than control group (P <0.01).The mRNA levels of PEPCK were also significantly increased (P <0.01). Conclusions] Increased expression of PGC-1and PEPCK and subsequent hepatic gluconeogenesis contribute to the insulin resistance observed in the IUGR rats.