中文摘要：

目的观察肝X受体（LXR）在不同糖代谢状态下肝内表达的变化情况及其对肝糖代谢酶磷酸烯醇式丙酮酸羧激酶（PEPCK）mRNA和葡萄糖激酶（GCK）mRNA表达的调节，阐明LXR信号通路对糖代谢的影响机制。方法SD雄鼠36只分为正常对照组、糖尿病组、肥胖组和肥胖伴糖尿病组。测定各组大鼠的体重、血糖、胆固醇和甘油三酯。采用实时PCR检测各组大鼠肝脏LXR mRNA、PEPCK mRNA和GCK mRNA的表达情况，应用Western印迹测定肝脏LXR蛋白质的表达。结果各实验组大鼠肝LXR mRNA表达均显著高于对照组（P〈0．05）。Western印迹结果示各组LXR蛋白表达量和转录水平一致。与对照组和肥胖组相比，肥胖伴糖尿病组和糖尿病组肝PEPCK mRNA表达均明显上调，GCK mRNA均明显下调；与对照组相比，肥胖组PEPCK mRNA表达明显下降，GCK mRNA明显上升（均P〈0．05）。结论在非糖尿病阶段，LXR可能作为糖代谢的保护性受体，通过调节肝糖代谢酶，使血糖保持稳态。进入糖尿病阶段后，LXR的保护作用并不能逆转因胰岛素不足所致的糖代谢相关酶的异常改变，血糖不能恢复正常。

英文摘要：

Objective To investigate the mechanism of liver X receptor（LXR） signal pathway in regulating glucose metabolism by observing the variety of LXR expression and its impacts on regulating the mRNA expression of PEPCK and GCK, the key enzyme of hepatic glucose metabolism in various glucose metabolic status in rats. Methods SD rats were chosen and divided into four groups： the CON group, the induced DM group, the OB group, and the induced OB＋DM group. For each group of rats,body weight,blood glucose,serum triglycerides, and cholesterol were measured. Then the rats were sacrificed and the livers were collected and studied. Real-time PCR was used to measure the expressions of LXR mRNA, PEPCK mRNA, and GCK mRNA in the livers. Finally, the Western Blot assay was used to measure the liver LXR protein expression. Results The expression of LXR mRNA was significantly higher in DM, OB, and OB ＋ DM groups than in CON group （ P 〈 0.05 ）. The Western blot results showed that the levels of protein were in accordance with the mRNA expression. Comparing to the CON and the OB groups,the PEPCK mRNA expression of the OB＋DM and the DM groups was significantly higher, while the GCK mRNA expression of these two groups was significantly lower（ P〈0. 05 ）. Comparing to the CON group, the PEPCK mRNA Expression of the OB group was significantly lower, while the GCK mRNA expression of OB group was significantly higher （ P 〈 0. 05 ）. Conclusions During non-diabetic phase, LXR could act as a protective receptor for glucose metabolism and keep glucose homeostasis by regulating the key enzymes of the hepatic glucose metabolism. While in the diabetic phase, the protective receptor LXR failed to reverse the change of the related enzymes caused by insulin deficiency, and finally the plasma glucose level was raised.