The expression of LXR and its impacts on hepatic glucose metabolism in different glucose metabolic statuses in rats
10.3760/cma.j.issn.1000-6699.2011.02.014
- VernacularTitle:不同糖代谢状态下大鼠肝X受体的表达及其对肝糖代谢的影响
- Author:
Ying DONG
;
Wei LIU
- Publication Type:Journal Article
- Keywords:
Liver X receptor;
Phosphoenolpyruvate carboxykinase;
Glucokinase
- From:
Chinese Journal of Endocrinology and Metabolism
2011;27(2):148-151
- CountryChina
- Language:Chinese
-
Abstract:
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 PGR 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.
