GCK对高脂饲料诱导的小鼠肥胖模型的降脂减肥作用

Inhibition of GCK on High Fat Diet-Induced Mouse Obesity

摘要: 目的：探讨GCK对高脂饲料诱导的小鼠肥胖模型的干预作用。方法：小鼠用高脂饲料喂养12个月造成肥胖模型。GCK口服给药6周，同时记录小鼠摄食量、体重变化；实验终点处死小鼠取血浆，全自动生化仪检测血浆中ALT、AST、TC、TG水平；取肝脏制作石蜡切片HE染色后显微镜下观察肝脏中脂肪滴含量；肝脏匀浆提取RNA，RT-PCR检测脂代谢相关蛋白FAS和PPARα水平。结果：GCK不影响小鼠摄食量，但是高剂量GCK能够导致肥胖小鼠体重减少；GCK能够有效降低小鼠血浆ALT、AST、TC、TG水平；GCK能够减少小鼠肝脏中的脂肪含量，其作用机制可能是诱导FAS的降低和PPARα的升高。结论：GCK能够在一定程度上抑制高脂饲料造成的肥胖。

Abstract: Objective: To investigate the effect of GCK on high fat diet-induced mouse obesity model. Methods: Mice were fed a high-fat diet for 12 months to develop an obesity model. GCK was intragastrical administered for 6 weeks, while the food intake and body weight were recorded. The mice were sacrificed at the end of the experiment. The plasma levels of ALT, AST, TC and TG were detected by automatic biochemical analyzer. The liver was prepared by paraffin section and stained by HE staining kit. The RNA was extracted from the liver homogenate, and the levels of lipid metabolism related proteins FAS and PPARα were detected by RT-PCR. Results: GCK did not affect the food in-take of mice, but high dose of GCK could cause weight loss in obese mice. GCK can effectively reduce plasma ALT, AST, TC, TG levels in mice; GCK can reduce the fat content in mouse liver. The mechanism of those effects may be to induce the FAS decrease and PPARα increase. Conclusion: GCK can inhibit the HFD-induced obesity.