玉竹多糖对高脂饲料喂养的小鼠脂代谢的影响

EFFECT OF POLYGONATUM ODORATUM POLYSACCHARIDES ON LIPID METABOLISM IN HIGH-FAT DIET FED MICE

目的研究玉竹多糖(POP)对小鼠脂肪代谢关键基因表达的影响,探讨POP干预肥胖形成的机制。方法采用C57BL/6健康清洁级小鼠,每天在喂饲高脂饲料的同时分别经口灌胃给予奥利司他(30mg/kg·d)和玉竹多糖(400 mg/kg·d),期间跟踪小鼠能量摄入量和体质量变化,8 w实验结束后检测小鼠脂肪和肝脏湿重,测定血清血脂含量,采用qPCR技术检测小鼠肝脏脂代谢关键基因表达水平。结果与高脂模型组相比,玉竹多糖能明显抑制小鼠体质量增加,显著降低Lee’s指数、身体质量指数、脂肪和肝脏系数、血清甘油三酯和低密度脂蛋白浓度(P<0.05);提高了血清高密度脂蛋白浓渡(P<0.05),对能量摄入量影响不明显。但显著减少肝脏脂肪合成相关基因脂蛋白脂酶、乙酰辅酶A羧化酶、脂肪酸合成酶、固醇调节元件结合蛋白-1c mRNA表达水平(P<0.05),上调脂肪分解相关基因激素敏感性甘油三酯脂肪酶mRNA表达(P<0.05),但对3-羟基-3-甲基戊二酰辅酶A还原酶mRNA表达影响不明显。结论玉竹多糖可以通过调节肝脏脂代谢相关基因的表达水平,促进脂肪氧化分解,抑制脂肪酸合成,抑制小鼠体质量的增加,从而有效预防小鼠肥胖的发生。

Objective To study the influence of polygonatum odoratum polysaccharides （POP） on the expression of key genes in lipid metabolism and explore the mechanism in obese. Methods C57BL/6 mice were fed a high fat diet and given orlistat（30 mg/kg·d） or POP（400 mg/kg·d） by gavage every day at the same time. After 8 weeks, body weight, energy intake, wet weights of liver and fat tissues, and levels of serum lipid profiles were detected. The mRNA expression of key genes in lipid metabolism were also analyzed using quantitative real-time polymerase chain reaction. Results Compared with the high-fat model group, POP could significantly inhibit weight gain in mice, decrease Lee＇s index, body mass index, fat and liver indexes, serum triglyceride and low density lipoprotein levels （P〈0.05）, increase serum high-density lipoprotein levels （P〈0.05）, but no influence was found on energy intake. Moreover, POP could significantly reduce hepatic mRNA expressions of the related to lipoprotein lipase （LPL）, acetyl-CoA carboxylase, fatty acid synthase and sterol regulatory element binding protein lc （P 〈 0.05）, up-regulate the mRNA expressions of the genes related to hormone-sensitive lipase and adipose triglyceride lipase （P 〈 0.05）, but no influence was detected on the mRNA expression of 3-hydroxy-3-methylpentyl-coenzyme A reductase gene. Conclusion The POP can regulate the mRNA expression of the genes related to lipid metabolism, promote fatty acid oxidation, and inhibit fatty acid synthesis, thus leading to weight loss in obese mice.