摘要
目的通过建立高脂饮食诱导的肥胖动物模型,观察肥胖对小鼠肝脏中铁代谢相关调控分子铁调素（hepcidin）、脂质运载蛋白-2（lipocalin-2,LCN2）和膜铁输出蛋白-1（ferroportin-1,FPN1）mRNA及蛋白表达的变化,初步探讨肥胖影响肝脏铁代谢相关分子表达调控的机制。方法将4-6周龄C57BL/6J小鼠随机分为正常对照组和膳食诱导的肥胖模型组,每组10只,对照组给予正常饲料喂养,肥胖组给予高脂饲料喂养,实验饲喂周期为15周。建模成功后取小鼠肝脏,采用实时荧光定量PCR法检测小鼠肝脏中铁代谢相关调控分子hepcidin、LCN2和FPN1 mRNA的表达,并应用Western Blot法检测小鼠肝脏LCN2和FPN1蛋白的表达。结果与对照组小鼠比较,肥胖模型组小鼠肝脏hepcidin mRNA表达水平显著升高,差异具有统计学意义（P〈0.05）,而LCN2和FPN1mRNA及蛋白表达水平差异无统计学意义（P〉0.05）。结论肥胖可以显著上调小鼠肝脏hepcidin的表达,而对肝脏铁代谢相关调控分子LCN2和FPN1的表达并无显著影响。故还不能够认为肥胖可以影响肝脏铁代谢调控分子lipocalin-2和ferroportin-1的表达,进而导致细胞摄取及释放铁的能力发生障碍,使得机体对铁的需求不能满足要求,出现铁代谢功能紊乱,导致肥胖性铁缺乏的发生,而是通过上调肝脏hepcidin表达直接或间接影响其他铁代谢相关调控分子或者存在更为复杂的调控机制,这仍需我们进一步的实验研究及探索。这也为进一步研究肥胖对肝脏铁代谢相关调控分子表达的影响及引起铁缺乏的机制提供了理论和实验基础。
Objective We established the animal models of obesity induced by high-fat diet, in order to study the mRNA and protein expression of regulation molecules related with iron metabolism about hepcidin, lipocalin-2 （ LCN2 ） , ferroportin-1 （FPN1） in obese mice’ s liver and the molecular regulation mechanism.Methods C57BL/6J （4 -6 weeks） mice were randomly divided into control group and obesity model group, each group of ten.The obesity group were fed with a high-fat diet and the control group were given the normal diet for lasting 15 weeks.After we successfully established the obesity animal model, the expression level of hepcidin, LCN2 and FPN1 mRNA in the liver were measured by Real-time fluorescent quantitative PCR method and the protein expression level of LCN2 and FPN1 were measured by Western-Blot.Results Compared with the control group, the expression level of hepcidin mRNA in the liver was increased in obesity group （P 〈0.05）, however, the expression level of LCN2, FPN1 was no significant difference （P 〉0.05）.Conclusion Obesity can increase the expression of hepcidin mRNA, however, there was no significantly effect on the expression of LCN2, FPN1.So, we can’t think that obesity can affect the expression of LCN2 and FPN1, lead to the ability of cells uptake and release iron abnormal, then appear iron metabolism disorders.As a result, leading to iron deficiency.Maybe obesity can affect other regulatory molecules related with iron metabolism through up-regulation the expression of Hepcidin or the more complex regulatory mechanisms.We still need further experimental research and exploration.This research also provides the basis of theoretical and experimental for the further study the effects of obesity on the expression of regulation molecules related with iron metabolism in obesity mice’ s liver and the mechanism of iron deficiency.
出处
《中国比较医学杂志》
北大核心
2015年第7期1-6,共6页
Chinese Journal of Comparative Medicine
基金
国家自然科学基金资助项目(81373020)
北京市自然科学基金资助项目(7112014)
