母鼠妊娠期和哺乳期日粮添加甜菜碱对子代雌性大鼠机体铁代谢的影响及其机制

Effects of maternal betaine supplementation during gestagation and lactation on iron metablism in female offsprings of rats and its mechanism

[目的]本文旨在研究母鼠日粮饲喂甜菜碱对子代雌性大鼠机体铁代谢的影响及其机制。[方法]随机选取56只10周龄Sprague Dawley雌性大鼠,与同种雄鼠自然交配,配种成功后,孕鼠随机分为对照组和甜菜碱组。对照组孕鼠在怀孕第1～21天饲喂基础日粮,甜菜碱组孕鼠同期饲喂在基础日粮上添加质量分数为1%甜菜碱的混合日粮。出生雌性大鼠于(3周龄)断奶后饲喂基础日粮至16周龄。记录13～16周龄子代雌性大鼠生产性能,测定16周龄子代雌性大鼠血液及组织铁代谢相关指标并分析其肝脏铁代谢相关基因及蛋白的表达。[结果]与对照相比,母体添加甜菜碱对子代雌性大鼠生长性能无明显影响,但显著或极显著降低16周龄子代雌性大鼠的血红蛋白含量(P<0.05)、血清铁含量、转铁蛋白结合铁含量和总铁结合力(P<0.01),促进肝脏铁摄取相关蛋白二价金属离子转运体(DMT1)及转铁蛋白受体1(TFR1)蛋白表达(P<0.05)。[结论]母体饲喂甜菜碱降低了子代雌性大鼠血清铁水平,但对肝脏铁含量没有显著影响。肝脏铁的稳态与甜菜碱诱导的肝脏铁摄取通路相关蛋白(TFR1和DMT1)的高表达密切相关。

[Objectives]This paper aimed to study the effects of maternal dietary betaine supplementation during gestagation and lactation on the iron metabolism in female offspring of rats.[Methods]Fifty-six 10 week-old Sprague Dawley female rats were randomly selected,mated and divided into two groups:control group(Con)and betaine group(Bet).Female rats were fed with basal diet and trail diet(basal diet plus 1%betaine)during pregnancy and lactation,respectively.The female offsprings of rats were selected and provided with basal diet from weaning up to 16-weeks.The growth performance was recorded during the experimental periods.The blood iron parameters,tissue iron content and hepatic iron metabolism related genes and protein expression were measured at the end of the experiment.[Results]Maternal betaine supplementation had no significant effect on growth performance,greatly decreased hemoglobin concentration,serum iron,transferrin-bound iron and total iron binding capacity(P<0.01),but significantly enhanced hepatic iron-uptake-related proteins DMT1(divalent metal transperfer 1)and TFR1(transferrin receptor protein 1)expression(P<0.05).[Conclusions]Maternal betaine exposure during pregnancy and lactation decreases serum iron content,but does not affect hepatic iron content in female offsprings of rats.Maintenance of hepatic iron homeostasis is strong associated with high expression of DMT1 and TFR1 induced by betaine in female offsprings of rats.