摘要
目的探讨长期(8 w)高果糖饮食对大鼠肝脏脂质沉积及肝脏炎症通路的影响。方法雄性C57BL/J6大鼠分为对照组及高果糖组,经喂养8 w后处死大鼠测定各组肝脏甘油三酯(TG)含量和谷丙转氨酶(ACT)含量,并测定大鼠肝脏内JNK途径(p-JNK/t-JNK)和IκBα途径(p-IKKα/β/t-IKKα/β)的蛋白表达变化。结果喂养8 w后,与对照组相比,高果糖组肝脏甘油三酯和谷丙转氨酶含量较对照组显著增加(P均<0.01);与对照组相比,高果糖组的p-JNK/t-JNK、p-IKKα/β/t-IKKα/β和t-IκB的蛋白表达均显著增加(P均<0.01)。结论 8 w高果糖喂养引起大鼠肝脏脂质沉积,同时伴有JNK和IKKα/β-NF-κB通路激活,提示肝脏两条炎症通路均介导了高果糖喂养诱导脂肪肝和肝胰岛素抵抗的发生发展。
Objective To investigate the effect of long-term （8 weeks） high fructose feeding on liver triglyceride （TG） content and hepatic inflammation pathways. Methods Male Wistar rats were fed a standard chow （Con） or high fructose diet （HFru） for 8 weeks. Rats were sacrificed and TG content and alanine transaminase （ALT） in liver were measured. The protein expressions of the markers of two inflammation pathways-JNK pathway （phosphorylated-JNK/total-JNK） and IKKa/β-NF- KB （p-IKKα/β/t-IKKα/β） pathway were detected. Results Compared with control group, TG content and ALT content were significantly increased after high fat feeding （both P 〈 0. 01 ）. The protein expressions of phosphorylated-JNK/total-JNK, phosphorylated -IKKa/β/ total-IKKa/β and IKB were all significantly increased in high-fructose group （P 〈 0. 01 ）. Conclusions 8-week long-term high-fructose feeding can induce liver steatosis in rats. Hepatic steatosis occurres simutaneouly with the activation of both JNK and IKKta/β-NF-KB inflammatory pathways in liver, which indicats both inflammatory pathways are involved in the development of fatty liver induced by high-fructose-feeding.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2013年第4期852-854,共3页
Chinese Journal of Gerontology
基金
河北省科技厅国际合作项目(No.11396406-D)
关键词
甘油三酯
脂肪肝
胰岛素抵抗
炎症
Triglyceride
Fatty liver
Insulin resistance
Inflammation
