摘要
研究运动对RBP4诱导的脂代谢异常鼠肝脏SREBP-1c信号通路和脂肪合成的影响;重组人RBP4注射建立脂代谢异常鼠模型,设一次性运动组(RBP4 One-time exercise group,ROE组)、8周有氧运动组(RBP4 aerobic exercise group,RAE组)和安静对照组(RBP4 control group,RC组)。结果发现:ROE组血清RBP4水平与RC组比较非常显著降低(P<0.01),血清TG和肝脏TG含量无显著性改变(P>0.05)。RAE组血清RBP4、TG和肝脏TG含量与RC组和ROE组比较均非常显著降低(P<0.01)。与RC组比较,ROE组和RAE组肝脏SREBP-1c m RNA表达均非常显著降低(P<0.01);ROE组SREBP-1c蛋白表达、FASm RNA和FAS蛋白表达均无显著性改变(P>0.05);RAE组SREBP-1c、FAS的m RNA和蛋白表达比ROE组均非常显著减少(P<0.01)。结果说明RBP4显著使小鼠肝脏SREBP-1c基因和蛋白表达增加、激活SREBP-1c信号通路、促进肝脏脂肪合成。8周有氧运动抑制了RBP4在肝脏的脂肪合成促进作用,改善脂代谢,机制涉及降低RBP4水平,减少肝脏SREBP-1c基因和蛋白表达,抑制SREBP-1c信号通路的激活,降低肝脏脂肪合成功能。
In order to study the effects of exercise on SREBP-1c signal pathway and fat synthesis of the liver ofmice with dyslipidemia induced by RBP4, the author established a dyslipidemia mouse model by means of RBP4intraperitoneal injection, set up a one-time exercise group (ROE), an 8-week aerobic exercise group (RAE) and acalm control group (RC), and revealed the following findings: comparing the mice in group ROE with the mice ingroup RC, serum RBP4 level decreased significantly (P〈0.01), serum TG and liver TG contents had no significantchange (P〉0.05); comparing the mice in group RAE with the mice in groups RC and ROE, serum RBP4, serum TGand liver TG contents decreased significantly (P〈0.01); comparing the mice in groups ROE and RAE with the micein group RC, liver SREBP-1c mRNA expression decreased significantly (P〈0.01); as for the mice in group ROE,SREBP-1c protein expression, FAS mRNA and FAS protein expression had no significant change (P〉0.05); comparingthe mice in group RAE with the mice in group ROE, SREBP-1c, FAS mRNA and protein expression decreasedsignificantly (P〈0.01). The said findings indicate the followings: RBP4 significantly increased mouseliver’s SREBP-1c gene and protein expressions, activated SREBP-1c signal pathway, and promoted liver fat synthesis;8-week aerobic exercise restrained the role of RBP4 in promoting fat synthesis in the liver, improved fat metabolism;the mechanism involved with reducing RBP4 level, reducing liver SREBP-1c gene and protein expres-sions, restraining SREBP-1c signal pathway activation, and reducing the liver’s fat synthesis function.
出处
《体育学刊》
CAS
CSSCI
北大核心
2015年第1期139-144,共6页
Journal of Physical Education
基金
福建省自然科学基金项目(2011J01151)
惠州学院重点学科培育项目(ZDPYXK1406)