Protective effects of aerobic swimming training on high-fat diet induced nonalcoholic fatty liver disease: regulation of lipid metabolism via PANDER-AKT pathway.
Protective effects of aerobic swimming training on high-fat diet induced nonalcoholic fatty liver disease: regulation of lipid metabolism via PANDER-AKT pathway.
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DOI：
10.1016/j.bbrc.2015.02.046
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发表时间：
2015-03
影响因子：
3.1
通讯作者：
Hao Wu;Meihua Jin;Donghe Han;Mingsheng Zhou;Xifan Mei;Y. Guan;Chang Liu
中科院分区：
文献类型：
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作者：
Hao Wu;Meihua Jin;Donghe Han;Mingsheng Zhou;Xifan Mei;Y. Guan;Chang Liu
本研究旨在探讨有氧游泳训练预防高脂饮食诱导的非酒精性脂肪性肝病(NAFLD)的机制。将42只雄性C57BL/6小鼠随机分为正常饮食久坐组(ND；n=8)、ND运动组(n=8)、高脂饮食久坐组(HFD；n=13)和高脂饮食运动组(n=10.13)。经过2周的训练适应后，小鼠接受每周5天的有氧游泳(60分钟/天)，为期10周。与ND组相比，HFD组的脂肪酸转运、脂肪生成和β氧化相关基因的表达水平显著升高。HFD组PANDER和FOXO1表达增加，AKT表达降低。带HFD的有氧游泳运动逆转了HFD对血小板反应素-1受体、肝脏脂肪酸结合蛋白、长链脂肪酸伸长酶-6、Fas细胞表面死亡受体、硬脂酰辅酶A脱饱和酶-1以及PANDER、FOXO1和AKT表达的影响。高脂运动组PPARα和AOX表达明显增强。我们的发现表明，有氧游泳训练可以通过调节脂肪酸运输、脂肪生成和β氧化相关基因来预防非酒精性脂肪肝。此外，有氧游泳训练的好处部分是通过Pander-AKT-FOXO1途径实现的。
This study aimed to investigate the mechanism by which aerobic swimming training prevents high-fat-diet-induced nonalcoholic fatty liver disease (NAFLD). Forty-two male C57BL/6 mice were randomized into normal-diet sedentary (ND; n = 8), ND exercised (n = 8), high-fat diet sedentary (HFD; n = 13), and HFD exercised groups (n = 13). After 2 weeks of training adaptation, the mice were subjected to an aerobic swimming protocol (60 min/day) 5 days/week for 10 weeks. The HFD group exhibited significantly higher mRNA levels of fatty acid transport-, lipogenesis-, and β-oxidation-associated gene expressions than the ND group. PANDER and FOXO1 expressions increased, whereas AKT expression decreased in the HFD group. The aerobic swimming program with the HFD reversed the effects of the HFD on the expressions of thrombospondin-1 receptor, liver fatty acid-binding protein, long-chain fatty-acid elongase-6, Fas cell surface death receptor, and stearoyl-coenzyme A desaturase-1, as well as PANDER, FOXO1, and AKT. In the HFD exercised group, PPARα and AOX expressions were much higher. Our findings suggest that aerobic swimming training can prevent NAFLD via the regulation of fatty acid transport-, lipogenesis-, and β-oxidation-associated genes. In addition, the benefits from aerobic swimming training were achieved partly through the PANDER-AKT-FOXO1 pathway.