Department of Sports and Education, School of Physical Education, Shanxi University, Taiyuan, Shanxi, China.
Department of Sports and Education, School of Physical Education, Shanxi University, Taiyuan, Shanxi, China.
Nutr Res. 2022 Sep;105:20-32. doi: 10.1016/j.nutres.2022.04.004. Epub 2022 Apr 27.
Adipogenesis is one of the triggers of obesity, which is a risk factor for various metabolic diseases. Long noncoding RNA steroid receptor RNA activator (lncRNA-SRA) is closely related to adipogenesis and p38/JNK mitogen-activated protein kinase mediates lipid production by regulating peroxisome proliferator-activated receptor gamma (PPARγ). Aerobic exercise can be efficient in improving adiposity and losing weight. Hence, we hypothesize that aerobic exercise ameliorates obesity by affecting the SRA/p38/JNK/PPARγ pathway and downstream target genes. The broad approaches used to test hypotheses are as follows. Spectrophotometer detected C57BL/6J mice blood lipid level; hematoxylin and eosin-stained fat tissue to check the grade of epididymis fat; quantitative polymerase chain reaction and Western blot detected messenger RNA expression and protein levels. Injected lncRNA-SRA virus vector to overexpress SRA. After 8 weeks of aerobic exercise intervention, obese mice showed significant improvements in body weight, white fat weight, lipid levels, and the Lee index. Aerobic exercise significantly inhibited the expression of SRA, activated the p38/JNK signaling pathway, further inhibited the expression of PPARγ and downstream target genes, and improved obesity. Aerobic exercise intervention improved lipid metabolism in obese mice, and the mechanism may be related to the regulation of the LncSRA/p38/JNK/PPARγ signaling pathway.
脂肪生成是肥胖的触发因素之一，而肥胖是各种代谢性疾病的风险因素。长链非编码 RNA 类固醇受体 RNA 激活物（lncRNA-SRA）与脂肪生成密切相关，p38/JNK 丝裂原活化蛋白激酶通过调节过氧化物酶体增殖物激活受体 γ（PPARγ）介导脂质生成。有氧运动可以有效地改善肥胖和减肥。因此，我们假设有氧运动通过影响 SRA/p38/JNK/PPARγ 通路及其下游靶基因来改善肥胖。测试假说的广泛方法如下。分光光度计检测 C57BL/6J 小鼠的血脂水平；苏木精和伊红染色脂肪组织检查附睾脂肪的等级；定量聚合酶链反应和 Western blot 检测信使 RNA 表达和蛋白水平。注射 lncRNA-SRA 病毒载体过表达 SRA。经过 8 周的有氧运动干预，肥胖小鼠的体重、白色脂肪重量、血脂水平和 Lee 指数均有明显改善。有氧运动显著抑制 SRA 的表达，激活 p38/JNK 信号通路，进一步抑制 PPARγ 及其下游靶基因的表达，改善肥胖。有氧运动干预改善了肥胖小鼠的脂质代谢，其机制可能与调节 LncSRA/p38/JNK/PPARγ 信号通路有关。
