Aerobic exercise improves adipogenesis in diet-induced obese mice via the lncSRA/p38/JNK/PPARγ pathway.

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.

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