The Effects of Errα (Estrogen-Related Receptor Alpha) Inhibition on the Serum Levels of Chemerin, Nesfatin-1, and Apelin After Endurance Training in Male Wistar Rats

Adipokines as lipid-secreted proteins play an important role in controlling the metabolism of the body. The aim of the present study was to investigate the effects of ERRα (Estrogen-related receptor alpha) inhibition on the serum levels of Chemerin, Nesfatin-1 ,and Apelin after 4 weeks of endurance training in male Wistar rats.
In this experimental study, 32 adult male Wistar rats were used. The animals were randomly divided into four equal groups including the control, control尤ﯷ, endurance training, and endurance training尤ﯷ. XCT790, as an ERRα inhibitor, was intraperitoneally injected at a dose of 0.48 mg /kg of body weight. The training groups performed running endurance training for four weeks (five sessions per week). At the start of the training, the speed was 15 meters per minute and the time was 20 minutes, and gradually increased to 27 meters per minute for 50 minutes. The ELIZA technique was utilized for measuring the serum levels of Apelin, Chemerin ,and Nesfatin-1. One-way analysis of variance followed by Tukey post hoc test was used for between groups comparisons.
Serum levels of Apelin (P=0.168) and Chemerin (P=0.397) in the endurance training group had no significant difference compared to the control group. Serum levels of Nesfatin-1in the endurance training group showed a significant increase compared to the control group (P=0.001). Also, Apelin serum levels (P=0.033) in the control尤ﯷ group significantly decreased compared to the control group, but the serum levels of Nesfatin-1 showed a significant increase (P= 0.001), while there was no significant difference in the serum levels of Chemerin compared to the control group (P= 0.718).
The results suggest that Nesfatin-1is a factor that can be changed by the endurance training, and it can probably play a compensatory role in energy homeostasis disorders, but Chemerin does not change with ERRα inhibition.