Background: Endurance exercise is known to promote a substantial effect on the energy balance in rats and humans. However, little is known about the exact mechanisms for the appetite-suppressive effects of endurance exercise. We hypothesized that endurance training might activate signaling cascades in the hypothalamus known to be involved in leptin signaling.
Methods: 16 male Wistar rats were randomly assigned to two groups: sedentary (n = 8) and exercise groups (n = 8). Animals in the exercise group started treadmill running at 30 m/min, 0% grade, for 1 min/bout. Running time was gradually increased by 2 min/bout every day. The training plan was one bout per day during initial two weeks, and two bouts per day during 3rd-9th week. At the end of nine-week experiment, blood was analyzed for low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), total cholesterol (TC), free fatty acid (FFA), interleukin (IL)-6, and leptin in both groups. Activations of janus kinase 2-signaling transducer and activator of transcription 3 (JAK2-STAT3), protein kinase B (Akt), extracellular regulated kninase (ERKs), and suppressor of cytokine signaling 3 (SOCS3) in hypothalamus were measured in the end of nine weeks of exercise protocol.
Results: Nine-week endurance exercise induced lower concentrations of LDL-C, TG, TC, FFA, and leptin in rats (P < 0.05 or P < 0.01). Nine-week endurance exercise significantly increased the circulating IL-6 concentration compared with sedentary group (239.6 ± 37.2 pg/ml vs. 151.8 ± 31.5 pg/ml, P < 0.01). Exercise rats showed significant increases in JAK2, STAT3, Akt, ERKs, and SOCS3 phosphorylations compared with sedentary rats (P < 0.01).
Conclusion: The data suggest that endurance exercise is a leptin signaling mimetic in hypothalamus of Wistar rats.