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Abstract
BackgroundEndurance 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.Methods16 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.ResultsNine-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).ConclusionThe data suggest that endurance exercise is a leptin signaling mimetic in hypothalamus of Wistar rats.
Highlights
There is an obesity epidemic in much of the developed and developing world [1,2,3,4,5,6]
It is possible that the effects of endurance exercise on leptin signaling pathways in hypothalamus may be dependent on IL-6
Effect of endurance exercise on serum lowdensity lipoprotein cholesterol (LDL-C), TG, total cholesterol (TC), free fatty acid (FFA), and leptin Nine-week endurance exercise induced lower concentrations of low-density lipoprotein cholesterol (LDL)-C, TG, TC, FFA, and leptin compared with sedentary rats (P < 0.05 or P < 0.01, Table 1)
Summary
There is an obesity epidemic in much of the developed and developing world [1,2,3,4,5,6]. Leptin is a cytokine originating mainly from white adipose tissue that plays an important role in regulating energy expenditure, food intake and obesity [7]. The mechanism by which leptin modulates these hypothalamic neurons involves the binding of leptin to the long form of leptin receptor (Ob-Rb) [8] and the subsequent intracellular signaling [9], initiated by autophosphorylation of Janus kinase 2 (JAK2) and activation of signal transducer and activator of transcription 2 (STAT3) [10]. It is possible that the effects of endurance exercise on leptin signaling pathways in hypothalamus may be dependent on IL-6. Endurance exercise is known to promote a substantial effect on the energy balance in rats and humans. 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
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