Animal studies demonstrate that nutritional programming during the early periods of postnatal life has numerous long-term growth consequences [5–9]. The ABT-263 intrauterine and lactation phases of life are crucial periods in brain growth and development processes; it is during these stages that this website critical events of cell migration and differentiation occur [10, 11]. Nutritional insults, by either low or overfeeding, on these stages may be responsible for the changes in the hypothalamic pathways involved in metabolic balance and energy homeostasis [12, 13]. As reported, early overfeed-programmed obese rats exhibit disrupted neuronal firing in the central nervous regulation of

body weight (bw) [14]. Several maternal environmental insult conditions have been linked to obesity in both human and rodent offspring, which, in turn, has been shown to affect neural development. Interestingly, both maternal caloric deprivation and maternal overfeeding can leads to metabolic syndrome in offspring [15, 16]. Overfeeding and obesity are

often accompanied by alterations in both sympathetic and parasympathetic autonomic BIRB 796 datasheet function. Several lines of evidence support the hypothesis that derangements in the autonomic nervous system (ANS) play an important role in the development of obesity [17, 18]. As reported, other different models of obesity display imbalanced function of the ANS [19, 20]. The sympathetic and parasympathetic nervous systems are critical in the coordination of the catabolic and anabolic responses, respectively. In response to physical activity, glucose uptake is increased in the adipose and skeletal muscle cells; which happens regardless of insulin action [21, 22]. The major metabolic changes induced

by exercise training are caused by the enhancement of sympathetic tonus. Adrenodemedullated rats that were submitted to swimming training showed low fat mobilization; where was showed that the long-term exercise training led to the mobilization of fat, and the fat gains in these adrenodemedullated rats were more unless consistent [23]. Thus, it is important to keep in mind that the exercise training may increase the basal metabolism to promote further increases in fat store consumption, even at rest. As previously reported by our group, the low-intensity and moderate swimming training was able to attenuate obesity onset induced by monosodium L-glutamate (MSG) in mice. However, the benefits of this protocol were observed only in cases where exercise was started early, soon after weaning [24]. Rat’s litter size reduction provokes overfeeding behavior in suckling pups, which induces a high chow intake post-weaning and subsequent obesity. The early overfeeding model of obesity is interesting because the development of obesity in childhood and adolescence is highly correlated with the onset of the metabolic syndrome in adulthood [25, 26].