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      Role of Exercise in the Central Regulation of Energy Homeostasis and in the Prevention of Obesity

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          Many of the small percentage of previously obese humans who successfully maintain weight loss report high levels of physical activity, suggesting a role for exercise in the maintenance of their lower body weights. The rat model of diet-induced obesity (DIO) has been particularly useful, since it shares several common characteristics with human obesity and, unlike the human condition, allows a thorough investigation of the effects of exercise on the central pathways which regulate energy homeostasis. In rats with DIO, voluntary wheel running selectively reduces adiposity without causing a compensatory increase in energy intake. These effects are likely mediated by signals generated by the exercising body such as interleukin-6, fatty acids, and heat which feed back on the brain to regulate central neuropeptide systems involved in the regulation of energy homeostasis. While exercise provides temporary reductions in obesity in adult rats, early postweaning exercise reduces adiposity in high-fat-fed DIO rats long after exercise is terminated. This suggests that early-onset exercise may permanently alter the development of the central pathways which regulate energy homeostasis. Therefore, identification of exercise-induced central and peripheral factors and elucidation of their interactions with central modulatory pathways may aid in the identification of new targets for the pharmacological treatment of human obesity.

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          Most cited references 30

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          Changes in energy expenditure resulting from altered body weight.

          No current treatment for obesity reliably sustains weight loss, perhaps because compensatory metabolic processes resist the maintenance of the altered body weight. We examined the effects of experimental perturbations of body weight on energy expenditure to determine whether they lead to metabolic changes and whether obese subjects and those who have never been obese respond similarly. We repeatedly measured 24-hour total energy expenditure, resting and nonresting energy expenditure, and the thermic effect of feeding in 18 obese subjects and 23 subjects who had never been obese. The subjects were studied at their usual body weight and after losing 10 to 20 percent of their body weight by underfeeding or gaining 10 percent by overfeeding. Maintenance of a body weight at a level 10 percent or more below the initial weight was associated with a mean (+/- SD) reduction in total energy expenditure of 6 +/- 3 kcal per kilogram of fat-free mass per day in the subjects who had never been obese (P < 0.001) and 8 +/- 5 kcal per kilogram per day in the obese subjects (P < 0.001). Resting energy expenditure and nonresting energy expenditure each decreased 3 to 4 kcal per kilogram of fat-free mass per day in both groups of subjects. Maintenance of body weight at a level 10 percent above the usual weight was associated with an increase in total energy expenditure of 9 +/- 7 kcal per kilogram of fat-free mass per day in the subjects who had never been obese (P < 0.001) and 8 +/- 4 kcal per kilogram per day in the obese subjects (P < 0.001). The thermic effect of feeding and nonresting energy expenditure increased by approximately 1 to 2 and 8 to 9 kcal per kilogram of fat-free mass per day, respectively, after weight gain. These changes in energy expenditure were not related to the degree of adiposity or the sex of the subjects. Maintenance of a reduced or elevated body weight is associated with compensatory changes in energy expenditure, which oppose the maintenance of a body weight that is different from the usual weight. These compensatory changes may account for the poor long-term efficacy of treatments for obesity.
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            Brain-derived neurotrophic factor regulates energy balance downstream of melanocortin-4 receptor.

            The melanocortin-4 receptor (MC4R) is critically involved in regulating energy balance, and obesity has been observed in mice with mutations in the gene for brain-derived neurotrophic factor (BDNF). Here we report that BDNF is expressed at high levels in the ventromedial hypothalamus (VMH) where its expression is regulated by nutritional state and by MC4R signaling. In addition, similar to MC4R mutants, mouse mutants that expresses the BDNF receptor TrkB at a quarter of the normal amount showed hyperphagia and excessive weight gain on higher-fat diets. Furthermore, BDNF infusion into the brain suppressed the hyperphagia and excessive weight gain observed on higher-fat diets in mice with deficient MC4R signaling. These results show that MC4R signaling controls BDNF expression in the VMH and support the hypothesis that BDNF is an important effector through which MC4R signaling controls energy balance.
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              Physical activity increases mRNA for brain-derived neurotrophic factor and nerve growth factor in rat brain.

              Brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) support the viability and function of many types of neurons, and are likely mediators of activity-dependent changes in the CNS. We examined BDNF and NGF mRNA levels in several brain areas of adult male rats following 0, 2, 4, or 7 nights with ad libitum access to running wheels. BDNF mRNA was significantly increased in several brain areas, most notably in the hippocampus and caudal 1/3 of cerebral cortex following 2, 4, and 7 nights with exercise. Significant elevations in BDNF mRNA were localized in Ammon's horn areas 1 (CA1) and 4 (CA4) of the hippocampus, and layers II-III of the caudal neocortex and retrosplenial cortex. NGF mRNA was also significantly elevated in the hippocampus and caudal 1/3 of the cortex, affecting primarily the dentate gyrus granular layer (DG) and CA4 of the hippocampus and layers II-III in caudal neocortex.

                Author and article information

                S. Karger AG
                December 2007
                19 March 2007
                : 87
                : 2
                : 65-70
                aDepartment of Neurology and Neurosciences, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, and bGraduate School of Biomedical Sciences, University of Medicine and Dentistry of New Jersey, Newark,N.J., and cNeurology Service, Veterans Administration Medical Center, East Orange, N.J., USA
                100982 Neuroendocrinology 2008;87:65–70
                © 2007 S. Karger AG, Basel

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                Page count
                Figures: 1, References: 65, Pages: 6
                Neuroendocrine Control of Peripheral Metabolic Function


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