Neuroendocrine Control of Peripheral Metabolic Function

Role of Exercise in the Central Regulation of Energy Homeostasis and in the Prevention of Obesity
Christa M. Patterson^{a, b}, Barry E. Levin<sup>a-c

a</sup>Department 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

Address of Corresponding Author

Neuroendocrinology 2008;87:65-70 (DOI: 10.1159/000100982)

  Key Words

• Energy homeostasis, central regulation
• Exercise role, energy homeostasis/obesity prevention
• Obesity prevention

  Abstract

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.

Copyright © 2007 S. Karger AG, Basel

  Author Contacts

Barry E. Levin
Neurology Service (127C), VA Medical Center
385 Tremont Avenue
East Orange, NJ 07018-1095 (USA)
Tel. +1 973 676 1000, ext. 1442, Fax +1 973 395 7112, E-Mail levin@umdnj.edu

  Article Information

Received: February 1, 2007
Accepted: February 12, 2007
Published online: March 19, 2007
Number of Print Pages : 6
Number of Figures : 1, Number of Tables : 0, Number of References : 65