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Am J Physiol Regul Integr Comp Physiol 294: R290-R301, 2008. First published November 7, 2007; doi:10.1152/ajpregu.00661.2007
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APPETITE, OBESITY, DIGESTION, AND METABOLISM

Three weeks of early-onset exercise prolongs obesity resistance in DIO rats after exercise cessation

Christa M. Patterson,1 Ambrose A. Dunn-Meynell,1,2 and Barry E. Levin1,2

1Department of Neurosciences, New Jersey Medical School, Newark; and 2Neurology Service, Veterans Affairs Medical Center, East Orange, New Jersey

Submitted 12 September 2007 ; accepted in final form 1 November 2007

We assessed the effect of early-onset exercise as a means of preventing childhood obesity using juvenile male rats selectively bred to develop diet-induced obesity (DIO) or to be diet resistant (DR) when fed a 31% fat high-energy diet. Voluntary wheel running begun at 36 days of age selectively reduced adiposity in DIO vs. DR rats. Other 4-wk-old DIO rats fed a high-energy diet and exercised (Ex) for 13 wk increased their core temperature, gained 22% less body weight, and had 39% lighter fat pads compared with sedentary (Sed) rats. When wheels were removed after 6 wk (6 wk Ex/7 wk Sed), rats gained less body weight over the next 7 wk than Sed rats and still had comparable adipose pad weights to 13-wk-exercised rats. In fact, only 3 wk of exercise sufficed to prevent obesity for 10 wk after wheel removal. Terminally, the 6-wk-Ex/7-wk-Sed rats had a 55% increase in arcuate nucleus proopiomelanocortin mRNA expression vs. Sed rats, suggesting that this contributed to their sustained obesity resistance. Finally, when Sed rats were calorically restricted for 6 wk to weight match them to Ex rats (6 wk Rstr/7 wk Al), they increased their intake and body weight when fed ad libitum and, after 7 wk more, had higher leptin levels and adiposity than Sed rats. Thus, early-onset exercise may favorably alter, while early caloric restriction may unfavorably influence, the development of the hypothalamic pathways controlling energy homeostasis during brain development.

diet-induced obesity; hypothalamus; caloric restriction; development; leptin; proopiomelanocortin



Address for reprint requests and other correspondence: B. E. Levin, Neurology Service (127C), Veterans Affairs Medical Center, 385 Tremont Ave., East Orange, NJ 07018-1095 (e-mail: levin{at}umdnj.edu)




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