Original Article

International Journal of Obesity (2006) 30, 722–727. doi:10.1038/sj.ijo.0803192; published online 10 January 2006

Differential effects of exercise on body weight gain and adiposity in obesity-prone and -resistant rats

B E Levin1,2 and A A Dunn-Meynell1,2

  1. 1Neurology Service, Veterans Affairs Medical Center, E Orange, NJ, USA
  2. 2Department of Neurosciences, New Jersey Medical School, Newark, NJ, USA

Correspondence: Dr BE Levin, Neurology Service (127C), VA Medical Center, 385 Tremont Ave., E. Orange, NJ 07018-1095, USA. E-mail: levin@umdnj.edu

Received 19 August 2004; Revised 21 February 2005; Accepted 24 February 2005; Published online 10 January 2006.

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Abstract

Objective:

 

To determine the effect of exercise on weight gain and adiposity in obesity-prone and -resistant rats.

Design:

 

Body weight gain, fat pad weights, food intake, plasma leptin and insulin levels were assessed in outbred male Sprague–Dawley rats, which remained sedentary or were given unrestricted access to running wheels either before or after they developed diet-induced obesity (DIO) or diet-resistance (DR) on a high energy (HE; 31% fat) diet.

Results:

 

When fed a low fat (4.5%) chow diet, rats which would later develop DIO (n=6) after 3 weeks on HE diet ran the same amount as DR rats (n=6). Other rats were first made DIO (n=12) or DR (n=12) after 10 weeks on HE diet and then either kept sedentary or given running wheels for 4 weeks on HE diet. DIO and DR rats ran comparable amounts but only the DIO rats reduced their body weight gain, fat pad relative to body weights and plasma leptin levels significantly, compared to their sedentary controls. Exercise had no effect on food intake in either DIO or DR rats but reduced feed efficiency (weight gain/caloric intake) in both.

Conclusion:

 

Although DIO and DR rats ran similar amounts, the greater reduction in body weight gain and adiposity of exercising DIO rats suggests that they are more sensitive to some metabolic or physiologic system that prevents them from increasing their intake sufficiently to compensate for their net reduction in energy stores.

Keywords:

diet-induced obesity, fat pads, insulin, leptin, food intake

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