AgResearch Ltd., Department of Nutrition, University of Auckland, Auckland, New Zealand.
Intake Compensates for Resting Metabolic Rate Variation in Female C57BL/6J Mice Fed High-fat Diets
Article first published online: 6 SEP 2012
2007 North American Association for the Study of Obesity (NAASO)
Volume 15, Issue 3, pages 600–606, March 2007
How to Cite
Johnston, S. L., Souter, D. M., Tolkamp, B. J., Gordon, I. J., Illius, A. W., Kyriazakis, I. and Speakman, J. R. (2007), Intake Compensates for Resting Metabolic Rate Variation in Female C57BL/6J Mice Fed High-fat Diets. Obesity, 15: 600–606. doi: 10.1038/oby.2007.550
- Issue published online: 6 SEP 2012
- Article first published online: 6 SEP 2012
- Received for review June 28, 2006, Accepted in final from September 25, 2006
- high-fat diet;
- fat mass;
- mouse models
Objective: The literature is divided over whether variation in resting metabolic rate (RMR) is related to subsequent obesity. We set out to see whether the effect of RMR on weight gain in mice could be revealed with high-fat feeding.
Research Methods and Procedures: Female C57BL/6J mice received a low- (10 kcal%fat n = 47), medium- (45 kcal%fat n = 50), or high-fat diet (60 kcal%fat n = 50) for 12 weeks. Pre-treatment RMR was measured by indirect calorimetry. Body composition was estimated using DXA before and after treatment.
Results: Mice on the high-fat diet gained 39% of body mass, whereas control animals gained 3.5%. There was no interaction between RMR and dietary type on weight gain, and there was no association between weight gain and RMR for any of the treatments. RMR accounted for 2.4% of the variation in pre-treatment food intake corrected for initial body mass; however, the gradient of this relationship indicated that variations in RMR were, on average, compensated for by adjustments in food intake.
Discussion: Individual variations in RMR did not predispose mice to weight gain independent of the dietary treatment. Deviations from the relationship between RMR and food intake were not associated with weight gain. This suggests that variations in energy expenditure, caused by RMR and physical activity, are closely linked to dietary intake, and, therefore, well compensated. Individual variations in the strength of this association may underpin individual variability in the responses to diet.