Abstract
Abstract. Using a mouse model long-term selected for high body mass (DU6i), we investigated if their higher degree of body fat as compared to unselected controls (DUKsi) was due to a greater fat accumulation, attributable to differences in substrate oxidation in response to a higher fat intake. We measured energy expenditure (EE) and substrate oxidation by indirect calorimetry at the ages of 42 d and 98 d in response to a fat rich diet compared to a standard diet (F, 20 %; C, 5 % fat) introduced at weaning (21 d). The EE to food energy intake ratio (Q) was calculated and uncoupling protein (UCP1) mRNA expression was analysed in brown adipose tissue in male mice of both strains. The F diet increased body and fat mass in DU6i (P<0.05) but not in DUKsi. Energy intake was not influenced by diet in both strains, but EE was lower in DU6i than in controls (P<0.05). In contrast to DU6i, fat oxidation was higher in DUKsi mice fed the F diet until the age of 42 d (P<0.05). At the age of 42 d, the Q value was lower in DU6i, and higher with F diet irrespective of strain. UCP1 mRNA expression was twice as high in DUKsi as in DU6i (P<0.05). Between 42 d and 98 d of age, DU6i mice were more susceptible to body mass gain and fat deposition in response to the F diet due to insufficient increase in fat oxidation and energy expenditure possibly related to lower UCP1 mRNA expression.
Highlights
Gain in body weight or body fat might be a consequence of increased food intake, a decline in resting metabolic rate or energy expenditure (EE), lower physical activity, and/or a decreased capacity to oxidise fat
One possible mechanism for high EE is the uncoupling of respiration rate from ATP production, which leads to decreased efficiency in food energy utilisation due to an increased expression of uncoupling protein 1 (UCP1), a protein expressed in brown adipose tissue (BAT) (Klaus 1991, Dulloo & Samec 2001)
High fat diets fed to mice have been shown to lead to a higher total energy intake (Lin et al 1979, Rippe et al 2000, Meyer et al 2009)
Summary
Gain in body weight or body fat might be a consequence of increased food intake, a decline in resting metabolic rate or energy expenditure (EE), lower physical activity, and/or a decreased capacity to oxidise fat. Various polygenic models of obesity in mice such as the New Zealand Obese (NZO) mouse (Crofford et al 1965), and other mouse strains display different susceptibility to body fat deposition in response to high fat diets (fat content 40 % and higher) (West et al 1992, Surwit et al 1995, Tschöp et al 2001, Hu et al 2004, Wagener et al 2006) This indicates the presence of a certain genetic background as well as gene-environmental interactions regulating growth and differentiation, which determine whether an individual becomes large or small, lean or fat (Marti et al 2008). It is currently unknown how sensitive this mouse strain is to a diet rich in fat
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