Degree Name

Master of Science (Research)


Faculty of Health and Behavioural Sciences


Some individuals become obese while others remain lean on a high energy diet. The cause of this susceptibility to the development of diet-induced obesity is still unknown. Variations in energy intake, expenditure and the type of substrate being oxidised, as well as Peptide YY (PYY) system regulation are believed to contribute to differential susceptibility to the development of dietinduced obesity. This project aimed to compare energy balance regulation including energy intake and expenditure, and the PYY system in diet-induced obese (DIO) and diet-resistant (DR) mice. To investigate energy balance this project measured food intake, body mass gain, spontaneous activity, 24h-metabolic rates and body composition in DIO, DR and low-fat-fed (LF) mice. Plasma PYY was measured by radioimmunoassay and its central binding sites (Neuropeptide YY1, 2 & 5 receptors) were measured by quantitative autoradiography. This study has shown that body weight gain was significantly (50%) higher in DIO mice compared to DR and LF mice (F2,32= 101.5, p<0.001). The higher net energy gain in DIO mice was due to their significantly higher food intake compared to DR mice (F2,33=7.79, p=0.002). There were no differences in the metabolic rate, spontaneous activity or type of substrate being oxidized between the DIO and DR mice. The levels of plasma PYY were 32% lower in the DIO mice than in LF mice (p=0.007). PYY and NPY-Y2 receptor binding densities in the DIO mice were significantly higher than DR mice (52% and 24%, respectively) and LF mice (44% and 37%, respectively) at the caudal medulla. Overall, the major contributing factor to diet-induced obesity in this animal model was increased viii energy intake, not a difference in energy expenditure, assimilation efficiency or the substrate types that were oxidized. Reduced plasma PYY in DIO mice may have resulted in the compensatory upregulation of PYY and NPY-Y2 receptor binding density in the caudal medulla. This may contribute at least partially towards the development of diet-induced obesity as this pathway suppresses food intake.

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