5 pp. / Recommendations for program planners, parents, teachers, school staff, and health professionals who are concerned about children and weight.

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Obesity is a major health problem that has reached epidemic proportions worldwide. Therapeutic intervention for obesity has proven extremely challenging. Obesity is a complex trait involving the interaction of genes involved in fundamental aspects of weight maintenance, exposure to an environment characterised by an over-abundance of food and sedentary life-style choices with limited physical activity (Poskitt 2009). A marked shift in diet has occurred worldwide (Popkin 2001) with greater saturated fat intake, reduced intake of complex carbohydrates and dietary fibre, and reduced fruit and vegetable intake (WHO 2003). In terms of pharmacological strategies, the current anti-obesity drugs on the market are primarily concerned with reducing appetite or fat absorption in the gut. However, serious side effects have been documented with some of these drugs, including an increased rate of cardiovascular events with Sibutramine use (Curfman et al., 2010). In 2007, the Scottish Medicines Consortium removed Rimonabant from use in the NHS Scotland due to risks of adverse psychiatric events (Burch et al., 2009). However, despite these setbacks, there have been considerable advancements in the treatment of obesity, achieved by combining pharmacological treatments with diet, exercise, behavioral approaches and surgery (gastric band surgery and liposuction). However, the prevalence of obesity continues to increase inexorably, particularly in the Asia Pacific region (Gill 2006; Low et al., 2009), and thus further advancements in obesity treatment are needed, ideally avoiding invasive procedures such as surgery.

Pharmacological blockade of the endocannabinoid system via rimonabant (SR141716) induced a sustained reduction in weight and fatness. Rimonabant-treated mice exhibited reduced metabolizable energy intake and increased daily energy expenditure on days 4-6 of treatment. However, these on the energy budget had disappeared by day 22-24. Rimonabant treatment increased daily physical activity levels throughout the study. These data suggested that rimonabant caused a negative energy balance by acting on both energy intake and expenditure. Melanin-concentrating receptor 1 (MCHR1) antagonism via GW803430 produced similar effects on energy  budget. However, only physical activity during the dark phase was increased by GW803430 treatment. MCHR1 antagonism produced a persistent anti-obesity effect and the initiation of weight loss resulted from a decrease in energy intake and an increase in active energy expenditure. With respect to environmental interventions, non-genetic individual variability in weightgain when fed a high fat diet (HFD) was investigated. I found that weight gain induced by HFD was associated positively with fat mass and fast free mass and negatively with physical activity prior to HFD exposure. Furthermore, fat mass and fat free mass were influenced by lactation litter size via weaning weight and post-weaning growth rate. Finally I used intermittent starvation to test whether the risk of starvation determines the lower intervention point as suggested by the dual intervention pointmodel. Overall, mice exhibited different behavioural and physiological responses to intermittent starvation dependent of the duration of treatment. This work contributes to a better understanding of the regulation of energy balance and provide useful insights for the prevention and treatment of obesity.