Childhood obesity: the genetic-environmental interface.

Obesity has a high prevalence in children living in industrialized countries. Excess adiposity is the result of a prolonged positive energy balance. Both genetic and environmental factors are involved. A genetic predisposition to obesity has been ascertained from, for example, twin studies. Animal models of genetic obesity have been used to identify candidate genes, which have, in some cases, also been demonstrated in humans. Genome scanning has highlighted some of the human genes that may be involved. Several environmental factors promote an imbalance between nutrient intake and nutrient oxidation in genetically predisposed children. Fat intake is associated with adiposity in children. The low thermogenesis induced by fat intake is another potential contributory factor. Oxidative activity in skeletal muscles greatly influences total energy expenditure as well as fat oxidation rate. Sedentary behaviour promotes low energy requirements in children. Moreover, low skeletal muscle activity reduces fat oxidation, favouring fat gain. Several socio-economic and cultural factors affect the dietary and physical activity habits of children. Finally, the enlargement of the fat mass induces compensatory metabolic reactions to oppose further fat gain. Further research on the factors responsible for the pathogenesis of obesity is necessary to identify more sensitive targets for the effective prevention and treatment of childhood obesity.