Laboratory rodents can be induced to overeat voluntarily when exposed to a choice of highly palatable human foods so-called" cafeteria diet". The hyperphagia of these animals is associated with marked increases in energy expenditure and reduced levels of energetic efficiency. Increases in Diet-Induced-Thermogenesis (DIT) in response to overfeeding have been demonstrated in several species including man. The studies with the cafeteria-fed rats confirm the large potential for DIT in young animals. In older (26-week-old rats) a dramatic decline in the capacity for DIT is observed. Increases in energy expenditure resulting from hyperphagia appear to be mediated by the sympathetic nervous system, which causes activation of heat production in brown adipose tissue (BAT). The high thermogenic potential of BAT is due to the physiological uncoupling of oxidative phosphorylation in the inner mitochondrial membrane. This activity is enhanced by overfeeding, which causes hypertrophy. DIT and BAT are controlled by hormonal action: noradrenaline appears to be the primary activator of BAT and insulin may be required for DIT and may even activate thermogenesis. Other hormones such as glucagon, thyroid, melatonin, TSH, endorphins and sex hormones are also implicated in one way or another in the regulation of energy balance and the control of thermogenesis.