The evidence reviewed here indicates that insulin can increase sympathetically-mediated thermogenesis, probably via its central actions. However, since hypoglycaemia appears to inhibit thermogenesis, the interpretation of data and design of the experiments to study this phenomenon are highly problematic and further confounded by marked changes in insulin sensitivity. This review has purposely concentrated on work performed on experimental animals without directly referring to man. This is because of the very limited number of studies carried out in man, and the fact that difficulties of interpretation discussed above are multiplied many-fold by the limitations of human studies. The evidence to support a role for DIT in energy balance regulation and the importance of brown fat in man has been reviewed elsewhere. A limited number of studies have reported increases in metabolic rate in human subjects infused with glucose and insulin. This response is partially inhibited by the beta-adrenergic antagonist propranolol, and the effects diminished in some grossly obese subjects (e.g. Pima Indians). Landsberg has recently presented and discussed data which indicate that insulin can stimulate thermogenesis in man, and concluded that 'insulin is a major signal that relates dietary intake to sympathetic activity'.