[Thermogenesis induced by nutrients in man: its role in weight regulation].

The maintenance of body weight at a stable level for an adult man requires the involvement of mechanisms which should adapt energy intake to energy expenditure (or vice versa). Energy balance is thus maintained near equilibrium. However, the nature of these mechanisms is poorly understood. The control of food intake has been studied often and will not be discussed in this presentation. This paper concerns the control of energy expenditure, particularly the control of nutrient-induced thermogenesis. The recent interest in this field has arisen following the demonstration of the role of nutrient-induced thermogenesis in rats and mice having free access to the "cafeteria diet". Under these conditions, these animals overeat, but the major part of the excess energy intake above maintenance, is dissipated as heat through the sympathetic activation of brown adipose tissue. By contrast, a thermogenic defect in brown adipose tissue is involved in the development of genetic or hypothalamic obesity in rats and mice. In man, diet-induced thermogenesis seems to play a smaller role in the control of energy balance than in small mammals. This is probably related to the partial atrophy of brown adipose tissue in adult man. Studies on thermogenesis induced by the intravenous infusion of glucose and insulin (euglycemic hyperinsulinemic clamp technique) in man have allowed us to identify two components: the first, the obligatory thermogenesis is due to the energetic cost of glucose storage (which mainly occurs as glycogen); the second has been called facultative thermogenesis, and is dependent upon stimulation of the sympathetic nervous system. Facultative thermogenesis can be suppressed by propranolol, a drug which blocks the beta-receptors of the sympathetic nervous system. The effector tissue which is responsible for the facultative thermogenesis in man is unknown. Overfeeding studies with carbohydrates in man have also shown the occurrence of facultative thermogenesis. The contribution of a thermogenesis defect to the development of obesity in predisposed individuals is shown by studies using the technique of the respiration chamber. About one third of obese subjects who have been studied in the chamber have shown a decreased postprandial thermogenic response. A thermogenic defect could explain a weight gain of about 10 kg. Other mechanisms which include eating behaviour and low physical activity are needed to explain weight gains greater than 10 kg.(ABSTRACT TRUNCATED AT 400 WORDS)