[Adaptation of food ingestion to energy expenditure]

Body energy balance is regulated in adults. The accuracy of the phenomenon is particularly evident in laboratory animals under steady conditions. Moreover, it has been repeatedly demonstrated that this balance is maintained in spite of fluctuations in food intake or energy expenditure. When animals such as rats, dogs or rabbits are presented with a diluted or concentrated version of familiar food, they compensate rapidly by increasing or decreasing their ponderal intake. This is achieved first by a change in meal frequency, then meal size adapts to the new caloric content and meal frequency returns to the original pattern. This adaptation is based on the learning of post-ingestive cues. Hypo or hyperphagia leads to reduced or increased energy expenditure, as the case may be; the basal metabolic rate is modulated by thyroid hormones and diet-induced thermogenesis by the sympathetic system. These variations are partly regulatory. In a cold environment, the increase in energy expenditure caused by increased thermogenesis is rapidly compensated by increased caloric intake. Physical activity activates the sympathetic system responsible for numerous hormonal changes, the most important of which is insulin hyposecretion. In animals or humans, moderate aerobic exercise induces a small weight loss; afterwards, weight gain is normalized and increased caloric intake compensates for energy expenditures such as exercise, increased basal metabolic rate and diet-induced thermogenesis. Extreme changes in body weight and fat are produced by gestation and lactation; they are satisfactorily explained by concomitant hormonal changes. Especially during lactation, food intake is regulated so that it allows body weight to return to pregestation level. Studies on the mechanisms implicated in the regulation of body energy balance are still in progress. Friedman and Ramirez (1985) suggest that the way fatty acids are utilized is important. Kasser et al. (1985) show a striking difference in the cellular metabolism of hypothalamic regions, depending on the metabolic state or the animal, and Woods et al. (1985) strongly suggest a role for the central insulin level. These hypotheses are well-documented and not exclusive of each other.