Abstract
Diet-induced thermogenesis (DIT) is defined as a regulatory, facultative component of energy expenditure, stimulated by overeating, which helps maintain energy balance. DIT may play a central role in the regulation of energy expenditure and in the etiology of certain types of obesity. Most experiments testing the existence or the mechanisms of DIT have used the cafeteria diet for the purposes of stimulating hyperphagia, a requisite for studies of DIT. Yet such a diet is inappropriate for studies of thermogenesis because its use prevents researchers from obtaining an experimental outcome that can be clearly interpreted. The primary limitation of the cafeteria diet is that its nutritional composition is uncontrolled. The diet is self-selected from a variety of supermarket foods that tend to be high in fat and/or carbohydrate and low in protein, vitamins and minerals. Hence, the diets consumed by the animals are likely to be deficient in protein, vitamins or minerals. There is evidence that 1) dietary deficiency of protein, vitamins and minerals can increase thermogenesis and 2) in protein-adequate diets, the balance of fat and carbohydrate in the diet can also influence thermogenesis with high carbohydrate diets increasing thermogenesis more than isoenergetic high fat diets. Hence, an observed increase in thermogenesis in cafeteria fed animals might be interpreted incorrectly to be the result of increased energy consumption when it is attributable to dietary imbalance or deficiency. Because the diet is self-selected, it is possible for each animal to choose a diet that varies in nutritional composition from that selected by every other animal, so control of dietary intake is compromised. Palatable diets of controlled macro- and micronutrient composition are capable of stimulating hyperphagia on the order of 50 to 60%. Thus, the use of the cafeteria diet is both unnecessary and inappropriate.