Evidence for diet-induced thermogenesis in hyperphagic cafeteria-fed rats.

Diet-induced thermogenesis (DIT) is the increase in heat production which follows the ingestion of food or alterations in the plane of nutrition, and therefore includes the energy costs of feeding, digestion and absorption, tissue synthesis and adaptive non-conservative mechanisms. Theoretical and empirically-derived values exist for the energy cost of processing nutrients and tissue synthesis, but the existence and importance of adaptive changes in heat production are more controversial and estimates of the magnitude of this component vary considerably. Evidence that D I T is important in energy balance regulation has been obtained from a number of experiments involving chronic overfeeding of human subjects (for review see Garrow, 1980) and animals maintained on low-protein diets (Miller & Payne, 1962; Lotfi, 1977; Gurr et al. 1980). However, detailed and accurate long-term energy balance studies are difficult to perform in man, and many of the animal experiments could be criticised because of the unphysiological and sometimes bizarre techniques employed to induce hyperphagia. This problem has now largely been overcome by the observation that the rat can be induced to overeat simply by presenting it with a choice of highly palatable food items, a dietary technique known as the ‘cafeteria’ feeding system (Rothwell & Stock, 1 9 7 9 ~ ) . Rats presented with the cafeteria diet overeat by up to 80% compared to controls maintained on a pelleted stock diet, but the effect of this hyperphagia on energy balance and body-weight depends on a number of factors such as age, strain and environmental temperature. Young (weanling) cafeteria-fed rats overeat by about 80% but also show large ( 7 ~ ~ 9 0 % ) increases in energy expenditure and therefore gain little or no excess weight and fat (Rothwell & Stock, 1 9 8 0 ~ ) . Older (6-8 week) animals gain slightly more weight than controls (Rothwell & Stock, 1979b) whereas 6-month-old rats gain weight rapidly (Rothwell & Stock, unpublished results). However, even in the latter group, expenditure was increased by 577’0, and therefore restricted the development of obesity. The levels of hyperphagia and thermogenesis are also dependent on environmental temperature and are much greater in cold environments (Rothwell & Stock, 1980b). It is therefore possible that attempts to induce large changes in energy intake and D I T in thermoneutral environments would be unsuccessful due to inhibitory thermoregulatory influences. In earlier studies on the energy balance of cafeteria-fed rats we have relied on determinations of metabolizable energy (ME) intake from food composition tables, body energy gain from body composition and energy expenditure by difference (i.e. the comparative carcass technique). The errors associated with these methods are