Combined effects of cafeteria and tube-feeding on energy balance in the rat.
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Biomedical subjects
Publications and source records attributed to M J Stock.
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Adult male rats were made obese either by tube feeding varying fractions (34%, 47%, 68% or 75%) of their normal food intake or by offering them a varied and palatable diet (cafeteria diet). After 17--30 days of these regimens, the treatments were withdrawn, and the animals were allowed free access to the normal stock diet. Tube-fed animals precisely adjusted voluntary food intake to compensate for the energy delivered by tube but nevertheless became obese as a result of an increased metabolic efficiency. Cafeteria-fed rats were hyperphagic and became obese without any apparent change in metabolic efficiency. Recovery from obesity was more rapid in the cafeteria animals and was due to a pronounced increase in heat production as well as concomitant hypophagia. Animals previously made obese by tube feeding exhibited hypophagia and returned to normal weight without any change in heat production. The relevance of these results to the concept of lipostasis and the relative roles of energy intake and expenditure in the regulation of energy balance are discussed.
Total body water was determined in vivo by tritium dilution in thirty-two male and female rats. Body water obtained by tritium dilution and body fat calculated from this value correlated significantly with body water and fat obtained by analysis (r 0.985, 0.855 respectively). There was no significant difference between values for fat assessed by the direct and indirect methods.
Oxygen consumption was monitored in fed and fasted, lean and obese mice of the ob/ob strain before and after subcutaneous injections of norepinephrine (NE). The increase in oxygen consumption after NE was of a similar magnitude in both lean and obese fed mice, but of a longer duration in the obese. Prior fasting caused a diminution of the response in the lean but was associated with an enhanced response in the obese mice. Fasting also resulted in a significant depression of the resting oxygen consumption of the obese mice but not of the lean. The relevance of these findings to the inability of the obese mouse to withstand cold exposure and to the maintenance of the obese state is discussed.
According to most existing theories, the regulation of energy balance is achieved by control of energy intake. This study was undertaken to find out whether there was control of energy output as well. Food intake, energy balance and the feed efficiency of weanling female mice made obese with injections of gold-thioglucose and monosodium glutamate indicate that the obesity is primarly due to an increased energetic efficiency, and suggest that the hypothalamus plays a role in controlling energy output. In the case of treatment with MSG, a relative obesity was observed, i.e. an increase in body fat without any change in body weight. This indicates that the CNS centres for the regulation of body weight and body fat are probably not the same. It is suggested that MSG obesity will be a suitable model for comparative studies of body weight and the regulation of fat content. It is concluded that chemically induced obesity is due more to a lower metabolic rate than to an elevated food intake.
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Measurements of metabolic rate and the thermic response (specific dynamic action) of a 400-kcal liquid meal were made in six subjects at rest and during light exercise. The tests were conducted before (LA1) and after (LA2) a 3-wk sojourn (HA1, HA2, HA3) at 3,650 m on the Monte Rosa. Fasting metabolic rate at rest increased inittally and then fell, as did fasting and fed exercising metabolic rates. The fall in metabolic rates, but not the initial increases, can be ascribed to the change in body weight. Resting thermic responses at altitude were only slightly lower than normal, although peak values were significantly depressed at HA2 (P less than 0.05). The mean exercising thermic response was also significantly lower at HA2 (P less than 0.05) but recovered in HA3 and LA2. In the time taken for thermic responses to decrease and recover there were interindividual differences that were best explained by the previous altitude experience of the subjects. The possibility of a cardiovascular shift during hypoxic exercise causing depression of postprandial metabolism is discussed.
Measurements of blood glucose and plasma free fatty acids (FFA), thyroxine (T4), free thyroxine (FT4), triiodothyronine (T3), and thyroid-stimulating hormone (TSH) were made on samples taken from fed and fasted human subjects while at rest and immediately after 20 min moderate exercise. Six subjects were studied on successive weeks before (LA1), during (HA1, HA2, HA3), and after (LA2) a 3-wk sojourn at high altitude (3,650 m). The subjects and location were the same as those used for the energy expenditure measurements described in the preceding paper (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 45:345--349, 1978). The most marked effect of altitude was to potentiate the rise in FFA due to exercise. This effect was most noticeable in fed subjects during HA1 and HA2. Changes in the plasma levels of the thyroid hormones correlated with the FFA changes and, once again, exercise at altitude caused the greatest increase in circulating levels. Possible causes of the parallel changes in FFA and thyroid hormone levels and their relationship to changes in energy metabolism are discussed.
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