Thermogenesis in response to various intakes of palatable food.

Complete energy balance studies were made on groups of overfed (A) and underfed (B) Wistar rats. In experiment A one group was fed cafeteria diet ad libitum (the intake was 29% larger than the control), two other groups were fed the same diet but in restricted quantities (18 and 9% above control), and a fourth group, fed a stock diet, served as control. In experiment B, caloric intake was restricted by 12 and 31% in two groups fed cafeteria diet, and by 21 and 34% in two other groups fed stock diet. The experiments lasted 41 days and during that period the protein gain was comparable between the control and the cafeteria-29% group (643.4 +/- 33.3 vs. 578.1 +/- 25.0) but the fat gain was significantly different between the two groups (863.2 +/- 81.6 vs. 1663.2 +/- 99.8 kJ). When energy expenditure (EE) (metabolizable energy less storage added to the cost of storage) is expressed as a percentage of metabolizable energy (ME) intake no significant difference was found among the groups. The average value was congruent to 75%. This finding would not support the presence of dietary-induced thermogenesis in animals overfed on the cafeteria diet. However, since the obligatory cost associated with storing energy would not explain the higher EE of the overfed groups, it is suggested that the level of ME intake exerts continuous proportional regulatory action on EE and, as a result, energy is spared by underfeeding and it is wasted by overfeeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of exercise-training in the prevention of hyperinsulinemia caused by high energy diet.

The present study was undertaken to determine whether exercise-training done in combination with feeding a high energy diet could modulate carbohydrate metabolism. Male rats were divided into exercise-trained or sedentary groups that received either a palatable high energy diet or merely standard laboratory diet. After 10 weeks of training, the animals were subjected to an intravenous glucose tolerance test. Body weight, epididymal fat pads, and adipocyte volume were reduced following training. The results also showed that exercise-training protects against deterioration of glucose tolerance produced by high energy diet. Training prevented the elevation of basal as well as glucose challenged insulin levels induced by the high energy diet in spite of a high fat as well as high overall energy intake. A highly significant coefficient of correlation (r = 0.78, P less than 0.01) was observed between the size of adipocytes and the insulin response to glucose load and suggests that the prevention of hyperinsulinemia in rats fed high energy foods while training could be associated with the ability to prevent obesity.

Catecholamines and triiodothyronine variations and the calorigenic response to norepinephrine in cold-adapted and exercise-trained rats.

A comparison was made of the thermogenic response to norepinephrine (NE) in cold-adapted (2 h per day at -15 degrees C for 5 weeks) and in exercise-trained rats (2 h swimming per day for 5 weeks). The oxygen consumption and the plasma catecholamine elevation were comparable for both conditions. Similarly plasma corticosterone determinations indicated comparable elevations in acute stress exposure and reduced responses in both exercise-trained and cold-adapted rats. The marked increase in colonic temperature which was observed in cold-adapted animals injected with NE (30 micrograms/100 g s.c.) was not found in exercise-trained rats. Similarly the brown adipose tissue was double in size in the cold-adapted rats but remained unchanged with exercise training. An important elevation of triiodothyronine (T3) was found in cold-exposed rats, either adapted or not. However, exercise was found to decrease plasma T3 in trained and nontrained rats. The results indicate that swimming for 2 h and exposure to cold (-15 degrees C) for 2 h produced comparable elevation of plasma corticosterone and catecholamine, and of oxygen consumption. However, only the cold-adapted animals develop a NE-induced thermogenesis. It is suggested that thyroid hormones are necessary as permissive factor, in stress-induced thermogenesis.

Effect of diet and exercise on norepinephrine-induced thermogenesis in male and female rats.

Male and female rats were fed standard laboratory chow or a highly palatable diet (cafeteria diet) for 10 wk. The cafeteria diet caused an increase in caloric intake and in body weight, and it induced thermogenesis that was associated with elevated plasma triiodothyronine (T3) levels, increased brown adipose tissue size, and enhanced metabolic response to norepinephrine. For a comparable caloric intake, body-weight gain was significantly greater in female than in male rats possibly because of difference in thermogenesis as suggested by the response to norepinephrine. Exercise training (swimming 2 h/day for 10 wk) reduced food intake and body-weight gain and failed to increase norepinephrine-induced thermogenesis in rats fed laboratory chow. In animals fed the cafeteria diet, food intake and body-weight gain were also reduced by exercise training, which at the same time diminished the diet-induced thermogenesis as evidenced by the diminution of 1) brown fat hypertrophy, 2) the elevation of plasma T3, and 3) the hyperthermic response to injected norepinephrine. It is suggested that the thyroid hormone and catecholamines through their actions on the brown adipose tissue are the important regulatory of thermogenesis. Exercise training would reduce the diet-induced thermogenesis by preventing increased T3 production. Enhanced thermogenesis may be considered an adaptive reaction as it serves to reduce fat deposition in animals fed cafeteria diet and to promote nonshivering heat production in the cold. On the other hand, exercise training reduces thermogenesis and thus prevents energy wasting.

Interactions between dietary obesity and exercise-training on carbohydrate metabolism.

The present study addressed the important question of whether exercise-training could reduce insulin levels in exercise-trained rats made obese by a diet composed of palatable foods. Female rats were divided in exercise-trained or in sedentary groups which receive either a palatable high-energy diet or merely a standard laboratory chow. The high-energy diet was composed of supermarket foods including chocolate chips cookies, pop-corn, bologna, etc. Exercise-training program consisted of forced swimming, 6 d per week, 2 h per d, in water maintained at 36 degrees C. At the end of both fattening and exercise-training program, the animals were subjected to an intravenous glucose tolerance test. The results showed that high-energy diet and exercise-training had opposite effects on both glucose tolerance and insulin secretion: the former impaired glucose tolerance and increased insulin levels, whereas the latter leads to opposite adaptations. In addition, some abnormalities in insulin metabolism persisted in rats simultaneously assigned to exercise-training and high-energy diet. Thus, the present results also suggested that physical training alone could not reduce plasma insulin under control levels, and that a change in energy balance is possibly necessary to achieve this purpose.