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New Findings: What is the central question of this study? What are the effects of different periods of REM sleep restriction (7, 14 and 21 days) on metabolic parameters in young rats? What is the main finding and its importance? Animals submitted to each period of REM sleep deprivation showed a negative energy balance, with reduced body weight gain, body energy gain and gross food efficiency, less body fat content, and increased energy expenditure. There was no increase in food intake after any of the REM sleep restriction periods. In young rats, negative energy balance is not compensated by increased dietary intake as observed in adult rats., Abstract: Reduced sleep is associated with metabolic alterations, not only in adults, but also in children and adolescents. Several studies have shown that sleep restricted (SR) adult rats exhibit metabolic changes, followed by increased food intake, but few have evaluated these functions in young animals. The aim of the present study was to establish the metabolic parameters of young rats subjected to different periods of REM sleep restriction and to propose a correction factor for the correct measurement of food intake. Young male Wistar rats were distributed in control and SR groups for 7, 14 or 21 days. Sleep restriction was performed by the single platform method for 18 h. Regardless of the length of sleep restriction, all SR rats had a negative energy balance, evidenced by reduction in body weight gain, body energy gain and gross food efficiency, accompanied by increased energy expenditure. In addition, sleep restriction reduced body fat content throughout the entire period. Discounting food spillage, there was no increase in food intake by SR rats. In conclusion, the present study revealed metabolic changes in SR young rats after different lengths of REM sleep restriction and that weight loss and increased energy expenditure were not compensated by increased dietary intake as occurs in adult rats, indicating that young rats use other mechanisms to cope with the negative energy balance caused by sleep restriction. In addition, we propose a correction factor for food intake, to prevent overestimation of this parameter, due to food spillage in the water containers., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

New Findings: What is the central question of this study? Sleep curtailment in infancy and adolescence may lead to long-term risk for obesity, but the mechanisms involved have not yet been determined. This study examined the immediate and long-term metabolic effects produced by sleep restriction in young rats. What is the main finding and its importance? Prolonged sleep restriction reduced weight gain (body fat stores) in young animals. After prolonged recovery, sleep-restricted rats tended to save more energy and to store more fat, possibly owing to increased gross food efficiency. This could be the first step to understand this association. Sleep curtailment is associated with obesity and metabolic changes in adults and children. The aim of the present study was to evaluate the immediate and long-term metabolic alterations produced by sleep restriction in pubertal male rats. Male Wistar rats (28 days old) were allocated to a control (CTL) group or a sleep-restricted (SR) group. This was accomplished by the single platform technique for 18 h per day for 21 days. These groups were subdivided into the following four time points for assessment: sleep restriction and 1, 2 and 4 months of recovery. Body weight and food intake were monitored throughout the experiment. At the end of each time period, blood was collected for metabolic profiling, and the carcasses were processed for measurement of body composition and energy balance. During the period of sleep restriction, SR animals consumed less food in the home cages. This group also displayed lower body weight, body fat, triglycerides and glucose levels than CTL rats. At the end of the first month of recovery, despite eating as much as CTL rats, SR animals showed greater energy and body weight gain, increased gross food efficiency and decreased energy expenditure. At the end of the second and fourth months of recovery, the groups were no longer different, except for energy gain and gross food efficiency, which remained higher in SR animals. In conclusion, sleep restriction affected weight gain of young animals, owing to reduction of fat stores. Two months were sufficient to recover this deficit and to reveal that SR rats tended to save more energy and to store more fat., (© 2015 The Authors. Experimental Physiology © 2015 The Physiological Society.)

Objective: The aim of this study was to evaluate the late effects of maternal obesity induced by lesion of the ventromedial hypothalamus on offspring metabolism., Materials and Methods: Thirty days after the bilateral lesion of the ventromedial hypothalamus, female rats were mated and divided into 2 groups of pregnant animals: Control (C) - false lesion (sham) and Obese (OB) - lesion. Three months after that, with the groups of mothers, offspring were divided into control and obese animals that received a normocaloric diet (C-N and OB-N), and control and obese animals that received a hypercaloric diet (C-H and OB-H). At 120 days of age, the animals were euthanized and their carcasses, feces and food were submitted to calorimetric analysis to determine energy balance and body composition., Results: During the growth period, offspring from obese mothers showed higher values of body weight and food intake than controls. Obese animals showed higher body weight gain and gross food efficiency than control animals in adulthood. The hypercaloric diet led to increased metabolizable energy intake, percentage of absorbed energy and energy expenditure in both groups. Body composition was only affected by the association of hypercaloric diet and maternal obesity that led to increased body fat., Conclusions: Maternal obesity has led to the development of later overweight in offspring, suggesting fetal programming. According to the trend presented, it is believed that the prolonged intake of hypercaloric diets in adult animals may, as an additional effect, induce worsening of the overweight induced by maternal obesity.

The neonatal administration of monosodium glutamate (MSG) to rodents leads to obesity in the adult animal, characterized by increased fat storages. Chronic food restriction is known to induce reduction in body energy expenditure, as an adaptive mechanism to save energy. Our purpose was to examine whether obesity can alter the mechanism of energy conservation in food-restricted animals. Newborn female Wistar rats were injected either MSG (obese) or saline (control). At the age of 90 days, the animals were fed daily ad libitum (control and MSG) or restricted (50%) (control-restricted and MSG-restricted). After 30 days the animals were sacrificed and the energy balance was determined by calorimetric analysis. Some parameters of energy balance and body composition were affected by MSG treatment as well as food restriction. The percent reduction of the energy expenditure and fat content in MSG-restricted animals was lower than control-restricted animals, when compared with their respective ad libitum groups. These results indicate that all food-restricted animals were able to develop the mechanism of energy conservation, regardless of the obesity, but it was less efficient in MSG-obese animals., (2009 S. Karger AG, Basel.)

Aim: Our objective was to verify the energy balance in streptozotocin-induced diabetic rats chronically treated with lipoic acid (LA)., Methods: Diabetes was induced in rats by streptozotocin and the animals divided into four groups, comprising controls and diabetic rats, with each group receiving either daily intraperitoneal LA (30 mg/kg) or a buffer solution for 30 days. Body weight, food intake and stool and urine collections were recorded daily. On day 30, animals were sacrificed and the carcasses, faeces and urine collected and processed for calorimetric analysis. Blood glucose and insulin were also determined., Results: All parameters of energy balance were affected by diabetes. LA treatment reduced weight gain, energy gain and gross food efficiency in both control and diabetic animals. However, the LA-treated animals tended to show higher energy expenditure than non-treated animals. Body composition was also affected by diabetes: fat content was impaired by LA treatment in both control and diabetic animals. The latter also showed increased glycaemia and decreased insulinaemia, but LA had no effect on these parameters., Conclusion: Our results indicate that chronic treatment with LA aggravates energy imbalances in diabetic animals. Moreover, our data suggest the need to reconsider the use of LA as an adjuvant in the prevention and treatment of type 1 diabetes.

Numerous studies indicate that sleep deprivation alters energy expenditure. However, this conclusion is drawn from indirect measurements. In the present study, we investigated alterations of energy expenditure, body composition, blood glucose levels, plasma insulin, adrenocorticotropic hormone (ACTH) and corticosterone levels immediately after 4 days of sleep deprivation or after 4 days of sleep recovery. Rats were sleep deprived or maintained in a control environment (groups sleep-deprived/deprivation and control/deprivation). One half of these animals were sacrificed at the end of the deprivation period and the other half was transported to metabolic cages, where they were allowed to sleep freely (groups sleep-deprived/recovery and control/recovery). At the end of the sleep recovery period, these rats were sacrificed. After sleep deprivation, sleep-deprived rats exhibited loss of body weight, augmented energy expenditure and reduced metabolic efficiency compared to control rats. These alterations were normalised during the sleep recovery period. The body composition of sleep-deprived rats was altered insofar as there was a loss of fat content and gain of protein content in the carcass compared to control rats. However, these alterations were not reversed by sleep recovery. Finally, plasma levels of insulin were reduced during the sleep deprivation period in both control and sleep deprived groups compared to the recovery period. After the deprivation period, plasma ACTH and corticosterone levels were increased in sleep-deprived rats compared to control rats, and although ACTH levels were similar between the groups after the sleep recovery period, corticosterone levels remained elevated in sleep-deprived rats after this period. By means of direct measurements of metabolism, our results showed that sleep deprivation produces increased energy expenditure and loss of fat content. Most of the alterations were reversed by sleep recovery, except for corticosterone levels and body composition.

Objective: To get some additional insight on the mechanisms of the effect of salt intake on body weight., Design and Methods: Rats were fed a low (LSD), normal (NSD), or high (HSD) salt diet. In a first set, body weight, tail-cuff blood pressure, fasting plasma thyroid-stimulating hormone, triiodothyronine, L-thyroxine, glucose, insulin, and angiotensin II were measured. Angiotensin II content was determined in white and brown adipose tissues. Uncoupling protein 1 expression was measured in brown adipose tissue. In a second set, body weight, food intake, energy balance, and plasma leptin were determined. In a third set of rats, motor activity and body weight were evaluated., Results: Blood pressure increased on HSD. Body weight was similar among groups at weaning, but during adulthood it was lower on HSD and higher on LSD. Food intake, L-thyroxine concentration, uncoupling protein 1 expression and energy expenditure were higher in HSD rats, while non-fasting leptin concentration was lower in these groups compared to NSD and LSD animals. Plasma thyroid-stimulating hormone decreased on both HSD and LSD while plasma glucose and insulin were elevated only on LSD. A decrease in plasma angiotensin II was observed in HSD rats. On LSD, an increase in brown adipose tissue angiotensin II content was associated to decreased uncoupling protein 1 expression and energy expenditure. In this group, a low angiotensin II content in white adipose tissue was also found. Motor activity was not influenced by the dietary salt content., Conclusions: Chronic alteration in salt intake is associated with changes in body weight, food intake, hormonal profile, and energy expenditure and tissue angiotensin II content.

Aims: Age can alter energy balance by decreasing the resting metabolic rate. Food restriction can also change energy balance by decreasing energy expenditure as a mechanism of energy conservation. We investigated the influence of food restriction on the energy balance of rats at different ages., Methods: Wistar EPM-1 female rats were used at ages of 3, 9, 15 and 21 months. At each age, two food intake schedules were provided: control (ad libitum) and food restriction (50%). Animals remained under these schedules for 30 days, and throughout this period body weight, food intake, and stool collection were controlled daily. On the 30th day, animals were killed, blood was collected and the carcasses and faeces were processed for analysis by pump calorimetry. Blood glucose, T(3), T(4) and rT(3) levels were determined., Results: Food restriction reduced energy gain and gross food efficiency of animals at different ages, but more so in older animals. Food-restricted rats also had lower energy expenditure than controls. This reduction was about 40% of the energy expenditure of control animals irrespective of age. Water content increased and fat content decreased in the carcass of food-restricted animals. Serum T(3) and T(4) levels were lower in food-restricted animals pointing out to a major role of thyroid hormones in the mechanism of energy conservation exhibited by food-restricted animals., Conclusions: The mechanism of energy conservation takes place in all restricted animals and is very important for survival and for species preservation, mainly in aged animals in which food restriction is frequently aggravated by senescence-related organic disorders.

Pregnancy and diabetes lead to metabolic alterations in the energy balance that may not be completely independent. The objective of the present study was to look at the alterations induced by type 1 diabetes mellitus on the energy balance of pregnant rats and the offspring. Diabetes was induced by streptozotocin injection 15 d before the starting of pregnancy. The rats had their energy balance variables followed for 21 d. Protein, fat and energy content of dams was determined from samples of the carcasses. Pregnancy led to increased energy intake, energy gain and energy expenditure as well as higher gross food efficiency than non-pregnant counterparts. Diabetes increased metabolizable energy intake but not the energy gain of the animals: they had very high energy expenditure, so that diabetes blocked the improvement in gross food efficiency shown during pregnancy. Offspring from diabetic dams were born with lower body weight. Pregnant animals did not present the usual energy storage as seen by lower energy gain of diabetic dams as well as by the lower fat content in the carcasses of pregnant diabetic rats. It is concluded that diabetes impairs the energy variables usually enhanced by pregnancy alone.

Food restriction, even when expressed per unit of metabolic mass, leads to energy conservation as seen by decreased oxygen consumption. The objective of the present study was to verify whether the energy conservation mechanism reduces energy expenditure for as long as food restriction lasts or whether a return to basal level may occur without realimentation, mainly in mildly food-restricted rats. Wistar rats were brought to the laboratory on weaning. They were then assigned to control group that received ad libitum food intake, R10 and R20 groups that received 90 and 80%, respectively, of the food eaten by control group and RM group that received an amount of food enough only to keep body weight. The food restriction period lasted for 3 months and was followed by another month during which all groups received ad libitum food intake. The results showed that even in animals subjected to mild food restriction (10%) there was a sustained decrease in oxygen consumption that lasted until refeeding of the animals. The results led to the conclusion that the energy conservation mechanism is active from little food restriction until more stronger levels of restriction, in a proportional manner, and the decreased energy expenditure is maintained during the whole food restriction period.

The study was performed to investigate possible alterations in oxygen consumption in an animal model with broad intestinal resection. Oxygen consumption and the thermal effect of a short meal were measured in rats subjected to short bowel syndrome. Four groups of rats were used. Group I was the control group, group II was sham operated, group III was submitted to 80% jejunum-ileum resection, and group IV was submitted to 80% jejunum-ileum resection with colon interposition. Ninety days after surgery, oxygen consumption was measured over a period of 6 h with the animals fasted overnight. The thermal effect of feeding was determined in another session of oxygen consumption measurement in animals fasted for 12 h. A 12-kcal meal was then introduced into the animal chamber and oxygen consumption was measured for a further 4 h. No differences in fasting oxygen consumption or in the thermal effect of the meal were detected among the groups studied. It is concluded that short bowel syndrome does not affect the overall energy expenditure of rats.

In pregnant and non-pregnant female rats at various ages the energy balance was determined to study the age-induced alterations in the mother and conceptus. The animals were anesthetized and the conceptus removed and separated into male, female, and placental tissues. The animals were then killed and the carcasses prepared for energy balance determination. The results obtained showed that the older animals gained less energy in the body and had lower gross food efficiency than the younger animals. The number, energy and weight of the offspring were not affected by the mother's age. Nevertheless, due to its constant growth during life, the rat is not the best model to study age-related processes.

Considering that the energy balance can be affected by factors such as pregnancy and food restriction and that the development of foetuses is different during different periods of pregnancy, the aim of this paper was to study the effects on the maternal and offspring energy balance of food restriction imposed at different periods of pregnancy. Pregnant and non-pregnant rats were subjected to four food intake treatments. Control groups received food ad libitum during the 20 days of the experiment. The other three groups were food restricted by receiving 50% of the control group food intake during the first half, the second half, or the whole experimental period. Food restriction imposed during the first half of the experimental period permitted a recuperation of energy intake, but compared to the control group, the rats gained less energy in the body. The offspring parameters studied were not affected by food restriction during the first half of the experimental period. Food restriction during the second half was more deleterious to the dams and to the offspring, which were born with less energy and weight. When food restriction was applied during the whole experimental period, the impairment in energy balance of offspring was similar to the one observed when food restriction occurred during the second half of pregnancy added to a decreased number of offspring. The dams, however, were more deeply affected than when food restriction was applied during the first half of the experimental period.

Energy balance of female rats that were either injected daily with ethanol or received the alcohol by gavage was determined and the results compared with saline animals. Food intake, feces elimination, and body weight were recorded daily. After a 20-day period of treatment the animals were sacrificed and the energy content of the carcasses and feces was determined by bomb calorimetry. The results indicated that ethanol-injected animals underwent an impairment in the energy balance, with losses in body weight and body energy. Also, there was a decrease in metabolized energy intake. The results of a group of saline rats pair-fed to alcohol-injected rats showed that the impairment of the energy balance was not only a consequence of the decreased energy intake, because the ethanol-fed animals had an energy balance that was worse than the one of the pair-fed rats, even though both had eaten the same amount of food. Nevertheless, when alcohol was given by gavage, no alteration in the energy balance parameters was detected. Macroscopic observation of the abdominal cavity showed adherences in the gut of the alcohol-injected animals. It is concluded that the ethanol by itself does not alter the energy balance; however, depending on the route of administration it could indirectly impair the energy balance.

Pregnant and nonpregnant rats were subjected to one of four food intake schedules: ad libitum, 20, 40 and 60% of food restriction, during 20 days, with the objective of studying the distribution of energy between food-restricted mothers and offspring. The animals were anesthetized and the conceptuses were removed and separated into male, female, and placental tissues. The rats were then killed and all carcasses were prepared for energy balance determination. A baseline group of weight-matched rats were killed in the first day of the experiment to evaluate the initial body energy. The results obtained showed that the energy balance of pregnant rats was impaired as a consequence of the food restriction imposed. The offspring from restricted mothers had lower body weight and energy content and were less in number than the ones from the control dams. It is also suggested that food restriction causes the mother to transfer similar percent energy to the offspring as in control animals which will deplete the mother energy stores more than in ad libitum fed rats.

Data from our laboratory have demonstrated that food restriction leads to alterations in energy balance such as reduced energy expenditure as an energy conservation mechanism. Food restriction may be imposed on the animals in different ways. The most common is to give equal daily amounts of restricted food. Alternatively, food may be given once every two or three days so that the food intake is not constant with the animal tending to eat more on the first day and be very restricted during the subsequent days of the period. The former model may elicit habituation to the low food intake while the latter may decrease the habituation stimulus since the food intake is not constant. Energy balance was determined in 3 groups of female rats weighing 206.7 +/- 2.0 g (N = 6 each): control (C), which received food ad libitum; continuously food restricted (CR), which received 8 g of food daily, and intermittently food restricted (IR), which received 24 g of food every 3 days. On the 21st day of treatment, the animals from both food-restricted groups showed a similar reduction of body weight (-47.9 +/- 5.1 and -55.8 +/- 4.0 g for CR and IR, respectively) and body energy (-501.0 +/- 65.5 and -427.0 +/- 82.1 for CR and IR, respectively), and they had similar energy expenditure (2643 +/- 72 and 2518 +/- 97 for CR and IR, respectively) which was different from ad libitum controls (4.6 +/- 2.9 body weight gain, 277.3 +/- 42.5 body energy gain and 4574 +/- 290 energy expenditure). Body weight decreased continuously in the CR group while in the IR group it followed the pattern of food intake with up-and-down shifts. We conclude that the energy balance pattern presented by food-restricted animals is the same regardless of the form of food restriction imposed.

Energy balance of pregnant and non-pregnant female rats was determined after 20 days of gestation. Energy contents of male and female pups and placentae were also determined. The metabolizable energy intake of pregnant rats was 33% higher than that of non-pregnant controls. Body weight gain was 9.4-fold that of non-pregnant rats. Gains in energy and body weight in pregnant rats exceeded those of pups and placentae. This implies that the excess energy was stored, probably for later use in an energy-requiring process such as lactation. Food was processed as expected in pregnant rats, since although gross food efficiency (gain in body energy divided by metabolizable energy intake) was greater in pregnant than in non-pregnant rats (5.4% vs 17.5%), only 53.7% of the extra energy intake was deposited in the dams.