The effect of parasympathetic drugs on energy expenditure: relevance to the autonomic hypothesis

The influence of the parasympathetic nervous system in the control of energy expenditure was investigated in obese and lean rodents during chronic administration of drugs that alter parasympathetic transmission. In the genetically obese ob/ob mice and fa/fa rats and in monosodium glutamate induced hypothalamic obese mice, administration of the parasympathetic inhibitors hyoscine, benztropine, and mecamylamine either had no effect on energy balance or caused losses in body weight that could entirely be accounted for by a reduction in food intake; 24-h oxygen consumption in drug-treated animals was no different from that of the nontreated controls. In the lean animals, both the parasympathetic inhibitors (hyoscine, benztropine, and mecamylamine) and stimulators (bethanecol and neostigmine) had no influence on energy balance nor on body composition. These studies refute the concept that an overactive parasympathetic tone underlies the elevated energetic efficiency of obese models and suggests that the parasympathetic nervous system is unlikely to play an important role in the long-term control of energy expenditure.     

Acutely reduced locomotor activity is a major contributor to Western diet-induced obesity in mice

The aim of the present study was to investigate the short- and long-term effects of a high-fat Western diet (WD) on intake, storage, expenditure, and fecal loss of energy as well as effects on locomotor activity and thermogenesis. WD for only 24 h resulted in a marked physiological shift in energy homeostasis, including increased body weight gain, body fat, and energy expenditure (EE) but an acutely lowered locomotor activity. The acute reduction in locomotor activity was observed after only 3-5 h on WD. The energy intake and energy absorption were increased during the first 24 h, lower after 72 h, and normalized between 7 and 14 days on WD compared with mice given chow diet. Core body temperature and EE was increased between 48 and 72 h but normalized after 21 days on WD. These changes paralleled plasma T(3) levels and uncoupling protein-1 expression in brown adipose tissue. After 21 days of WD, energy intake and absorption, EE, and body temperature were normalized. In contrast, the locomotor activity was reduced and body weight gain was increased over the entire 21-day study period on WD. Calculations based on the correlation between locomotor activity and EE in 2-h intervals at days 21-23 indicated that a large portion of the higher body weight gain in the WD group could be attributed to the reduced locomotor activity. In summary, an acute and persisting decrease in locomotor activity is most important for the effect of WD on body weight gain and obesity in mice.     

Energy balance in exercise-trained rats acclimated at two environmental temperatures

The present study was carried out to investigate the effects of exercise training on energy balance in male rats acclimated at two different environmental temperatures. Sedimentary and exercised rats were housed and trained at either 24 or 4 degrees C, with the training program consisting of running on a motor-driven treadmill within their respective environments. After 45 days, energy, protein, and fat contents of rats were determined together with the energy content of food and feces. The results show that metabolizable energy intake was reduced by 10% in exercise-trained groups. Substantial differences in energy gains were observed between sedentary and trained rats; sedentary rats showed almost three times more energy gain than trained rats. Carcass analysis revealed the energy gain differences to be mainly due to varied amounts of fat deposition. Energy expenditure (kJ) excluding the cost of exercise training was corrected for metabolic body size (BW 0.75), which in turn showed no significant differences between trained rats and their respective sedentary controls. The present results suggested that exercise training in rats leads to neither increase nor decrease in energy expenditure through components additional to physical activity. The present results also indicated that brown adipose tissue thermogenesis, as assessed through mitochondrial guanosine 5'-diphosphate binding, was not significantly modified by exercise training, regardless of the temperature at which the rats were housed and trained.     

The 24-h energy intake of obese adolescents is spontaneously reduced after intensive exercise: a randomized controlled trial in calorimetric chambers

Background

Physical exercise can modify subsequent energy intake and appetite and may thus be of particular interest in terms of obesity treatment. However, it is still unclear whether an intensive bout of exercise can affect the energy consumption of obese children and adolescents.

Objective

To compare the impact of high vs. moderate intensity exercises on subsequent 24-h energy intake, macronutrient preferences, appetite sensations, energy expenditure and balance in obese adolescent.

Design

This randomized cross-over trial involves 15 obese adolescent boys who were asked to randomly complete three 24-h sessions in a metabolic chamber, each separated by at least 7 days: (1) sedentary (SED); (2) Low-Intensity Exercise (LIE) (40% maximal oxygen uptake, VO₂max); (3) High-Intensity Exercise (HIE) (75%VO₂max).

Results

Despite unchanged appetite sensations, 24-h total energy intake following HIE was 6–11% lower compared to LIE and SED (p<0.05), whereas no differences appeared between SED and LIE. Energy intake at lunch was 9.4% and 8.4% lower after HIE compared to SED and LIE, respectively (p<0.05). At dinner time, it was 20.5% and 19.7% lower after HIE compared to SED and LIE, respectively (p<0.01). 24-h energy expenditure was not significantly altered. Thus, the 24-h energy balance was significantly reduced during HIE compared to SED and LIE (p<0.01), whereas those of SED and LIE did not differ.

Conclusions

In obese adolescent boys, HIE has a beneficial impact on 24-h energy balance, mainly due to the spontaneous decrease in energy intake during lunch and dinner following the exercise bout. Prescribing high-intensity exercises to promote weight loss may therefore provide effective results without affecting appetite sensations and, as a result, food frustrations.

Trial Registration

ClinicalTrial.gov {"type":"clinical-trial","attrs":{"text":"NCT01036360","term_id":"NCT01036360"}}NCT01036360     

Characterization of the diurnal rhythm of peptide YY and its association with energy balance parameters in normal-weight premenopausal women

PYY may play a role in modulating satiety and energy expenditure; increasing PYY postprandially has been studied largely in single-meal responses. The diurnal rhythm of PYY and its role in energy balance have not been fully characterized. The purpose of our study was to characterize features of the diurnal rhythm of PYY and determine its role in regulating energy balance. This study was a cross-sectional analysis of 11 subjects in whom 24-h repeated blood sampling was conducted at baseline of a larger prospective study. Breakfast (B), lunch (L), dinner (D), and a snack (S) occurred between 0900 and 1900. Total PYY was assayed every hour from 0800 to 1000, every 20 min from 1000 to 2000, and every hour from 2000 to 0800. PYY variables included total AUC, postprandial peaks, and 24-h mean. Energy balance variables included energy intake, RMR, RQ, and NEAT. PYY postprandial peaks were significantly higher than fasting (P < 0.05). Twenty-four-hour peak PYY occurred after L and was significantly higher than all other peaks (P < 0.05). A cubic curve function accounted for most of the variance in PYY (r(2) = 69.9%, P < 0.01). Fasting PYY (0800) correlated with postprandial peaks at B (r = 0.77, P = 0.01), L (r = 0.71, P = 0.01), and D (r = 0.65, P = 0.03). The only significant association between PYY and energy expenditure was that RMR (kcal/24 h) correlated with 24-h mean PYY (r = 0.71, P = 0.013) and total AUC (r = 0.69, P = 0.019). We conclude that PYY displays a meal-driven diurnal rhythm and is correlated to RMR, a major contributor to energy expenditure. Thus, PYY varies in accordance with energy content and RMR, supporting a role for PYY in energy balance modulation.     

Regulatory alterations of daily energy expenditure induced by fasting or overfeeding in unrestrained rats

The consequences of fasting or overfeeding during 2 days on energy expenditure were investigated by continuously monitoring O2 consumption in unrestrained, unanesthetized rats. O2 consumption decreased by 15% on the 1st day of fasting and then by an additional 15% on the 2nd day. On the 3rd day, when rats were fed again, energy intake increased by 30% above control (prefasting) values, whereas energy expenditure rapidly increased but no more than control values. On the other hand, when ad libitum fed animals were offered a sucrose solution (32%) for 2 days, energy intake increased by 30% and energy expenditure by 9-12%. On the 3rd day, when the rats were fed with their normal diet, energy intake significantly decreased under control (preoverfeeding) values during one day, but energy expenditure rapidly returned to normal values. The results show that fasting decreases, whereas hyperphagia increases 24-h energy expenditure during the treatments. When the treatments are terminated, energy expenditure rapidly returns to normal values, but fasting induces a postfasting increase of energy intake (during 2 days), whereas hyperphagia, on the contrary, results in a transient decrease of appetite. This indicates that alterations of food intake induce compensatory changes of energy expenditure during the treatments, but that after the treatments, energy balance is normalized via regulatory adjustments in the ratio of energy expenditure over energy intake.     

Indirect calorimetry in laboratory mice and rats: principles, practical considerations, interpretation and perspectives

In this article, we review some fundamentals of indirect calorimetry in mice and rats, and open the discussion on several debated aspects of the configuration and tuning of indirect calorimeters. On the particularly contested issue of adjustment of energy expenditure values for body size and body composition, we discuss several of the most used methods and their results when tested on a previously published set of data. We conclude that neither body weight (BW), exponents of BW, nor lean body mass (LBM) are sufficient. The best method involves fitting both LBM and fat mass (FM) as independent variables; for low sample sizes, the model LBM + 0.2 FM can be very effective. We also question the common calorimetry design that consists of measuring respiratory exchanges under free-feeding conditions in several cages simultaneously. This imposes large intervals between measures, and generally limits data analysis to mean 24 h or day-night values of energy expenditure. These are then generally compared with energy intake. However, we consider that, among other limitations, the measurements of Vo(2), Vco(2), and food intake are not precise enough to allow calculation of energy balance in the small 2-5% range that can induce significant long-term alterations of energy balance. In contrast, we suggest that it is necessary to work under conditions in which temperature is set at thermoneutrality, food intake totally controlled, activity precisely measured, and data acquisition performed at very high frequency to give access to the part of the respiratory exchanges that are due to activity. In these conditions, it is possible to quantify basal energy expenditure, energy expenditure associated with muscular work, and response to feeding or to any other metabolic challenge. This reveals defects in the control of energy metabolism that cannot be observed from measurements of total energy expenditure in free feeding individuals.     

Absence of circadian and photoperiodic conservation of energy expenditure in three rodent species

According to a traditional homeostatic view, living beings spend metabolic energy at a constant rate, just like a light bulb spends electrical energy, so that energy expenditure can be expressed in units of watts. However, research conducted during the last half-century has evinced pronounced circadian variation in physiological processes, not only demonstrating circadian rhythmicity in energy expenditure but also raising the hypothesis that energy expenditure may be regulated on a daily (circadian) basis rather than on a constant-rate (homeostatic) basis. In the present study, the hypothesis of circadian (and photoperiodic) conservation of energy expenditure was tested in three rodent species: domestic mice, Nile grass rats, and Syrian hamsters. Two correlates of energy expenditure (running-wheel activity and food intake) and a classic index (oxygen consumption) were used. Changes in energy expenditure were studied in animals maintained under light-dark cycles (LDs) with periods shorter or longer than 24 h as well as in animals maintained under 24-h LDs with short and long photophases. In none of the conditions in any of the species was evidence found in support of the hypothesis of circadian (or photoperiodic) conservation of energy expenditure. Energy expenditure was generally conserved on a homeostatic basis.     

Comparison of heart rate monitoring combined with indirect calorimetry and the doubly labelled water (2H218O) method for the measurement of energy expenditure in children

The aim of the present study was to compare data on 24-h energy expenditure (EE24h) in nine boys and ten girls (mean age 9.3 and 8.1 years, respectively) by heart rates (fc) combined with energy expenditure obtained from a 1-day stay in an indirect calorimeter (EEcal) and a 2-week period of normal living using the doubly labelled water method (EEdlw). Individual calibration curves were derived from fc and oxygen uptake measured during sleep (in the calorimeter), standing and walking on a treadmill. An estimation of energy expenditure based on 24-h fc monitoring (EEfc) was made during the stay in the calorimeter and on a normal school-day. Mean results showed an overestimation in EEfc compared to EEcal and EEdlw of 10.4% and 12.3% respectively, varying from 6.3% to 16.2%. These results confirmed earlier observations in adults that for a group the fc method overestimates EE24h by about 10%.     

Metabolic Determinants of Weight Gain in Humans

One of the fundamental challenges in obesity research is to identify subjects prone to weight gain so that obesity and its comorbidities can be promptly prevented or treated. The principles of thermodynamics as applied to human body energetics demonstrate that susceptibility to weight gain varies among individuals as a result of interindividual differences in energy expenditure and energy intake, two factors that counterbalance one another and determine daily energy balance and, ultimately, body weight change. This review focuses on the variability among individuals in human metabolism that determines weight change. Conflicting results have been reported about the role of interindividual differences in energy metabolism during energy balance in relation to future weight change. However, recent studies have shown that metabolic responses to acute, short‐term dietary interventions that create energy imbalance, such as low‐protein overfeeding or fasting for 24 hours, may reveal the underlying metabolic phenotype that determines the degree of resistance to diet‐induced weight loss or the propensity to spontaneous weight gain over time. Metabolically “thrifty” individuals, characterized by a predilection for saving energy in settings of undernutrition and dietary protein restriction, display a minimal increase in plasma fibroblast growth factor 21 concentrations in response to a low‐protein overfeeding diet and tend to gain more weight over time compared with metabolically “spendthrift” individuals. Similarly, interindividual variability in the causal relationship between energy expenditure and energy intake (“energy sensing”) and in the metabolic response to cold exposure (e.g., brown adipose tissue activation) seems, to some extent, to be indicative of individual propensity to weight gain. Thus, an increased understanding and the clinical characterization of phenotypic differences in energy metabolism among individuals (metabolic profile) may lead to new strategies to prevent weight gain or improve weight‐loss interventions by targeted therapies on the basis of metabolic phenotype and susceptibility to obesity in individual persons.     

Impaired Control of Body Cooling during Heterothermia Represents the Major Energetic Constraint in an Aging Non-Human Primate Exposed to Cold

Daily heterothermia is used by small mammals for energy and water savings, and seems to be preferentially exhibited during winter rather than during summer. This feature induces a trade-off between the energy saved during daily heterothermia and the energy cost of arousal, which can impact energy balance and survival under harsh environmental conditions. Especially, aging may significantly affect such trade off during cold-induced energy stress, but direct evidences are still lacking. We hypothesized that aging could alter the energetics of daily heterothermia, and that the effects could differ according to season. In the gray mouse lemur (Microcebus murinus), a non-human primate species which exhibits daily heterothermia, we investigated the effects of exposures to 25 and 12°C on body composition, energy balance, patterns of heterothermia and water turnover in adult (N = 8) and aged animals (N = 7) acclimated to winter-like or summer-like photoperiods.Acclimation to summer prevented animals from deep heterothermia, even during aging. During winter, adult animals at 12°C and aged animals at 25°C exhibited low levels of energy expenditure with minor modulations of heterothermia. The major effects of cold were observed during winter, and were particularly pronounced in aged mouse lemurs which exhibited deep heterothermia phases. Body composition was not significantly affected by age and could not explain the age-related differences in heterothermia patterns. However, aging was associated with increased levels of energy expenditure during cold exposure, in concomitance with impaired energy balance. Interestingly, increased energy expenditure and depth of heterothermia phases were strongly correlated.In conclusion, it appeared that the exhibition of shallow heterothermia allowed energy savings during winter in adult animals only. Aged animals exhibited deep heterothermia and increased levels of energy expenditure, impairing energy balance. Thus, an impaired control of the heterothermic process induced high energy costs in the aging mouse lemur exposed to cold.     

Metabolic activity in isolated hepatocytes from cold exposed rats subjected to 24-hour fasting.

The aim of this work was to study the metabolic activity in isolated hepatocytes from control rats and rats exposed for 15 or 30 days to cold, all subjected to 24-h fasting. Hepatocyte oxygen consumption was used as an index of metabolic activity. The results show that 24-h fasting induces a decrease in energy expenditure at the level of the liver in cold-exposed rats but not in control animals.     

Mice lacking melanin-concentrating hormone receptor 1 demonstrate increased heart rate associated with altered autonomic activity

Melanin-concentrating hormone (MCH) plays an important role in energy balance. The current studies were carried out on a new line of mice lacking the rodent MCH receptor (MCHR1(-/-) mice). These mice confirmed the previously reported lean phenotype characterized by increased energy expenditure and modestly increased caloric intake. Because MCH is expressed in the lateral hypothalamic area, which also has an important role in the regulation of the autonomic nervous system, heart rate and blood pressure were measured by a telemetric method to investigate whether the increased energy expenditure in these mice might be due to altered autonomic nervous system activity. Male MCHR1(-/-) mice demonstrated a significantly increased heart rate [24-h period: wild type 495 +/- 4 vs. MCHR1(-/-) 561 +/- 8 beats/min (P < 0.001); dark phase: wild type 506 +/- 8 vs. MCHR1(-/-) 582 +/- 9 beats/min (P < 0.001); light phase: wild type 484 +/- 13 vs. MCHR1(-/-) 539 +/- 9 beats/min (P < 0.005)] with no significant difference in mean arterial pressure [wild type 110 +/- 0.3 vs. MCHR1(-/-) 113 +/- 0.4 mmHg (P > 0.05)]. Locomotor activity and core body temperature were higher in the MCHR1(-/-) mice during the dark phase only and thus temporally dissociated from heart rate differences. On fasting, wild-type animals rapidly downregulated body temperature and heart rate. MCHR1(-/-) mice displayed a distinct delay in the onset of this downregulation. To investigate the mechanism underlying these differences, autonomic blockade experiments were carried out. Administration of the adrenergic antagonist metoprolol completely reversed the tachycardia seen in MCHR1(-/-) mice, suggesting an increased sympathetic tone.     

Effect of randomly interesterified triacylglycerols containing medium- and long-chain fatty acids on energy expenditure and hepatic fatty acid metabolism in rats

In our previous studies, medium- and long-chain triacylglycerols (MLCT), randomly interesterified triacylglycerols containing medium-chain and long-chain fatty acids in the same glycerol molecule, significantly reduced body fat accumulation in humans and rats. To clarify mechanism(s) for this effect of MLCT, we measured energy expenditure and hepatic fatty acid metabolism in rats by comparison with long-chain triacylglycerols (LCT) or medium-chain triacylglycerols (MCT). MLCT, compared with LCT, showed significantly lower body fat accumulation, higher 24-h energy expenditure and acyl-CoA dehydrogenase activity measured using octanoyl-CoA as a substrate, and similar lipogenic activity. MCT, compared with LCT, showed significantly higher energy expenditure, but fat accumulation was comparable. Additionally, MCT exhibited significantly higher lipogenic activity than the other oils. These data suggest that enhancement of energy expenditure and medium-chain fatty acids (MCFA) oxidation without activating de novo lipogenesis are responsible at least for the lower body fat accumulation in rats fed MLCT. The activation of hepatic lipogenesis by excessive intake of MCFA might counteract their preventive effects on body fat accumulation.     

Effect of moderate physical activity on plasma leptin concentration in humans

In subjects who maintain a constant body mass, the increased energy expenditure induced by exercise must be compensated by a similar increase in energy intake. Since leptin has been shown to decrease food intake in animals, it can be expected that physical exercise would increase energy intake by lowering plasma leptin concentrations. This effect may be secondary either to exercise-induced negative energy balance or to other effects of exercise. To delineate the effects of moderate physical activity on plasma leptin concentrations, 11 healthy lean subjects (4 men, 7 women) were studied on three occasions over 3 days; in study 1 they consumed an isoenergetic diet (1.3 times resting energy expenditure) over 3 days with no physical activity; in study 2 the subjects received the same diet as in study 1, but they exercised twice daily during the 3 days (cycling at 60 W for 30 min); in study 3 the subjects exercised twice daily during the 3 days, and their energy intake was increased by 18% to cover the extra energy expenditure induced by the physical activity. Fasting plasma leptin concentration (measured on the morning of day 4) was unaltered by exercise [8.64 (SEM 2.22) 7.17 (SEM 1.66), 7.33 (SEM 1.72) 1 microg x l(-1) in studies 1, 2 and 3, respectively]. It was concluded that a moderate physical activity performed over a 3-day period does not alter plasma leptin concentrations, even when energy balance is slightly negative. This argues against a direct effect of physical exercise on plasma leptin concentrations, when body composition is unaltered.     

Changes in 24-h substrate oxidation in older and younger men in response to exercise.

The purpose of this study was to compare 24-h substrate oxidation in older (OM; 60-75 yr, n = 7) and younger (YM; 20-30 yr, n = 7) men studied on sedentary day (Con) and on a day with exercise (Ex; net energy expenditure = 300 kcal). Plasma glucose and free fatty acids were also measured at several time points during the 24-h measurement. Weight was not different in OM and YM (means +/- SD; 84.8 +/- 16.9 vs. 81.4 +/- 10.4 kg, respectively), although percent body fat was slightly higher in OM (25.9 +/- 3.5 vs. 21.9 +/- 9.7%; P = 0.17).Values of 24-h energy expenditure did not differ in OM and YM on the Con (means +/- SE; 2,449 +/- 162 vs. 2,484 +/- 104 kcal/day, respectively) or Ex (2,902 +/- 154 vs. 2,978 +/- 122 kcal/day) days. Under both conditions, 24-h respiratory quotient was significantly lower and fat oxidation significantly higher in OM. Glucose concentrations were not different at any time point, but plasma free fatty acid concentrations were higher in OM, particularly following meals. Thus, under these controlled conditions, 24-h fat oxidation was not reduced and was in fact greater in OM. We speculate that differences in the availability of circulating free fatty acids in the postprandial state contributed to the observed differences in 24-h fat oxidation in OM and YM.     

Impact of leucine on energy balance

Body weight is determined by the balance between energy intake and energy expenditure. When energy intake exceeds energy expenditure, the surplus energy is stored as fat in the adipose tissue, which causes its expansion and may even lead to the development of obesity. Thus, there is a growing interest to develop dietary interventions that could reduce the current obesity epidemic. In this regard, data from a number of in vivo and in vitro studies suggest that the branched-chain amino acid leucine influences energy balance. However, this has not been consistently reported. Here, we review the literature related to the effects of leucine on energy intake, energy expenditure and lipid metabolism as well as its effects on the cellular activity in the brain (hypothalamus) and in peripheral tissues (gastro-intestinal tract, adipose tissue, liver and muscle) regulating the above physiological processes. Moreover, we discuss how obesity may influence the actions of this amino acid.     

Central orexin sensitivity, physical activity, and obesity in diet-induced obese and diet-resistant rats

Nonexercise activity thermogenesis (NEAT), the most variable component of energy expenditure, can account for differential capacities for human weight gain. Also highly variable, spontaneous physical activity (SPA) may similarly affect weight balance in animals. In the following study, we utilized the rat model of obesity, the diet-induced obese (DIO) rat, as well as the diet-resistant (DR) rat strain, to investigate how access to a high-fat diet alters SPA and the associated energy expenditure (i.e., NEAT). DIO and DR rats showed no differences in the amount of SPA before access to the high-fat diet. After 29 days on a high-fat diet, the DIO rats showed significant decreases in SPA, whereas the DR rats did not. Next, we wanted to determine whether the DIO and DR rats showed differential sensitivity to microinjections of orexin into the paraventricular nucleus of the hypothalamus (PVN). Unilateral guide cannulae were implanted, aimed at the PVN. Orexin A (0, 0.125, 0.25, and 1.0 nmol in 500 nl) was microinjected through the guide cannula into the PVN, then SPA and energy expenditure were measured for 2 h. Using the response to vehicle as a baseline, the DR rats showed significantly greater increase in NEAT compared with the DIO rats. These data indicate that diet-induced obesity is associated with decreases in SPA and a lack of increase in NEAT. A putative mechanism for changes in NEAT that accompany obesity is a decreased sensitivity to the NEAT-activating effects of neuropeptides such as orexin.     

Acutely decreased thermoregulatory energy expenditure or decreased activity energy expenditure both acutely reduce food intake in mice

Despite the suggestion that reduced energy expenditure may be a key contributor to the obesity pandemic, few studies have tested whether acutely reduced energy expenditure is associated with a compensatory reduction in food intake. The homeostatic mechanisms that control food intake and energy expenditure remain controversial and are thought to act over days to weeks. We evaluated food intake in mice using two models of acutely decreased energy expenditure: 1) increasing ambient temperature to thermoneutrality in mice acclimated to standard laboratory temperature or 2) exercise cessation in mice accustomed to wheel running. Increasing ambient temperature (from 21°C to 28°C) rapidly decreased energy expenditure, demonstrating that thermoregulatory energy expenditure contributes to both light cycle (40±1%) and dark cycle energy expenditure (15±3%) at normal ambient temperature (21°C). Reducing thermoregulatory energy expenditure acutely decreased food intake primarily during the light cycle (65±7%), thus conflicting with the delayed compensation model, but did not alter spontaneous activity. Acute exercise cessation decreased energy expenditure only during the dark cycle (14±2% at 21°C; 21±4% at 28°C), while food intake was reduced during the dark cycle (0.9±0.1 g) in mice housed at 28°C, but during the light cycle (0.3±0.1 g) in mice housed at 21°C. Cumulatively, there was a strong correlation between the change in daily energy expenditure and the change in daily food intake (R² = 0.51, p<0.01). We conclude that acutely decreased energy expenditure decreases food intake suggesting that energy intake is regulated by metabolic signals that respond rapidly and accurately to reduced energy expenditure.     

Role of thermogenesis in the regulation of energy balance in relation to obesity

Obligatory thermogenesis is a necessary accompaniment of all metabolic processes involved in maintenance of the body in the living state, and occurs in all organs. It includes energy expenditure involved in ingesting, digesting, and processing food (thermic effect of food (TEF]. At certain life stages extra energy expenditure for growth, pregnancy, or lactation would also be obligatory. Facultative thermogenesis is superimposed on obligatory thermogenesis and can be rapidly switched on and rapidly suppressed by the nervous system. Facultative thermogenesis is important in both thermal balance, in which control of thermoregulatory thermogenesis (shivering in muscle, nonshivering in brown adipose tissue (BAT] balances neural control of heat loss mechanisms, and in energy balance, in which control of facultative thermogenesis (exercise-induced in muscle, diet-induced thermogenesis (DIT) in BAT) balances control of energy intake. Thermal balance (i.e., body temperature) is much more stringently controlled than energy balance (i.e., body energy stores). Reduced energy expenditure for thermogenesis is important in two types of obesity in laboratory animals. In the first type, deficient DIT in BAT is a prominent feature of altered energy balance. It may or may not be associated with hyperphagia. In a second type, reduced cold-induced thermogenesis in BAT as well as in other organs is a prominent feature of altered thermal balance. This in turn results in altered energy balance and obesity, exacerbated in some examples by hyperphagia. In some of the hyperphagic obese animals it is likely that the exaggerated obligatory thermic effect of food so alters thermal balance that BAT thermogenesis is suppressed. In all obese animals, deficient hypothalamic control of facultative thermogenesis and (or) food intake is implicated.