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Rats learned to press a lever for intravenous self-injection of liquid diet during periods of several weeks when oral food was not available. The intakes were low but regulated, and were sufficient to balance energy expenditures at low body weight. Systemic receptors alone are thus adequate to motivate feeding behavior and meter the caloric yield of the intravenous injections.
A model for changes in energy balance and body weight is described which can be written as an iterative computer program. Medium and long-term changes in body weight resulting from random daily fluctuations in energy balance are quantitatively predicted. Body weight varies periodically about a mean value to to the extent of +/- 1 kg over a span of a few weeks. Long-term weight stabilization is the result of a dynamic equilibrium between energy intake and output which depends on activity and tissue metabolism. A lean : fat tissue deposition ratio defines the metabolic type of individual. This ration, which is constant for each individual, governs the proportions in which these tissues are both deposited and mobilized. In the model, the ratio has an important effect on the magnitude and composition of the weight gains resulting from over-eating. It is suggested that the differences in response which have been observed in over-eating experiments result from inter-individual differences in this ratio.
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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This report presents an account of energy balance of young Jamaican children recovering from protein-energy malnutrition (PEM). This was done in three steps. Initially the true gross energy of a formula used in the treatment of PEM was determined by bomb calorimetry. Then its metabolizable energy content was determined in a group of nine children recovering from PEM. In a similar but different group of eight children total daily metabolizable energy intake (EI), average rate of weight gain (g/kg/day) (WG), and total daily energy expenditure (TDEE) were determined. TDEE was determined by indirect calorimetry using a heart rate counter and is based on the relationship of heart rate to oxygen consumption. In this group, the mean EI was 122.5 kcal, WG was 8.4 g, and TDEE was 92 kcal. The difference between EI and TDEE was 30.7 kcal/kg, or 3.3 kcal/g of weight gain. This difference is presumed to be the stored energy in new tissue and corresponds to a proposed new tissue composition of 31% fat and 14% protein. A regression curve comparison of WG versus EI showed that at zero weight gain EI was 85.5 kcal and each additional gain. The difference of 1.0 kcal between total energy cost and stored energy reflects the energy required to deposit new tissue. Gram weight gain required 4.4 kcal. The latter figure is felt to reflect the total energy cost of weight. From three independent measurements, an estimate of maintenance energy requirements was estimated to be about 82 kcal/kg/day.
Since previous saturation dives have caused loss of body weight despite apparently adequate-to-high food intake, a complete study of energy balance was undertaken during the saturation dive Hana Kai II. Over a 30-day period in the hyperbaric chamber (3 days of predive control, 1 day of compression, 16 days at 18.6 ATA, 7 days of decompression, and 3 days of postdive control), all food, urine, and feces for five men were analyzed by bomb calorimetry; 24-h energy expenditure (M) was measured from continuous VO2, VCO2, and urine N. Body weight was taken daily; body composition was assessed from density, total body water, and skinfold thickness. Food intake was high throughout the 30 days (about 3500 kcal/day) while fecal and urinary losses were a normal 6-8% of intake. Energy expenditure was increased a little by the hyperbaric condition, but averaged only 2431 kcal/day for the 30 days and yet there was an average loss of adipose tissue of 0.8 kg for each man for the entire period. Nitrogen balance was positive. There was no evidence of heat gain or loss. The energy balance, total fuel compared with energy expenditure, required an additional 919 kcal/man-day for 30 days, an unidentified term which is not measured by conventional techniques.
An investigation was undertaken of the changes in metabolic energy balance which occur in weightlessness. Daily energy intake was determined each day throughout the 28-, 59-, and 84-day flights for each of the nine Skylab astronauts. The energy content of the urine and feces was also measured. Changes in body composition were inferred from measurements of weight, volume, water, and total exchangeable potassium before and after flight. During flight changes were followed by a daily measurement of body mass and by metabolic balance. Examination of the data reveal losses in body weight during the 1st and 2nd mo of flight, a loss in body water and protein during the 1st mo, and a loss of fat during the 1st, 2nd, and 3rd mo of flight. The energy input was about 41.7 kcal/kg per day on the ground, and 43.7 kcal/kg per day after 3 mo in space. The increase in net energy input of about 1.6% per mo is significant (P less than 0.05). When the net energy input is expressed on the basis of total body potassium, the increase in the resulting "noramlized" net energy input of about 3.7% per mo is also significant (P less than 0.05).
NEFA, total lipids, bilirubin, GOT, acetoacetate and glucose in blood plasma of cows were measured during early lactation. Feeding and yield were also recorded. NEFA and bilirubin values showed a gradual decrease with advancing lactation, while total lipids rose gradually during the first months of lactation. GOT showed no definite trend during early lactation. Acetoacetate values were at maximum 21--30 days post partum and glucose values were high at partus and low during the first weeks of lactation. NEFA were negatively correlated to energy balance during the first month of lactation. Total lipids, bilirubin and GOT seemed not to be dependent on energy balance in cows with normal appetite. NEFA, bilirubin and GOT were significantly elevated in cows with reduced appetite. NEFA were positively correlated to bilirubin, GOT and acetoacetate and negatively correlated to glucose. The correlation coefficients were higher during the first month of lactation than during the second and third month. Cows contracting clinical ketosis showed high values of NEFA a long time before any clinical symptoms appeared. Significantly increased values of acetoacetate occurred only the last days before treatment when plasma glucose had reached low values.
Biomass growth, consumption of carbon and energy source, specific rates of formation of metabolic byproducts, biomass yield referred to the C-source and to oxygen, respiration rate and the value of RQ were studied in Klebsiella aerogenes CCM 2318 (on a synthetic glucose medium) at different specific growth rates. Maintenance coefficients and the total energy balance of the cultivation process were evaluated for a multistage tower fermentor with a defined interstage mixing. The results pointed to changes in both glucose metabolism and the physiological state of the population, brought about by changes in specific growth rate. As compared with a chemostat, the culture was found to exhibit a different physiological character is stages 1 and 4 despite a considerable interstage mixing.
1. Groups of lean and genetically obese (ob/ob) mice were adapted to varying energy intakes and the rates of total protein turnover in liver, gut and kidney were measured. 2. Lean mice gained less weight when fed above maintenance and lost less weight when fed below maintance than obese mice. 3. Hepatic protein turnover (mg/d) was sigmoidally related to digestible energy intake in lean mice but showed no significant changes with dietary intake in obese mice. 4. The changes in protein turnover resulted from changes in both the half-lives of protein synthesis and catabolism and in tissue protein content. 5. In the lean mice, protein turnover in kidney and gut was not significantly changed with increasing energy intake until the highest level was reached. 6. The findings suggest that protein turnover may be an important cycle for the regulation of energy balance in mice and that this cycle is impaired in the genetically obese (ob/ob) mice.
The impact of intraventricular injections of 100 microng of the biogenic amines, norepinephrine or dopamine, upon the energy balance of white leghorn hens Gallus domesticus was examined. Both drugs reduce metabolic heat production (about 35% at 9 and 20 degrees C, and about 15% at 35 degrees C) by inhibiting shivering or by reducing activity or both. Also the drugs inhibit the opposing thermal response, evaporative heat loss (about 3% at 9 and 20 degrees C, and about 20% at 35 degrees C) by reducing respiration rate. The relative balance of inhibiting these opposing responses by the drugs results in hypothermia at 9 and 20 degrees C, and hyperthermia or no change in body temperature at 35 degrees C. Both drugs usually caused an initial vasodilation of the feet and comb at all temperatures tested but did not persist long enough to have much of an impact on body temperature. It was concluded that differing ambient temperatures do not alter the action of the biogenic amines upon the modes of physical thermoregulation in chickens even though the direction of body temperature change is reversed at different ambient temperatures.
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A survey is made of a number of experiments conducted in our laboratory over the last six years. Our working hypothesis assumes that positive energy balance, which should not be prematurely defined as the cause of obesity, is itself caused by disturbances in appetite and satiation control which, given certain environmental conditions, can favour the occurrence of obesity. Three points are considered: (1) The hyperphagic reaction as a response to stress. The experimental findings suggest that the hyperphagic reaction is not primarily a biologically determined phenomenon but rather a learned response. The hyperphagic reaction is found more frequently in female and overweight persons. Most children react to stress with a decrease in food consumption. (2) Disturbances of satiation control. The food intake of obese Ss has a linear time function, whilst children and normal weight adults reveal a biological, negatively accelerated satiation curve. (3) Increased responsiveness to external cues. The concept of externality is extended to include the aspect of an internal-external stimulus discrepancy. The findings show that not only manifest obese Ss but also latent obese Ss are characterized by an increased responsiveness to external cues. In three different experiments with the same Ss it could be demonstrated that externality is to a greater or lesser extent independent of the experimental procedure. Finally, methodological aspects are discussed, because in studies on human appetite the possibility exists that experimental procedure, sample composition and laboratory conditions can exert a direct influence on the results.
Training with low carbohydrate availability (LCA) has been proposed as an independent determinant of physiological perturbations commonly attributed to low energy availability (LEA) and to increase skeletal muscle oxidative machinery, yet the effects of LCA in isolation from LEA remain unclear. We examined whether short-term carbohydrate restriction under energy balance alters endocrine and metabolic markers associated with LEA and skeletal muscle proteomic response. In a randomized crossover design, eight trained males completed 4 days of either a low-carbohydrate high-fat diet (LOW; 12% carbohydrate, 69% fat, 19% protein) or a normal-carbohydrate diet (NORM; 62% carbohydrate, 19% fat, 19% protein), while undertaking daily cycloergometer exercise (15 kcal kg FFM-1 day-1) and maintaining energy availability at 45 kcal kg FFM-1 day-1. LOW induced a clear metabolic shift consistent with LCA, evidenced by elevated circulating free fatty acids, glycerol and β-hydroxybutyrate, in fasting conditions and fat oxidation at rest and during exercise, alongside reduced exercise glucose concentrations. Despite these responses, LOW did not alter insulin, testosterone, triiodothyronine, leptin, hepcidin, or P1NP. In contrast, β-CTX increased and IGF-1 decreased relative to NORM. Muscle glycogen concentration decreased only in LOW (40% ± 14%). Proteomic analysis identified 671 proteins; 57 differentially expressed in LOW relative to NORM were limited to fatty acid metabolism pathways and suppression of ribosomal, sarcomeric, and extracellular matrix proteins. These findings indicate that isolated LCA exerts limited endocrine disruption but may selectively compromise bone turnover and muscle anabolic response, suggesting that without acute LEA, LCA has limited influence on muscle oxidative phenotype.
Adult female chickens were force-fed a corn-soy base diet at 150% of the daily amount consumed by those allowed the same diet ad libitum. Other hens were force-fed diets isocaloric to the 150% group just mentioned, but diet composition was adjusted so that 2/3 of the metabolizable energy (M.E.) came from the corn-soy diet and 1/3 from either corn oil or glucose; or force-fed a low energy diet accounting for 2/3 of the M.E. and corn oil 1/3 of M.E., or a purified diet accounting for all M.E. Fatty liver-hemorrhagic syndrome (FLHS) was induced in all force-fed groups with only the low energy diet plus corn oil having produced a significantly lower score for FLHS. However, the livers from the hens of the latter group had as much lipid, and the hens gained at least as much weight as those in other force-fed groups. During the third week of the experiment M.E. was determined along with a partition of energy among eggs, basal metabolism, body weight gain, and subsistance plus heat increment (H.I). The data showed that the hens force-fed corn oil had lower H.I. values indicative of associative dynamic action of fats at a plane of nutrition above normal. The data revealed that various types of diets and sources of energy in excess can induce FLHS, and this is discussed in terms of FLHS arising out of a positive energy balance.
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.
Neuropeptide SIFamide (SIFa) neurons in Drosophila melanogaster have been characterized by their exceptionally elaborate arborization patterns, which extend from the brain into the ventral nerve cord (VNC). SIFa neurons are equipped to receive signals that integrate both internal physiological cues and external environmental stimuli. These signals enable the neurons to regulate energy balance, sleep patterns, metabolic status, and circadian timing. These peptidergic neurons are instrumental in orchestrating the animal's internal states and refining its behavioral responses, yet the precise molecular underpinnings of this process remain elusive. Here, we demonstrate that SIFa neurons coordinate a range of behavioral responses by selectively integrating inputs and outputs in a context-dependent manner. These neurons engage in a feedback loop with sNPF neurons in the VNC, modifying behaviors such as longer mating duration (LMD) and shorter mating duration (SMD). Additionally, SIFa neurons interact with dopamine and glutamate to differentially regulate sleep and mating duration. Activating SIFa neurons leads to reduced mating duration and increased food intake, while deactivating them reduces food intake. Overall, these findings demonstrate the importance of SIFa neurons in absorbing inputs and turning them into behavioral outputs, shedding light on animal's intricate behavioral orchestration.
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