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At least 991 records · Page 55Linked to original sources
PubMed2000

Leptin: a possible link between food intake, energy expenditure, and reproductive function.

Several regulatory substances participate in the regulation of both food intake/energy metabolism and reproduction in mammals. Most of these neuropeptides originate and act in the central nervous system, mainly at specific hypothalamic areas. Leptin represents a signal integrating all these functions, but originating from the periphery (adipose tissue) and carrying information mainly to central structures. Observations in rodent models of leptin deficiency have suggested that leptin participates in the control of reproduction, in conjunction with that of food intake and energy expenditure. Indeed, leptin administration resulted in the restoration of normal body weight, food intake, and fertility in the ob mouse, lacking circulating leptin. Specific targets of leptin in the hypothalamus are neurons expressing neuropeptide Y, proopiomelanocortin and gonadotropin-releasing hormone, but the presence of leptin receptors in peripheral reproductive structures suggests that leptin might also act at these sites. Human obesity is often associated with reproductive disturbances. The situation in humans is more complex than in the animal models of leptin deficit and the presence of leptin resistance in these subjects is suggested. In conclusion, leptin fits many requirements for a molecule linking the regulation of energy balance and the control of reproduction.

Animals↗
PubMed1999

The effect of inactivity on dietary intake and energy homeostasis.

Reduced physical activity commonly occurs in patients with disease or chronic disabilities, in the elderly, and in certain patients with obesity. Surprisingly, information on the effect of inactivity on energy homeostasis is scarce and often difficult to interpret. In models of reduced physical activity, such as space flights, bed-rest and confinement, subjects frequently lose weight (< 5%), predominantly in the form of fat-free mass. In some cases this is compensated by an increase in fat mass, which means that changes in weight are poor indicators of energy balance. The extent to which spontaneous reduction in energy intake (in most studies energy intake is fixed) compensates or overcompensates for the reduction in energy expenditure (mainly physical activity and to a small extent in BMR, typically < 6%) is largely underexamined. Preliminary observations suggesting that there is a preferential selection of low-energy-dense foods (low in fat) require confirmation under carefully controlled experimental conditions. It is concluded that a comprehensive and systematic evaluation is needed to address the effects and relevance of various degrees of physical inactivity to energy homeostasis, in relation to disease and space medicine.

Anorexia↗
PubMed1986

Energy intake and body weight in ovo-lacto vegetarians.

Vegetarians have a lower body weight than omnivores. In this study the relationship between the weight/height ratio and food consumption was evaluated in 92 ovo-lacto vegetarians and 113 omnivores in Israel. The average weight of the vegetarians was significantly lower than that of the omnivores (60.8 kg vs. 69.1 kg), even though the vegetarian diet supplied a significantly higher amount of calories than the nonvegetarian diet (3,030.5 cal/day vs. 2,626.8 cal/day). Consumption of fat was similar in both groups. Carbohydrate consumption was higher in the vegetarians while protein consumption was lower. The prevalence of obesity was significantly lower in the vegetarian group (5.4%) as compared to 19.5% among the omnivores. The lower body weight of vegetarians despite a higher caloric intake is of considerable interest.

Adult↗
PubMed2006

Effects of higher dietary protein intake on energy balance and metabolic control in children with long-chain 3-hydroxy acyl-CoA dehydrogenase (LCHAD) or trifunctional protein (TFP) deficiency.

The incidence of overweight and obesity is increasing among children with long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) or mitochondrial trifunctional (TFP) deficiency. Traditional treatment includes fasting avoidance and consumption of a low-fat, high-carbohydrate diet. A diet higher in protein and lower in carbohydrate may help to lower total energy intake while maintaining good metabolic control. To determine the short-term safety and efficacy of a high protein diet, subjects were admitted to the General Clinical Research Center and fed an ad-libitum high-protein diet and a high-carbohydrate diet for 6 days each using a randomized, crossover design. Nine subjects with LCHAD or TFP deficiency, age 7-14 were enrolled. Body composition was determined by DEXA. Total energy intake was evaluated daily. Resting energy expenditure and substrate utilization were determined by indirect calorimetry. Post-prandial metabolic responses of plasma glucose, insulin, leptin, ghrelin, acylcarnitines, and triglyceride were determined in response to a liquid meal. Subjects had a higher fat mass, lower lean mass and higher plasma leptin levels compared to reference values. While on the high protein diet energy consumption was an average of 50 kcals/day lower (p = 0.02) and resting energy expenditure was an average of 170 kcals/day higher (p = 0.05) compared to the high carbohydrate diet. Short-term higher protein diets were safe, well tolerated, and resulted in lowered energy intake and increased energy expenditure than the standard high-carbohydrate diet. Long-term studies are needed to determine whether higher protein diets will reduce the risk of overweight and obesity in children with LCHAD or TFP deficiency.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed2001

Limits to sustained energy intake. IV. Effect of variation in food quality on lactating mice Mus musculus.

Observations were made on 30 MF1 mice with their litters. The animals were fed either normal pelleted mouse food (SDS BP Nutrition Ltd) containing 13.4 kJ x g(-1) digestible energy or a specially formulated diet that provided 25% less digestible energy (9.75 kJ x g(-1)) but equivalent amounts of protein and essential minerals and vitamins per gram as the normal diet. Half the animals were switched to the low-energy diet during early pregnancy and half after parturition. The food intake of the two groups increased enormously following parturition, reaching an asymptote over the last few days of lactation. In both groups, the asymptotic food intake exceeded that previously observed across 71 litters of this strain of mice fed the normal diet throughout pregnancy and lactation; the intake of the group fed the low-energy diet from early lactation significantly exceeded that of the mice switched to the low-energy diet after parturition. The increased intakes of the experimental groups were, however, insufficient to offset the lower digestible energy content of the food during lactation. The body mass of the mothers at the end of lactation did not differ between the two experimental groups and the controls. Offspring mass at weaning was inversely related to litter size, but also did not differ between the three groups; pup mortality did not differ between the experimental and control groups. Behavioural observations showed that during both the dark and light phases the general activity of the mother declined enormously from early pregnancy to late lactation. In the dark phase, the time spent in general activity was replaced by time spent both feeding and resting (suckling young), but in the light phase it was replaced only by feeding. At peak lactation, the mice fed for 30-50% of the dark phase and for 30-40% of the light phase. The data indicate that a previously observed asymptote in food intake during peak lactation at 23 g x day(-1) is unlikely to be a limit mediated centrally by the alimentary tract. A higher central limit may exist, at 26.9 g x day(-1), but this is unlikely to reflect the time available for feeding. The data are consistent with limits on sustainable daily energy intake being mediated by the performance of the mammary glands. Animals appeared to accommodate the demands for milk production within a constrained total energy budget by compensating their behaviour, most notably by reductions in the time spent in 'general activity'.

Animals↗
PubMed1993

Short-term effects of different amounts of sweet and nonsweet carbohydrates on satiety and energy intake.

If a sweet taste sensation increases appetite it can be hypothesized that sweet carbohydrates (CHOs) are less satiating than nonsweet CHOs. We studied this hypothesis in two experiments. In two within-subjects repeated measures experiments, subjects (n = 28 in study 1, n = 29 in study 2) got lunches of varying energy content. There were five energy levels (250, 350, 450, 550, and 650 kcal) in the first experiment, and three energy levels (250, 500, and 750 kcal) in the second experiment. Within each energy level there was one lunch with sweet, and one lunch with nonsweet CHOs. The weight, protein, fat, carbohydrate, and fibre level was kept constant within each energy level. The results of the first study confirmed the hypothesis that sweet CHOs were less satiating than nonsweet CHOs. The results of the second study did not show a difference between the satiating effect of sweet and nonsweet CHOs. There was a strong sensory specific effect in both studies. Sweet CHOs had a suppressing effect on appetite for something sweet, whereas nonsweet CHOs suppressed appetite for something savoury. In the second study, sweet CHOs suppressed the intake of sweet food items in a test meal 2 h later in a dose-response manner. Nonsweet CHOs suppressed the intake of nonsweet food items, also in a dose-response manner. It is concluded that energy (or a food property related to energy) has a strong effect on appetite. The taste had a sensory specific effect on subsequent appetite and food selection.

Adult↗