scholarly journals High leptin in pregnant mink (Mustela vison) may exert anorexigenic effects: a permissive factor for rapid increase in food intake during lactation

2004 ◽  
Vol 91 (3) ◽  
pp. 411-421 ◽  
Author(s):  
Anne-Helene Tauson ◽  
Mats Forsberg ◽  
André Chwalibog
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Heat Production ◽  
Plasma Concentrations ◽  
Negative Energy ◽  
Late Gestation ◽  
Negative Energy Balance ◽  
Food Intake Regulation ◽  
Anorexigenic Effect ◽  
Intake Regulation

The role for leptin in food intake regulation in the mink, a polytocous seasonal breeder with altricial young, was investigated in pregnant and lactating dams and data were related to quantitative energy metabolism measurements and plasma concentrations of other important metabolic hormones. A total of nine mink dams were measured in consecutive 1-week balance periods, each including a 22h measurement of heat production by means of indirect calorimetry, and blood was sampled at weekly intervals throughout gestation and during lactation weeks 1–4. Intake of metabolisable energy (ME) was high and energy balance was positive until the first third of true gestation. During mid- and late gestation ME intake decreased (P<0·001) while heat production remained almost constant, resulting in negative energy balance and the loss of body weight. From late gestation until lactation week 4, ME intake increased by 3·5 times, but weight loss continued. Plasma concentrations of leptin were approximately doubled during the last two-thirds of true gestation (P<0·01), demonstrating a clear gestational hyperleptinaemia. Concentrations declined rapidly after parturition and then remained stable. Insulin was independent of leptin, with low concentrations coincident with hyperleptinaemia. Also, concentrations of thyroid hormones declined during gestation, probably reflecting the low food intake. Hyperleptinaemia concomitant with low ME intake, negative energy balance and mobilisation of body reserves suggested an anorexigenic effect of leptin in pregnant mink. This suppression of food intake in late gestation might be permissive for the rapid increase in food intake occurring after parturition.

scholarly journals Lipoprotein Subclass Profile after Progressive Energy Deficits Induced by Calorie Restriction or Exercise

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1814 ◽  
Author(s):  
Yu Chooi ◽  
Cherlyn Ding ◽  
Zhiling Chan ◽  
Jezebel Lo ◽  
John Choo ◽  
...  
Keyword(s):  
Energy Balance ◽  
Aerobic Exercise ◽  
Calorie Restriction ◽  
Plasma Concentrations ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Energy Deficit ◽  
Dependent Manner ◽  
Blood Lipid Profile ◽  
Diet And Exercise

Weight loss, induced by chronic energy deficit, improves the blood lipid profile. However, the effects of an acute negative energy balance and the comparative efficacy of diet and exercise are not well-established. We determined the effects of progressive, acute energy deficits (20% or 40% of daily energy requirements) induced by a single day of calorie restriction (n = 19) or aerobic exercise (n = 13) in healthy subjects (age: 26 ± 9 years; body mass index (BMI): 21.8 ± 2.9 kg/m2). Fasting plasma concentrations of very low-, intermediate-, low-, and high-density lipoprotein (VLDL, LDL, IDL, and HDL, respectively) particles and their subclasses were determined using nuclear magnetic resonance. Total plasma triglyceride and VLDL-triglyceride concentrations decreased after calorie restriction and exercise (all p ≤ 0.025); the pattern of change was linear with an increasing energy deficit (all p < 0.03), with no evidence of plateauing. The number of circulating large and medium VLDL particles decreased after diet and exercise (all p < 0.015), with no change in small VLDL particles. The concentrations of IDL, LDL, and HDL particles, their relative distributions, and the particle sizes were not altered. Our data indicate that an acute negative energy balance induced by calorie restriction and aerobic exercise reduces triglyceride concentrations in a dose-dependent manner, by decreasing circulating large and medium VLDL particles.

Session 2: Calorie-Cutting Keys

2016 ◽  
pp. 15-26
Author(s):  
Evan M. Forman ◽  
Meghan L. Butryn
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Eating Behavior ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Calorie Intake ◽  
Self Monitoring ◽  
Serving Size ◽  
High Calorie

This chapter (Session 2) discusses the importance of self-monitoring to gain awareness of calorie intake and to recognize patterns in eating behavior. Clients are provided with information on how to self-monitor food intake, including recording type of food, serving size, method of preparation, and time of eating. Strategies for beginning to reduce calories are discussed, such as limiting high-calorie foods in the environment, eating regular meals, and planning meals in advance. The idea of achieving a negative energy balance is introduced, meaning that in order to lose weight, clients must expend a greater amount of energy than they consume in the form of calories.

scholarly journals Metabolic adaptations during negative energy balance and their potential impact on appetite and food intake

2019 ◽  
Vol 78 (3) ◽  
pp. 279-289 ◽  
Author(s):  
Nuno Casanova ◽  
Kristine Beaulieu ◽  
Graham Finlayson ◽  
Mark Hopkins
Keyword(s):  
Weight Loss ◽  
Energy Balance ◽  
Food Intake ◽  
Negative Energy ◽  
Fat Free Mass ◽  
Negative Energy Balance ◽  
Energy Deficit ◽  
Behavioural Responses ◽  
Compensatory Responses ◽  
Metabolic Adaptations

This review examines the metabolic adaptations that occur in response to negative energy balance and their potential putative or functional impact on appetite and food intake. Sustained negative energy balance will result in weight loss, with body composition changes similar for different dietary interventions if total energy and protein intake are equated. During periods of underfeeding, compensatory metabolic and behavioural responses occur that attenuate the prescribed energy deficit. While losses of metabolically active tissue during energy deficit result in reduced energy expenditure, an additional down-regulation in expenditure has been noted that cannot be explained by changes in body tissue (e.g. adaptive thermogenesis). Sustained negative energy balance is also associated with an increase in orexigenic drive and changes in appetite-related peptides during weight loss that may act as cues for increased hunger and food intake. It has also been suggested that losses of fat-free mass (FFM) could also act as an orexigenic signal during weight loss, but more data are needed to support these findings and the signalling pathways linking FFM and energy intake remain unclear. Taken together, these metabolic and behavioural responses to weight loss point to a highly complex and dynamic energy balance system in which perturbations to individual components can cause co-ordinated and inter-related compensatory responses elsewhere. The strength of these compensatory responses is individually subtle, and early identification of this variability may help identify individuals that respond well or poorly to an intervention.

scholarly journals Regulation of serum leptin and its role in the hyperphagia of lactation in the rat

2003 ◽  
Vol 176 (2) ◽  
pp. 193-203 ◽  
Author(s):  
RG Denis ◽  
G Williams ◽  
RG Vernon
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Milk Production ◽  
Litter Size ◽  
High Energy ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Calorie Intake ◽  
Serum Leptin ◽  
Nocturnal Rise

The factors regulating serum leptin concentration and its relationship to the hyperphagia of lactation have been investigated in rats. Lactation results in hypoleptinaemia and loss, or at least marked attenuation, of the nocturnal rise in serum leptin. Litter removal resulted in a fall in food intake and restoration of the nocturnal rise in serum leptin. Returning the litter to the mother after a 48-h absence increased food intake and began to reinitiate milk production, but the nocturnal serum leptin levels were still increased at 48 h after litter restoration. Adjusting litter size to four, eight, ten or fourteen pups at parturition resulted in different rates of litter growth and food intake during the subsequent lactation, but had no effect on the degree of hypoleptinaemia. Reducing litter size from ten to four pups at mid-lactation resulted in a transient increase in both serum leptin and pup growth rate, while food intake fell to a level found in rats suckling four pups throughout lactation. Reducing milk production by injection of bromocriptine increased serum leptin, but did not restore the nocturnal rise in serum leptin; food intake decreased, but remained much higher than in non-lactating rats. Feeding a varied, high-energy diet resulted in a decrease in the weight of food ingested, but no change in calorie intake, and had no effect on the hypoleptinaemia. These studies suggested that the hypoleptinaemia of lactating rats is due to negative energy balance, but the loss of the nocturnal rise in serum leptin is due to the suckling stimulus. The negative energy balance of lactation does not appear to be caused by a physical constraint on food intake. While the hypoleptinaemia should facilitate the hyperphagia of lactation, other orexigenic signals must also be involved.

Relationships between energy balance and health traits of dairy cattle in early lactation

1999 ◽  
Vol 24 ◽  
pp. 171-175 ◽  
Author(s):  
B. L. Collard ◽  
P. J. Boettcher ◽  
J. C. M. Dekkers ◽  
L. R. Schaeffer ◽  
D. Petitclerc
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Total Energy ◽  
Milk Production ◽  
Additive Genetic Variance ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Energy Deficit ◽  
Research Station ◽  
Daily Energy

AbstractData were records of daily food intake and milk production, periodic measures of milk composition and all health and reproductive information from 140 multiparous Holstein cows involved in various experiments at the Agriculture Canada dairy research station in Lennoxville, Quebec. Energy concentrations of the total mixed rations were also available. Daily energy balance was calculated by multiplying the food intake by the concentration of energy in the diet and then subtracting from this quantity the expected (National Research Council) amount of energy required for maintenance (based on parity and body weight) and for milk production (based on yield and concentrations of fat, protein and lactose). Four energy balance traits were defined: (1) average daily energy balance within the first 10 to 100 days of lactation, (2) minimum daily energy balance, (3) days in negative energy balance and (4) total energy deficit during the period of negative energy balance. Health traits were the numbers of incidences of each of the following: (1) all udder problems, (2) mastitis, (3) all locomotive problems, (4) laminitis, (5) digestive problems and (6) reproductive problems. Reproductive traits were the number of days to first observed oestrous and number of inseminations. Phenotypic relationships between energy balance and health were investigated by regressing the energy balance traits on each health trait. Parity and treatment (according to the research trial that the cow was involved with) were also included in the model. Genetic parameters were estimated with restricted maximum likelihood and a model that included effects of parity, treatment and animal. Phenotypically, several significant (P<0.10) relationships between energy balance and health were observed. Cows with longer periods of negative energy balance had increased digestive problems. Cows with greater total energy deficit had more digestive problems and laminitis. Estimates of heritabilities for energy intake and milk energy were 0.42 and 0.12, respectively but estimates of heritability for all energy balance traits were zero. The low estimates for these traits may have been due to (1) low true additive genetic variance, (2) small amount of data, or (3) relatively few genetic ties among cows.

Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation

2010 ◽  
Vol 298 (3) ◽  
pp. E726-E734 ◽  
Author(s):  
Paulo José Forcina Martins ◽  
Marina Soares Marques ◽  
Sergio Tufik ◽  
Vânia D'Almeida
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Sleep Deprivation ◽  
Weight Control ◽  
Time Course ◽  
Energy Homeostasis ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Mrna Levels

Several pieces of evidence support that sleep duration plays a role in body weight control. Nevertheless, it has been assumed that, after the identification of orexins (hypocretins), the molecular basis of the interaction between sleep and energy homeostasis has been provided. However, no study has verified the relationship between neuropeptide Y (NPY) and orexin changes during hyperphagia induced by sleep deprivation. In the current study we aimed to establish the time course of changes in metabolite, endocrine, and hypothalamic neuropeptide expression of Wistar rats sleep deprived by the platform method for a distinct period (from 24 to 96 h) or sleep restricted for 21 days (SR-21d). Despite changes in the stress hormones, we found no changes in food intake and body weight in the SR-21d group. However, sleep-deprived rats had a 25–35% increase in their food intake from 72 h accompanied by slight weight loss. Such changes were associated with increased hypothalamus mRNA levels of prepro-orexin (PPO) at 24 h followed by NPY at 48 h of sleep deprivation. Conversely, sleep recovery reduced the expression of both PPO and NPY, which rapidly brought the animals to a hypophagic condition. Our data also support that sleep deprivation rapidly increases energy expenditure and therefore leads to a negative energy balance and a reduction in liver glycogen and serum triacylglycerol levels despite the hyperphagia. Interestingly, such changes were associated with increased serum levels of glucagon, corticosterone, and norepinephrine, but no effects on leptin, insulin, or ghrelin were observed. In conclusion, orexin activation accounts for the myriad changes induced by sleep deprivation, especially the hyperphagia induced under stress and a negative energy balance.

scholarly journals A Negative Energy Balance Is Associated with Metabolic Dysfunctions in the Hypothalamus of a Humanized Preclinical Model of Alzheimer’s Disease, the 5XFAD Mouse

2021 ◽  
Vol 22 (10) ◽  
pp. 5365
Author(s):  
Antonio J. López-Gambero ◽  
Cristina Rosell-Valle ◽  
Dina Medina-Vera ◽  
Juan Antonio Navarro ◽  
Antonio Vargas ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Mouse Model ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
5Xfad Mouse ◽  
5Xfad Mice ◽  
Metabolic Dysfunctions

Increasing evidence links metabolic disorders with neurodegenerative processes including Alzheimer’s disease (AD). Late AD is associated with amyloid (Aβ) plaque accumulation, neuroinflammation, and central insulin resistance. Here, a humanized AD model, the 5xFAD mouse model, was used to further explore food intake, energy expenditure, neuroinflammation, and neuroendocrine signaling in the hypothalamus. Experiments were performed on 6-month-old male and female full transgenic (Tg5xFAD/5xFAD), heterozygous (Tg5xFAD/-), and non-transgenic (Non-Tg) littermates. Although histological analysis showed absence of Aβ plaques in the hypothalamus of 5xFAD mice, this brain region displayed increased protein levels of GFAP and IBA1 in both Tg5xFAD/- and Tg5xFAD/5xFAD mice and increased expression of IL-1β in Tg5xFAD/5xFAD mice, suggesting neuroinflammation. This condition was accompanied by decreased body weight, food intake, and energy expenditure in both Tg5xFAD/- and Tg5xFAD/5xFAD mice. Negative energy balance was associated with altered circulating levels of insulin, GLP-1, GIP, ghrelin, and resistin; decreased insulin and leptin hypothalamic signaling; dysregulation in main metabolic sensors (phosphorylated IRS1, STAT5, AMPK, mTOR, ERK2); and neuropeptides controlling energy balance (NPY, AgRP, orexin, MCH). These results suggest that glial activation and metabolic dysfunctions in the hypothalamus of a mouse model of AD likely result in negative energy balance, which may contribute to AD pathogenesis development.

Adolescent Inhalant Abuse Results in Adrenal Dysfunction and a Hypermetabolic Phenotype with Persistent Growth Impairments

2018 ◽  
Vol 107 (4) ◽  
pp. 340-354 ◽  
Author(s):  
Rose Crossin ◽  
Zane B. Andrews ◽  
Natalie A. Sims ◽  
Terence Pang ◽  
Michael Mathai ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Adrenal Insufficiency ◽  
Fasting Blood Glucose ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Metabolic Phenotype ◽  
Adolescent Male ◽  
Inhalant Abuse

Background/Aims: Abuse of toluene products (e.g., glue-sniffing) primarily occurs during adolescence and has been associated with appetite suppression and weight impairments. However, the metabolic phenotype arising from adolescent inhalant abuse has never been fully characterised, and its persistence during abstinence and underlying mechanisms remain unknown. Methods: Adolescent male Wistar rats (post-natal day 27) were exposed to inhaled toluene (10,000 ppm) (n = 32) or air (n = 48) for 1 h/day, 3 days/week for 4 weeks, followed by 4 weeks of abstinence. Twenty air rats were pair-fed to the toluene group, to differentiate the direct effects of toluene from under-nutrition. Food intake, weight, and growth were monitored. Metabolic hormones were measured after exposure and abstinence periods. Energy expenditure was measured using indirect calorimetry. Adrenal function was assessed using adrenal histology and hormone testing. Results: Inhalant abuse suppressed appetite and increased energy expenditure. Reduced weight gain and growth were observed in both the toluene and pair-fed groups. Compared to the pair-fed group, and despite normalisation of food intake, the suppression of weight and growth for toluene-exposed rats persisted during abstinence. After exposure, toluene-exposed rats had low fasting blood glucose and insulin compared to the air and pair-fed groups. Consistent with adrenal insufficiency, adrenal hypertrophy and increased basal adrenocorticotropic hormone were observed in the toluene-exposed rats, despite normal basal corticosterone levels. Conclusions: Inhalant abuse results in negative energy balance, persistent growth impairment, and endocrine changes suggestive of adrenal insufficiency. We conclude that adrenal insufficiency contributes to the negative energy balance phenotype, potentially presenting a significant additional health risk for inhalant users.

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