scholarly journals Hypothalamic Structural and Functional Imbalances in Anorexia Nervosa

2019 ◽  
Vol 110 (6) ◽  
pp. 552-562 ◽  
Author(s):  
Vincent Florent ◽  
Marc Baroncini ◽  
Patrice Jissendi-Tchofo ◽  
Renaud Lopes ◽  
Matthieu Vanhoutte ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Energy Balance ◽  
Food Intake ◽  
Treatment Strategies ◽  
Negative Energy ◽  
Normal Weight ◽  
Structural Variations ◽  
Hypothalamic Area ◽  
Physiological Processes ◽  
Maladaptive Response

The hypothalamus contains integrative systems that support life, including physiological processes such as food intake, energy expenditure, and reproduction. Here, we show that anorexia nervosa (AN) patients, contrary to normal weight and constitutionally lean individuals, respond with a paradoxical reduction in hypothalamic levels of glutamate/glutamine (Glx) upon feeding. This reversal of the Glx response is associated with decreased wiring in the arcuate nucleus and increased connectivity in the lateral hypothalamic area, which are involved in the regulation on a variety of physiological and behavioral functions including the control of food intake and energy balance. The identification of distinct hypothalamic neurochemical dysfunctions and associated structural variations in AN paves the way for the development of new diagnostic and treatment strategies in conditions associated with abnormal body mass index and a maladaptive response to negative energy balance.

scholarly journals Hypothalamic neuropeptide expression following chronic food restriction in sedentary and wheel-running rats

2005 ◽  
Vol 35 (2) ◽  
pp. 381-390 ◽  
Author(s):  
C E de Rijke ◽  
J J G Hillebrand ◽  
L A W Verhagen ◽  
T A P Roeling ◽  
R A H Adan
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Mrna Expression ◽  
Food Restriction ◽  
Wheel Running ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Energy Status ◽  
Hypothalamic Area ◽  
Expression Levels

When rats are given access to a running-wheel in combination with food restriction, they will become hyperactive and decrease their food intake, a paradoxical phenomenon known as activity-based anorexia (ABA). Little is known about the regulation of the hypothalamic neuropeptides that are involved in the regulation of food intake and energy balance during the development of ABA. Therefore, rats were killed during the development of ABA, before they entered a state of severe starvation. Neuropeptide mRNA expression levels were analysed using quantitative real-time PCR on punches of separate hypothalamic nuclei. As is expected in a state of negative energy balance, expression levels of agouti-related protein (AgRP) and neuropeptide Y (NPY) were increased 5-fold in the arcuate nucleus (ARC) of food-restricted running ABA rats vs 2-fold in sedentary food-restricted controls. The co-regulated expression of AgRP and NPY strongly correlated with relative body weight and white adipose tissue mass. Arcuate expression of pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART) was reduced 2-fold in the ABA group. In second-order neurons of the lateral hypothalamic area (LHA), melanin-concentrating hormone (MCH) mRNA expression was upregulated 2-fold in food-restricted running rats, but not in food-restricted sedentary controls. Prepro-orexin, CART and corticotropin-releasing hormone expression levels in the LHA and the paraventricular nucleus (PVN) were unchanged in both food-restricted groups. From this study it was concluded that during the development of ABA, neuropeptides in first-order neurons in the ARC and MCH in the LHA are regulated in an adequate response to negative energy balance, whereas expression levels of the other studied neuropeptides in secondary neurons of the LHA and PVN are unchanged and are probably regulated by factors other than energy status alone.

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.

Energy Balance and Reproductive Function in Active Women

2004 ◽  
Vol 29 (1) ◽  
pp. 48-58 ◽  
Author(s):  
Vicki J. Harber
Keyword(s):  
Menstrual Cycle ◽  
Energy Balance ◽  
Training Programs ◽  
Treatment Strategies ◽  
Reproductive Function ◽  
Negative Energy ◽  
Energy Availability ◽  
Menstrual Disorders ◽  
Improve Performance ◽  
Lh Pulsatility

Athletes engaged in rigorous training programs expend large amounts of energy and require appropriate energetic compensation to maintain or improve performance. If these exercise regimens are not fueled sufficiently, a negative energy balance will likely emerge and lead to a broad spectrum of menstrual cycle disturbances and less than optimal performance. This review examines the theory and evidence surrounding energy availability and reproductive function. Implications for performance and treatment strategies are also addressed. Key words: energy intake, energy expenditure, energy availability, menstrual disorders, LH pulsatility, amenorrhea

Eating Disorders: Implications for the 1990's*

1987 ◽  
Vol 32 (7) ◽  
pp. 624-631 ◽  
Author(s):  
Paul E. Garfinkel ◽  
David M. Garner ◽  
David S. Goldbloom
Keyword(s):  
Eating Disorders ◽  
Anorexia Nervosa ◽  
Bulimia Nervosa ◽  
Treatment Strategies ◽  
Risk Groups ◽  
Normal Weight ◽  
Stepped Care ◽  
Endogenous Opiates ◽  
Populations At Risk ◽  
The Relationship

In the past decade much has been learned about the clinical features, diagnosis and understanding of people with anorexia nervosa and bulimia nervosa. In order to provide the next level of improvement in our care for these patients, our understanding of certain problems must be addressed by empirical research. Areas which require further study include the definition of high risk groups, the refinement of diagnoses, understanding factors which result in chronicity, determining the complications of chronicity and comparative evaluations of different treatments. These five areas are outlined in this article. Populations at risk for anorexia nervosa and bulimia nervosa may be those who must be thin and achieve according to career choice, those with a particular family and personal psychiatric history; obesity and chronic medical illnesses may be further risks. Improved diagnostic understanding has occurred by the differentiation of bulimic from restricting subtypes of anorexia nervosa. Further work must determine the relationship between the bulimic subtype of anorexia nervosa and bulimia in normal weight women and to further clarify the relationship between eating disorders and affective disorders. A number of factors may result in a chronic illness. These have been described on a variety of levels. The consequences of starvation in altering an individual's thinking, feeling and behaviour do play a role. It is not clear what factors at a neurochemical level contribute to this. Elevated endogenous opiates decreased noradrenergic function and decreased serotonin may be important. Information about the chronic complications is required for clinicians to understand the broad range of difficulties that may develop over time so that clinicians may use this information in planning treatment strategies. Two examples, those of osteoporosis and the pregnant woman with an eating disorder, highlight this problem. Finally, treatment is briefly reviewed in terms of options available and the idea of developing a stepped-care approach to treatment.

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.

Peripheral and Central Glucocorticoid Signaling Contributes to Positive Energy Balance in Rats

2017 ◽  
Vol 49 (06) ◽  
pp. 472-479
Author(s):  
Tássia Borba ◽  
Lígia Galindo ◽  
Kelli Ferraz-Pereira ◽  
Raquel da Silva Aragão ◽  
Ana Toscano ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Glucocorticoid Receptors ◽  
Negative Energy ◽  
Positive Energy ◽  
Obesity Epidemic ◽  
Routes Of Administration ◽  
Glucocorticoid Signaling ◽  
Positive Energy Balance

AbstractThe obesity epidemic has been the target of several studies to understand its etiology. The pathophysiological processes that take to obesity generally relate to the rupture of energy balance. This imbalance can result from environmental and/or endogenous events. Among the endogenous events, the hypothalamic-pituitary-adrenal axis, which promotes stress response via glucocorticoid activity, is considered a modulator of energy balance. However, it remains controversial whether the increase in plasma levels of glucocorticoids results in a positive or negative energy balance. Furthermore, there are no studies comparing different routes of administration of glucocorticoids in this context. Here, we investigated the effects of intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) administration of a specific agonist for glucocorticoid receptors on food intake and energy expenditure in rats. Sixty-day old rats were treated with i.p. or i.c.v. dexamethasone. Food intake and satiety were evaluated, as well as locomotor activity in order to determine energy expenditure. Both i.p. and i.c.v. dexamethasone increased food intake and decreased energy expenditure. Moreover, i.c.v. dexamethasone delayed the onset of satiety. Together, these results confirm that central glucocorticoid signaling promotes a positive energy balance and supports the role of the glucocorticoid system as the underlying cause of psychological stress-induced obesity.

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.

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