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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Palatable food is rich in fat and/or sucrose. In this study we examined the long-term effects of such diets on food intake, body weight, adiposity and circulating levels of the satiety peptide leptin and the hunger peptide ghrelin. The experiments involved rats and mice and lasted 5 weeks. In rats, we examined the effect of diets rich in fat and/or sucrose and in mice the effect of a high fat diet with or without sucrose in the drinking water. Animals fed with the palatable diets had a larger intake of calories, gained more weight and became more adipose than animals fed standard rat chow. Fasted animals are known to have low serum leptin and high serum ghrelin and to display elevated serum leptin and lowered serum ghrelin postprandially. With time, a sucrose-rich diet was found to raise the fasting level of leptin and to lower the fasting level of ghrelin in rats. A fat-rich diet suppressed serum ghrelin without affecting serum leptin; high sucrose and high fat in combination greatly reduced serum ghrelin and raised serum leptin in the fasted state. The mRNA expression of leptin in the rat stomach was up-regulated by sucrose-rich (but not by fat-rich) diets, whereas the expression of ghrelin seemed not to be affected by the palatable diets. Mice responded to sucrose in the drinking water with elevated serum leptin (fasted state) and to all palatable diets with low serum ghrelin. The expression of both leptin and ghrelin mRNA in the stomach was suppressed in fasted mice that had received a high fat diet for 5 weeks. We conclude that the expression of leptin mRNA in stomach and the concentration of leptin in serum were elevated in response to sucrose-rich rather than fat-rich diets, linking leptin with sucrose metabolism. In contrast, the expression of ghrelin and the serum ghrelin concentration were suppressed by all palatable diets, sucrose and fat alike. In view of the increased body weight and adiposity neither elevated leptin nor suppressed ghrelin were able to control/restrain the overeating that is associated with palatable diets.
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PMID:Overeating of palatable food is associated with blunted leptin and ghrelin responses. 1596 41

Chronic sleep loss as a consequence of voluntary bedtime restriction is an endemic condition in modern society. Although sleep exerts marked modulatory effects on glucose metabolism, and molecular mechanisms for the interaction between sleeping and feeding have been documented, the potential impact of recurrent sleep curtailment on the risk for diabetes and obesity has only recently been investigated. In laboratory studies of healthy young adults submitted to recurrent partial sleep restriction, marked alterations in glucose metabolism including decreased glucose tolerance and insulin sensitivity have been demonstrated. The neuroendocrine regulation of appetite was also affected as the levels of the anorexigenic hormone leptin were decreased, whereas the levels of the orexigenic factor ghrelin were increased. Importantly, these neuroendocrine abnormalities were correlated with increased hunger and appetite, which may lead to overeating and weight gain. Consistent with these laboratory findings, a growing body of epidemiological evidence supports an association between short sleep duration and the risk for obesity and diabetes. Chronic sleep loss may also be the consequence of pathological conditions such as sleep-disordered breathing. In this increasingly prevalent syndrome, a feedforward cascade of negative events generated by sleep loss, sleep fragmentation, and hypoxia are likely to exacerbate the severity of metabolic disturbances. In conclusion, chronic sleep loss, behavioral or sleep disorder related, may represent a novel risk factor for weight gain, insulin resistance, and Type 2 diabetes.
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PMID:Sleep loss: a novel risk factor for insulin resistance and Type 2 diabetes. 1622 62

Hunger and satiety have conventionally provided the framework for understanding eating and overeating. We argue that hunger and satiety play a relatively small role in everyday eating. The normative control of food intake refers to the fact that our eating is largely governed by the motive to avoid eating excessively. Dieters impose a restrictive intake norm on themselves, but often violate the norm. Personal norms are individualized rules that people develop to help themselves decide how much is appropriate to eat in a given situation. Situational norms are derived from the eating situation itself; examples include portion size and social influence, which exert powerful effects on intake. We discuss the implications of a normative approach to the analysis of eating and overeating.
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PMID:Normative influences on food intake. 1624 66

The authors compared eating patterns, disordered eating, features of eating disorders, and depressive symptoms in persons with binge eating disorder (BED; n = 177), with night eating syndrome (NES; n = 68), and in an overweight comparison group without BED or NES (comparison; n = 45). Participants completed semistructured interviews and several established measures. Depressive symptoms were greater in the BED and NES groups than in the comparison group. NES participants ate fewer meals during the day and more during the night than BED and comparison participants, whereas BED participants ate more during the day than the comparison participants. BED participants reported more objective bulimic and overeating episodes, shape/weight concerns, disinhibition, and hunger than NES and comparison participants, whereas NES participants reported more eating pathology than comparison participants. This evaluation provides strong evidence for the distinctiveness of the BED and NES constructs and highlights their clinical significance.
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PMID:Binge eating disorder and night eating syndrome: a comparative study of disordered eating. 1639 84

Obesity is a major global epidemic, with over 300 million obese people worldwide, and nearly 1 billion overweight adults. Being overweight carries significant health risks, reduced quality of life, and impaired socioeconomic success, with profound consequences for health expenditure. The most successful treatment for obesity is gastric bypass surgery, which acts in part by reducing appetite through alterations in gut hormones. Circulating gut hormones, secreted or suppressed after eating food, act in the brain, particularly the hypothalamus, to alter hunger and fullness. Stomach-derived ghrelin increases food intake even in those with anorexia from chronic illness, while pancreatic polypeptide (PP), intestinal peptide YY 3-36 (PYY), oxyntomodulin, and other hormones reduce food intake and appetite. While obese subjects have appropriate reductions in orexigenic ghrelin, other gut-hormone disturbances may contribute to obesity such as reduced anorexigenic PYY and PP. Prader-Willi syndrome (PWS) arises from the loss of paternally inherited genes on chromosome 15q11-13, leading to life-threatening insatiable hunger and obesity from early childhood, through developmental brain, particularly hypothalamic defects. The study of genetically homogenous causes of abnormal-feeding behavior helps our understanding of appetite regulation. PWS subjects have inappropriately elevated plasma ghrelin for their obesity, at least partly explained by preserved insulin sensitivity. It remains unproven if their hyperghrelinemia or other gut-hormone abnormalities contribute to the hyperphagia in PWS, in addition to brain defects. Postmortem human hypothalamic studies and generation of animal models of PWS can also provide insight into the pathophysiology of abnormal-feeding behavior. Changes in orexigenic NPY and AGRP hypothalamic neurons, or anorexigenic oxytocin neurons have been found in illness and PWS. Functional neuroimaging studies, using PET and fMRI, will also allow us to tease apart the hormonal and brain pathways responsible for controlling human appetite, and their defects in obesity.
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PMID:The hypothalamus, hormones, and hunger: alterations in human obesity and illness. 1687 68

Two experiments explored the hypothesis that distraction causes a reduced sensitivity to the physiological and sensory cues that signal when to terminate a meal. In Experiment 1, eighty-eight females ate five 'Jaffa Cakes' either while distracted by a computer game or while sitting in silence. Analysis of the difference in rated hunger, fullness and desire to eat (pre- to post-intake) revealed that distracted participants experienced smaller changes in their desire to eat and fullness than did non-distracted participants. Experiment 2 assessed whether changes in ratings are attenuated because sensory-specific satiety (or a related process) fails to develop. Using a similar procedure, eighty-four females provided desire to eat, pleasantness and intensity ratings for Jaffa Cakes and for two 'uneaten' foods, both before and at three time-points after consuming five Jaffa Cakes. Non-distracted participants reported a reduction in their desire to eat the eaten food relative to the uneaten food (food-specific satiety), whereas distracted participants maintained a desire to eat all foods. Moreover, this difference between distracted and non-distracted participants was evident 5 and 10 min after the eating episode had terminated. The present findings invite speculation that distraction attenuates the development of sensory-specific satiety, and that this effect persists (at least for a brief period) after the distractor has terminated. More generally, this kind of phenomenon warrants further scrutiny because it holds the potential to contribute towards overeating, either by prolonging an eating episode or by reducing the interval between meals.
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PMID:Effects of distraction on the development of satiety. 1701 Feb 37

Complementary neurophysiological recordings in rhesus macaques (Macaca mulatta) and functional neuroimaging in human subjects show that the primary taste cortex in the rostral insula and adjoining frontal operculum provides separate and combined representations of the taste, temperature and texture (including viscosity and fat texture) of food in the mouth independently of hunger and thus of reward value and pleasantness. One synapse on, in the orbitofrontal cortex, these sensory inputs are for some neurons combined by learning with olfactory and visual inputs. Different neurons respond to different combinations, providing a rich representation of the sensory properties of food. In the orbitofrontal cortex feeding to satiety with one food decreases the responses of these neurons to that food, but not to other foods, showing that sensory-specific satiety is computed in the primate (including the human) orbitofrontal cortex. Consistently, activation of parts of the human orbitofrontal cortex correlates with subjective ratings of the pleasantness of the taste and smell of food. Cognitive factors, such as a word label presented with an odour, influence the pleasantness of the odour, and the activation produced by the odour in the orbitofrontal cortex. Food intake is thus controlled by building a multimodal representation of the sensory properties of food in the orbitofrontal cortex and gating this representation by satiety signals to produce a representation of the pleasantness or reward value of food that drives food intake. Factors that lead this system to become unbalanced and contribute to overeating and obesity are described.
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PMID:Sensory processing in the brain related to the control of food intake. 1734 76

To better understand the relation between emotional eating and dietary choices, dietary correlates of emotional eating were investigated in an adolescent sample. Participants were 617 predominantly Latino middle school students from seven schools in Los Angeles County. Analyses of cross-sectional data revealed that emotional eating was associated with increased frequency of intake of sweet high energy-dense foods, such as cake and ice cream, salty high energy-dense foods like chips, and soda. Gender stratified analyses revealed an association between emotional eating and more frequent fruit and vegetable intake in boys only, and a positive association between emotional eating and salty high energy-dense intake in both boys and girls. These data support previous literature that reports a preference for high energy-dense food in emotional eating, and shows that this association may be generalizable to Latino youth. Considering that emotional eating may lead to overeating because it often takes place in the absence of hunger, it may be appropriate to develop interventions to teach youth healthier substitutions and regulate mood by means other than eating in order to reduce risk for obesity, especially in high risk populations, such as Latinos.
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PMID:Dietary correlates of emotional eating in adolescence. 1746 8

The neural systems regulating food intake in obese individuals remain poorly understood. Previous studies applied positron emission tomography and manipulated hunger and satiety to investigate differences in appetitive processing between obese and normal-weight individuals. However, it is not known whether manipulation of stimulus value may yield different neural activity in obese as compared to control subjects when intrinsic physiological states are kept constant. We used functional magnetic resonance imaging to investigate 13 obese and 13 normal-weight subjects and manipulated food motivation by presenting visual food stimuli differing in their caloric content and energy density. In contrast to controls, obese women selectively activated the dorsal striatum while viewing high-caloric foods. Moreover, in the high-calorie condition body mass index (BMI) predicted activation in the dorsal striatum, anterior insula, claustrum, posterior cingulate, postcentral and lateral orbitofrontal cortex. The results indicate that in obese individuals simple visual stimulation with food stimuli activates regions related to reward anticipation and habit learning (dorsal striatum). Additionally, high-calorie food images yielded BMI-dependent activations in regions associated with taste information processing (anterior insula and lateral orbitofrontal cortex), motivation (orbitofrontal cortex), emotion as well as memory functions (posterior cingulate). Collectively, the results suggest that the observed activation is independent of the physiological states of hunger and satiation, and thus may contribute to pathological overeating and obesity. Some of the observed activations (dorsal striatum, orbitofrontal cortex) are likely to be dopamine-mediated.
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PMID:Differential activation of the dorsal striatum by high-calorie visual food stimuli in obese individuals. 1756 68

Ghrelin is produced primarily in the stomach in response to hunger, and circulates in the blood. Plasma ghrelin levels increase during fasting and decrease after ingesting glucose and lipid, but not protein. The efferent vagus nerve contributes to the fasting-induced increase in ghrelin secretion. Ghrelin secreted by the stomach stimulates the afferent vagus nerve and promotes food intake. Ghrelin also stimulates pituitary gland secretion of growth hormone (GH) via the afferent vagus nerve. GH inhibits stomach ghrelin secretion. These findings indicate that the vagal circuit between the central nervous system and stomach has a crucial role in regulating plasma ghrelin levels. Moreover, body mass index modulates plasma ghrelin levels. In a lean state and anorexia nervosa, plasma ghrelin levels are increased, whereas in obesity, except in Prader-Willi syndrome, plasma ghrelin levels are decreased and the feeding- and sleeping-induced decline in plasma ghrelin levels is disrupted. There are two forms of ghrelin: active n-octanoyl-modified ghrelin and des-acyl ghrelin. Fasting increases both ghrelin types compared with the fed state. Hyperphagia and obesity are likely to decrease plasma des-acyl ghrelin, but not n-octanoyl-modified ghrelin levels. Hypothalamic serum and glucocorticoid-inducible kinase-1 and serotonin 5-HT2C/1B receptor gene expression levels are likely to be proportional to plasma des-acyl ghrelin levels during fasting, whereas they are likely to be inversely proportional to plasma des-acyl ghrelin levels in an increased energy storage state such as obesity. Thus, a dysfunction of the ghrelin feedback systems might contribute to the pathophysiology of obesity and eating disorders.
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PMID:Ghrelin and feedback systems. 1798 56


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