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

The regulation of body weight is a complex process which relies on a balance between supply of nutrients and demand on these nutrients in the form of energy expenditure. Various central and peripheral mechanisms play a crucial role in maintaining this balance. While various neuropeptides in the central nervous system (CNS), particularly in the hypothalamus, maintain the necessary harmony between hyperphagia and anorexia, peripheral signals arising from the gastrointestinal tract (cholecystokinin-8 [CCK-8], amylin), pancreas (insulin) and adipose tissue (leptin) provide the necessary stimuli or a feedback inhibition for the synthesis and secretion of these hypothalamic neuropeptides. Various metabolites of the carbohydrate and fat metabolism are also involved in regulating the neuronal activity in the hypothalamus which ultimately leads to a release of key neuropeptides. In addition to the central mechanisms, peripheral mechanisms that regulate energy expenditure, particularly in the brown adipose tissue and skeletal muscle, are critical in maintaining the overall balance. Insight into these mechanisms sets the stage for developing novel strategies in the treatment of emerging childhood diseases such as obesity, anorexia nervosa, and bulimia. Further, delineation of these processes in the fetus and newborn sets the stage for investigating their role in molding the adult phenotype due to intrauterine adaptations.
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PMID:Neurohumoral regulation of body weight gain. 1501 96

In this article, the authors deal with clinical and psycho-social aspects as well as treatment measures for nervous bulimia, overeating attacks and obesity. By studying these disorders, we have been able to notice the existence of common psycho-pathological characteristics. Impulsive behavior, more or less compulsive eating habits, and the presence of certain personality traits are different from nervous anorexia according to our study. However, our manner of viewing these disorders consists of considering nervous bulimia and overeating attacks as being clear psychiatric entities, while obesity can be a consequence, or not as seen in the majority of cases, of a psychiatric disorder, although there always exists a special weakness which causes one to suffer from these disorders and there exists a need for psychological support to complement a nutritional treatment program.
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PMID:[Bulimia nervosa and obesity. Clinical and psycho-social features, and intervention]. 1506 41

Acute gastric dilatation with necrosis is a rare and severe complication associated with anorexia nervosa, bulimia, and psychogenic polyphagia. The Authors report an unusual case without underlying psychiatric context. Gastric necrosis was suspected based on imaging findings (plain radiograph and computed tomography). The detection of these imaging signs in an appropriate clinical setting, even without underlying psychiatric context, is important to avoid any delay in diagnosis and reduce mortality.
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PMID:[Gastric necrosis from acute dilatation without underlying psychiatric disorder]. 1520 57

Binge eating disorder (BED), characterized by ingestion of very large meals without purging afterwards, is found in a subset of obese individuals. We showed previously that stomach capacity is greater in obese than in lean subjects, and in this study, we investigated capacity in obese individuals with BED. We also determined ad-libitum intake of a test meal until extremely full. Furthermore, we measured various appetitive hormones (insulin, leptin, glucagon, CCK, ghrelin) and glucose before a fixed meal and for 120 min afterwards. An acetaminophen tracer was used to assess gastric emptying rate. We compared three groups of overweight women: 11 BED, 13 BE (subthreshold BED), and 13 non-binge-eating normals. The BED individuals had the largest stomach capacity as assessed by either maximum volume tolerated (P=.05) or by gastric compliance to pressure (P=.02) using an intragastric balloon. Although test meal intake did not differ between groups, it correlated (P=.03) with gastric capacity. The BED group showed a tendency (P=.06) to have greater area under the curve (AUC) and had higher values at 5 and 60 min (P<.05) for insulin compared to normals. Moreover, the BED subjects had lower ghrelin baselines premeal, and lower AUC for ghrelin, which then declined less postmeal than for the normals (P<.05). None of the other blood values differed, including glucose, leptin glucagon, and CCK, as well as acetaminophen, reflecting gastric emptying. The lower ghrelin in BED, although contrary to what was expected, is consistent with lower ghrelin in obesity, and suggests down-regulation of ghrelin by overeating. The lack of differences in CCK is consistent with the lack of differences in gastric emptying rate, given that CCK is released when nutrients reach the intestine. The results show that BED subjects have a large gastric capacity as well as abnormalities in meal-related ghrelin and insulin patterns that may be factors in binge eating.
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PMID:Gastric capacity, test meal intake, and appetitive hormones in binge eating disorder. 1523 78

Eating disorders are a group of disease states including anorexia nervosa, bulimia nervosa and binge eating on one end as well as episodic or chronic overeating resulting in obesity at the other end of the spectrum. These disorders are characterized by decreased and/or increased energy intake and are frequently associated with hormonal and metabolic disorders. The discovery of leptin, an adipocyte-secreted hormone acting in the brain to regulate energy homeostasis, and its subsequent study in human physiology have significantly advanced our understanding of normal human physiology and have provided new opportunities for understanding and possibly treating disease states, such as anorexia and bulimia nervosa. It has been recently discovered that leptin levels above a certain threshold are required to activate the hypothalamic-pituitary-gonadal and hypothalamic-pituitary-thyroid axes in men, whereas the hypothalamic-pituitary-adrenal, renin-aldosterone, and growth hormone-IGF-1 axes may be largely independent of circulating leptin levels in humans. In this review, we summarize the latest findings related to the role of leptin in the regulation of several neuroendocrine axes, such as the hypothalamic-pituitary-gonadal and the hypothalamic-pituitary-thyroid axes in humans and discuss its potential pathophysiologic role in eating disorders.
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PMID:The role of leptin in regulating neuroendocrine function in humans. 1533 44

Although neurochemical changes have been reported in the brain in animal models of binge eating, biochemical changes of specific proteins in the brain are unknown. Our aim was to elucidate brain proteins altered in rats during enhanced rebound hyperphargia. Rats were deprived of food for 22 h/day for 6 days, then allowed free access to food for 24 h in normal cages (rebound hyperphargia) or in space-restricted cages (enhanced rebound hyperphargia). Proteins extracted from the rat brain were separated by two-dimensional gel electrophoresis, and compared with those from control rats freely fed for 7 days in normal cages. Proteins expressed differently from controls were identified by N-terminal amino acid sequencing and mass fingerprinting using a MALDI-TOF mass spectrometer. Among proteins in the corpus striatum, frontal lobe, hippocampus and thalamus/hypothalamus, ubiquitin C-terminal hydrolase L1 and peroxiredoxin 2 decreased in the hippocampus and phosphatidylethanolamine-binding protein increased in the thalamus/hypothalamus of rats with the enhanced rebound hyperphargia induced by space-restriction. In this study, we first demonstrated that three brain proteins changed in rats during enhanced rebound hyperphagia. These proteins might have pathophysiologic relevance to binge eating.
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PMID:A comparative proteomic analysis of the rat brain during rebound hyperphagia induced by space-restriction. 1613 81

The present study tested the dual pathway model of Stice [. A review of the evidence for a sociocultural model of bulimia nervosa and an exploration of the mechanisms of action. Clinical Psychology Review, 14, 633-661 and . A prospective test of the dual-pathway model of bulimic pathology: mediating effects of dieting and negative affect. Journal of Abnormal Psychology, 110, 124-135.] in a non-clinical sample of female adolescents and a clinical sample of female eating disorder patients. The model assumes that negative affect and restrained eating mediates the link between body dissatisfaction and overeating. We also tested an extended version of the model postulating that negative affect and overeating are not directly related, but indirectly through lack of interoceptive awareness and emotional eating. Structural equation modelling was used to test our models. First, in the two samples, body dissatisfaction and drive for thinness were associated with overeating/binge eating. In both clinical and adolescent sample, we found support for the negative affect pathway and not for the restraint pathway. Lack of interoceptive awareness and emotional eating appear to (partly) explain the association between negative affect and overeating. Emotional eating was much more strongly associated with overeating in the clinical than in the adolescent sample. In sum, we found substantial evidence for the negative affect pathway in the dual pathway model. The link between body dissatisfaction and overeating in this respect might be explained by the fact that negative affect, due to body dissatisfaction, is related to a lack of awareness of personal feelings and to eating when dealing with negative emotions, which on its turn is associated with overeating.
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PMID:The Stice model of overeating: tests in clinical and non-clinical samples. 1624 9

This study examined the test-retest reliability of the Eating Disorder Examination-Questionnaire (EDE-Q) in patients with binge eating disorder (BED). Short-term (mean days = 4.8; SD = 3.6) test-retest reliability of the EDE was examined in a sample of 86 patients with BED. Test-retest reliability was excellent for objective bulimic episodes (correlation = .84), but poor to unacceptable for subjective bulimic episodes and objective overeating episodes (correlations = .51 and .39, respectively). Test-retest reliabilities were good for the EDE-Q scales (correlations = .66 to .77), albeit somewhat variable for the individual EDE-Q items (.54 to .78). These findings support the reliability of the EDE-Q for patients with BED. The EDE-Q has utility for assessing the number of binge eating episodes (objective bulimic episodes) and associated features of eating disorders in patients with BED. The results for subjective bulimic episodes are consistent with previous studies in suggesting that these eating behaviors may not be reliable indicators of eating disorders for patients with BED.
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PMID:Reliability of the Eating Disorder Examination-Questionnaire in patients with binge eating disorder. 1630 Oct 13

A questionnaire that assessed a broad range of eating-related characteristics for unselected, normal subjects was factor analyzed in a two-step process proposed by Comrey (1984). Twelve "factored homogeneous item dimensions" were identified first and yielded three primary-level factors in a second factor analysis: Predisposition to Obesity (including Dieting and Preoccupation with, and Fear Of, Gaining Weight), Uncontrollable Urges to Eat (including Eating Momentum Beyond Control, Food a Panacea and Constant Temptation, and Secret Binging), and Predisposition to Anorexia (including Insufficient Eating Obvious to Others, Food Phobia, Inability to Eat, and Vomiting After Meals). The three primary-level factors were positively intercorrelated and exhibited significant positive, though weak, correlations with a measure of trait arousability. Also, weak results tentatively indicated that individuals with more pleasant and/or more arousable temperaments were less likely to be overweight. Subjects reported sharply higher levels of food consumption when feeling "depressed" (i.e., bored, lonely, sad) than when feeling "distressed" (i.e., uncomfortable, anxious, in pain). Uncontrollable Urges to Eat correlated positively and significantly with self-reports of food consumption while depressed, showing that those lacking control over eating ate especially more while feeling bored, lonely, or sad. Predisposition to Obesity correlated negatively and significantly with self-reports of food consumption while distressed, showing that those tending more toward obesity ate less while upset or anxious.
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PMID:Measures of eating-related characteristics for the general population: relationships with temperament. 1636 30

Patients with eating disorders are increasing in number. Some neurocircuits concerned with feeding behavior might be dysfunctional in these patients with repeated expression of disorganized eating behavior like long-lasting dieting. These neuronal, or endocrinological dysfunctions might even be enhanced by psychological stress. To understand the biological bases of eating disorders is necessary to establish effective treatment. According to the clinical features of the patients, we have conducted some rat studies. We have found that space restriction stress enhances rebound hyperphagia induced by time-restricted scheduled feeding, and propose the phenomenon as a possible rat model of binge eating. We can speculate some part of the biological bases of human eating disorders, and effective prevention and treatment through such animal models.
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PMID:[Animal model of eating disorders]. 1672 66


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