Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bulimia nervosa has been recently identified. DSM III-R gives more restrictive criteria for the trouble than DSM III. One may doubt it allows to better understand the probable psychopathological heterogeneity of this eating disorder. Biological indexes up to now only led to partial results. Their interpretation is made more difficult because of the small size of the samples of patients, studied in conditions which are often ill-defined. The biological parameters which are investigated are similar to those studied in depression: monoamines, hypothalamic-pituitary-adrenal axis, hypothalamic-pituitary-thyroid axis, hypothalamic-pituitary-gonadal axis, Growth Hormone, prolactin , melatonin, beta-endorphin, EEG mapping. Antidepressants and anticonvulsants remain the most often mentioned drugs. Tryptophane, lithium, opiate antagonists, amphetamines, serotoninergic drugs are currently being studied.
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PMID:[Bulimic behaviors. Clinical, biochemical, pharmacologic data]. 266 2

In order to establish possible alterations in the secretory patterns of adrenocorticotropic hormone (ACTH), cortisol and/or beta-endorphin in bulimia nervosa, the circadian fluctuations of these hormones were evaluated in blood samples taken at 1-hour intervals over 24 h. Eleven bulimic women with normal body weight and 8 weight- and age-matched normal controls were tested during the follicular phase (days 6-8) of normal menstrual cycles. All women were hospitalized for bulimia or for checkup examinations and were tested 3 days after hospital admission. Both normal and bulimic women showed maximal ACTH, cortisol and beta-endorphin levels at 08.00 h, with minimal ACTH and beta-endorphin levels at midnight and cortisol levels at 02.00 h. The general temporal structure of all hormonal secretions coincided in the two groups. However, whereas all measured ACTH/cortisol levels were quantitatively similar in the two groups, plasma beta-endorphin concentrations were significantly higher in bulimic than in control subjects at all examined time points. The enhancement in the overall 24-hour beta-endorphin secretion suggests the presence of an increased opioid tonus in bulimic women, which might play a role in the pathophysiology of the eating disorder.
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PMID:Circadian variations in plasma ACTH, cortisol and beta-endorphin levels in normal-weight bulimic women. 892 31

Bulimia nervosa is an eating disorder characterised by recurrent episodes of binge eating and associated efforts to purge the ingested calories through self-induced vomiting, laxative or diuretic abuse, fasting or intensive exercise. The aetiopathogenesis and pathophysiology of the disorder are currently unclear. Biological bases have been proposed repeatedly, based on several lines of evidence: hunger, satiety and food choice are regulated by neurotransmitters and neuropeptides, and impairment of eating habits may be related to alterations in the secretion of these chemicals; genetic studies suggest that these neurotransmitter systems are dysfunctional in individuals with bulimia nervosa; and the frequent comorbidity of bulimia nervosa with major depressive and obsessive-compulsive disorders, conditions in which multiple alterations of brain biochemical functions have been demonstrated. Data in the literature suggest that levels of noradrenaline (norepinephrine) and serotonin (5-hydroxytryptamine; 5-HT) are lower in individuals with bulimia nervosa than in healthy controls. Levels of dopamine are similar to, or lower than, those in controls. After remission of the disorder, noradrenergic function returns to that seen in controls, whereas dopaminergic and serotonergic function rebound to levels higher than in controls. Among the neuropeptides, alterations in the levels of neuropeptide Y, peptide YY, beta-endorphin, corticotrophin-releasing hormone, somatostatin, cholecystokinin and vasopressin have been found in the symptomatic phase of bulimia nervosa, with a return to levels seen in controls after remission. Pharmacological treatment of bulimia nervosa that is directed at correction of the neurochemical alterations observed is difficult because of the complexity of the impairments. However, such treatment is necessary and should be continued long after symptomatic remission to ensure reinstitution of cerebral biochemical homeostasis.
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PMID:Aetiopathogenesis and pathophysiology of bulimia nervosa: biological bases and implications for treatment. 1146 Aug 90

Previously, we identified that a majority of patients with anorexia nervosa (AN) and bulimia nervosa (BN) as well as some control subjects display autoantibodies (autoAbs) reacting with alpha-melanocyte-stimulating hormone (alpha-MSH) or adrenocorticotropic hormone, melanocortin peptides involved in appetite control and the stress response. In this work, we studied the relevance of such autoAbs to AN and BN. In addition to previously identified neuropeptide autoAbs, the current study revealed the presence of autoAbs reacting with oxytocin (OT) or vasopressin (VP) in both patients and controls. Analysis of serum levels of identified autoAbs showed an increase of IgM autoAbs against alpha-MSH, OT, and VP as well as of IgG autoAbs against VP in AN patients when compared with BN patients and controls. Further, we investigated whether levels of these autoAbs correlated with psychological traits characteristic for eating disorders. We found significantly altered correlations between alpha-MSH autoAb levels and the total Eating Disorder Inventory-2 score, as well as most of its subscale dimensions in AN and BN patients vs. controls. Remarkably, these correlations were opposite in AN vs. BN patients. In contrast, levels of autoAbs reacting with adrenocorticotropic hormone, OT, or VP had only few altered correlations with the Eating Disorder Inventory-2 subscale dimensions in AN and BN patients. Thus, our data reveal that core psychobehavioral abnormalities characteristic for eating disorders correlate with the levels of autoAbs against alpha-MSH, suggesting that AN and BN may be associated with autoAb-mediated dysfunctions of primarily the melanocortin system.
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PMID:Autoantibodies against neuropeptides are associated with psychological traits in eating disorders. 1619 79

Anorexia nervosa is an eating disorder, characterized by low body weight, distorted body image, amenorrhea and an intense fear of gaining weight. The occurrence of anorexia nervosa has increased over the past 10 years among adolescents and young women and it is estimated to occur in 0,5-1% of population. The Anorexia nervosa is not only a psychiatric illness may have many serious gynecological and medical ramifications. Preventive measures to reduce the incidence of anorexia are not known at this time. However, early detection, intervention and cooperation between many specialists can reduce the severity of symptoms and health consequences. Gynecologists assume a broader role in preventative medicine and health maintenance, that is why their awareness of anorexia nervosa is needed. Anorectic patients have metabolic and endocrine complications. Most of them are caused by the dysfunction of hypothalamus, which produces many nueropeptides and neurotransmitters. Anorexia nervosa is characterized by numerous aberrations in neuropeptides and neurotransmitters, such as gonadotropin-releasing hormone, corticotropin-releasing hormone, neuropeptyd Y, leptin, beta-endorfins and serotonine, dopamine. The relationship of anorexia nervosa with genetic factor is being enhanced lower the last few years. However, the studies on the role of polymorphism in some genes brought conflicting results.
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PMID:[Anorexia nervosa--new view on neuroendocrine and genetic determinations]. 1707 96