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)

Abnormal growth hormone (GH) and adrenocorticotropic hormone (ACTH)/cortisol secretory patterns in response to a glucose load have been observed in underweight anorectic women. The present study was performed in an attempt to establish whether changes in the hypothalamic/pituitary sensitivity to hyperglycemia occur in bulimia in the absence of weight disturbance. Therefore, serum GH, plasma cortisol, and plasma insulin concentrations were measured in eight women with normal weight bulimia and in eight normal women during an intravenous glucose (0.33 g/kg as an IV bolus) tolerance test (IGTT). In addition, since abnormal pituitary hormone responses to a glucose load might reflect alterations in somatostatin (SRIH) release, TSH secretion also was measured, in view of its sensitivity to SRIH inhibition. Both GH and cortisol levels progressively and significantly declined during IGTT in the normal subjects. In the bulimic women, cortisol levels remained unchanged, whereas GH concentrations rose significantly after glucose injection. Plasma cortisol and serum GH levels were significantly higher in the bulimic than in the control subjects. No significant differences between groups were observed in hyperglycemia-induced insulin increments or in TSH decrements. These data indicate that an altered sensitivity to hyperglycemia affects the hypothalamic/pituitary centers controlling the secretion of the counterregulatory hormones GH and ACTH/cortisol in bulimia nervosa. The lack of a simultaneous change in the TSH secretory pattern argues against a possible involvement of SRIH in the pathophysiology of this disorder.
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PMID:Abnormal growth hormone and cortisol, but not thyroid-stimulating hormone, responses to an intravenous glucose tolerance test in normal-weight, bulimic women. 136 37

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

Considerable evidence exists of hypothalamic dysfunction in patients with anorexia nervosa and bulimia nervosa. This dysfunction is reflected in disturbances of endocrine function including abnormalities of gonadotropin, growth hormone, and corticotropin-releasing hormone secretion. Whereas these disturbances are generally reversed with nutritional rehabilitation and weight restoration, it is not evident to what extent nutritional factors are the primary etiology or whether they unmask an otherwise existing but compensated central disturbance. Similarly, endocrine disturbances may be a final common pathway in which disturbances of diet, weight, activity, stress, and mood as well as hypothalamic dysfunction are expressed.
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PMID:The endocrinology of anorexia nervosa and bulimia nervosa. 289 9

Considerable evidence exists of hypothalamic dysfunction in patients with anorexia nervosa and bulimia nervosa. This dysfunction is reflected in disturbances of endocrine function including abnormalities of gonadotropin, growth hormone, and corticotropin-releasing hormone secretion. Whereas these disturbances are generally reversed with nutritional rehabilitation and weight restoration, it is not evident to what extent nutritional factors are the primary etiology or whether they unmask an otherwise existing but compensated central disturbance. Similarly, endocrine disturbances may be a final common pathway in which disturbances of diet, weight, activity, stress, and mood as well as hypothalamic dysfunction are expressed.
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PMID:The endocrinology of anorexia nervosa and bulimia nervosa. 328 60

Dissociation is made manifest by a failure to integrate thoughts, feelings, memories, and actions into a unified sense of consciousness. Although dissociation is presumed to be a special state of consciousness manifested by state-dependent memory and physiology, the psychobiology of dissociation is poorly understood. In this study, we examined cerebrospinal fluid levels of the major monoamine metabolites and beta-endorphin in patients with eating disorders (11 with anorexia nervosa, 16 with bulimia nervosa), while they were acutely ill. Dissociative capacity was measured using the Dissociative Experiences Scale (DES). We provide evidence that neurochemical changes in dopaminergic, serotonergic, and opioid systems may be associated with the clinical expression of dissociation in patients with eating disorders during the acute phase of their illness. These preliminary results are compatible with previous studies of neurochemical disturbances in the eating disorders and suggest that future work in dissociation should specifically include examination of these neurobiologic systems.
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PMID:Relation of dissociative phenomena to levels of cerebrospinal fluid monoamine metabolites and beta-endorphin in patients with eating disorders: a pilot study. 751 Dec 47

This paper reviews the recent progress in the understanding of the neurobiology of the eating disorders. The analysis of the biochemical abnormalities present in the patients with bulimia nervosa indicates the decrease of central serotonin and noradrenalin activity, elevation of the levels of cerebrospinal fluid peptide YY, alterations of the endogenous opioids and also reduction of peripheral cholecystokinin levels. As these studies were performed on patients who were actively binging and purging it is conceivable that the above abnormalities can results from a pathological feeding pattern. It is also suggested that the reduction of central serotoninergic activity is the stable, trait-related dysregulation of neurotransmitter system activity. In patients with anorexia nervosa the endocrine disturbances of the hypothalamic-pituitary-ovarian and hypothalamic-pituitary-adrenal axes were thoroughly studied. Underweight anorectic patients have been found to have elevations of cerebrospinal fluid level of neuropeptide Y, corticotropin releasing hormone and vasopressin as well as reductions of beta-endorphin and oxytocin level. However, most of the neuropeptide alterations normalize following weight recovery. The only exception is a persistent increase of central serotonin activity postulated to be responsible for the obsessive-compulsive personality traits and disturbed eating behaviors found in these patients.
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PMID:[Selected issues of biological aspects of eating disorders]. 799 11

The effects of the opiate receptor antagonist, naltrexone, were examined on antecedent thoughts of binging and plasma beta-endorphin concentrations in an adolescent girl who was hospitalized with bulimia nervosa. Significant decreases in urge to binge were obtained during naltrexone administration compared with control sessions. Baseline plasma beta-endorphin concentrations for the bulimic adolescent were not different from those of nonbulimic controls, but plasma beta-endorphins increased significantly during naltrexone administration. After discharge from the hospital, the adolescent refused to take naltrexone because she felt she could not deal with her life without the "pleasure of binging." The case points to the interplay of biological and psychological factors in bulimia nervosa.
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PMID:Effects of the opiate antagonist, naltrexone, on binging antecedents and plasma beta-endorphin concentrations. 805 38

Concentrations of cholecystokinin-8 (CCK-8) and beta-endorphin (beta-EP) in T-lymphocytes of 26 women with bulimia nervosa (BN) and in 26 age- and sex-matched healthy comparison subjects were measured. Ten patients were then treated with 300 mg/day of fluvoxamine, p.o., and five patients were treated with 300 mg/day of amineptine, p.o., for 4 months. Concentrations of the two peptides were measured again after 1, 2, and 4 months of therapy. Basal CCK-8 values were significantly lower in patients than in healthy subjects. During fluvoxamine therapy, CCK-8 values increased, reaching normal levels by month 4 of treatment. No such increase occurred during amineptine therapy. Baseline beta-EP values were normal in the bulimic patients but had declined by month 4 of fluvoxamine therapy.
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PMID:T-lymphocyte concentrations of cholecystokinin-8 and beta-endorphin in eating disorders: II. Bulimia nervosa. 877 Dec 20

The purpose of this article is to summarize briefly potential biological pathways that are common among anorexia nervosa, bulimia nervosa, and obesity. We conclude that data on serotonergic and beta-endorphin regulatory systems provide the most promising leads for potential trait-based etiological theories. We then discuss the contribution of current data to a better understanding of the etiology and maintenance of eating disorders. Finally, we comment on how the exploration for common biological mechanisms highlights problems in nosological diagnosis (i.e., the lack of symptom specificity among disorders) and obscures the etiological significance of social stressors and cultural factors.
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PMID:Common biological pathways in eating disorders and obesity. 890 39

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


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