Disease relevance of Bulimia

• Conclusions: Obese adult carriers of functionally relevant MC4R mutations do not specifically present with binge-eating disorder or a history of early-onset obesity [1].
• METHODS: The dopamine release and metabolism in the prefrontal cortex (PFC) and in the ventrolateral striatum (VLS) of rats were studied using microdialysis during enhanced rebound hyperphagia induced by space restriction (an animal model of binge eating) [2].
• Dysregulation of both lipid and glucose metabolism and changes in body weight and body fat mass have been reported in bulimia nervosa (BN) and/or binge eating disorder (BED); hence, investigation of adiponectin secretion is of obvious interest in these eating disorders [3].
• In patients with bulimia or anorexia nervosa, both initially and after weight gain, the maximal effect of prostaglandin E1 (PGE1) on platelet cAMP production was greatly increased, while the half-maximally effective dose was unchanged [4].
• Polycystic ovary syndrome, gestational diabetes, and bulimia nervosa [5].

Psychiatry related information on Bulimia

• Disturbances were studied in the nocturnal circadian pattern of serum melatonin and plasma cortisol levels in 33 female patients with an eating disorder (anorexia nervosa, n = 11; bulimia nervosa, n = 12; or both, n = 10) and in ten female control subjects of comparable age [6].
• The blunted PRL responses to m-CPP administration suggest that postsynaptic 5-HT receptor sensitivity is altered in bulimia nervosa, and that similar alterations in 5-HT receptors at or above the level of the hypothalamus may contribute to binge eating and other behavioral symptoms [7].
• Anorexia nervosa is associated with changes in the noradrenergic, serotonergic, and opioid systems; bulimia nervosa is accompanied by marked alterations in serotonin and norepinephrine activity [8].
• Of these disorders, five were "internalizing" (major depression, phobias, generalized anxiety disorder, panic disorder, and bulimia nervosa), and four were "externalizing" (nicotine dependence, alcohol dependence, drug abuse or dependence, and adult antisocial behavior) [9].
• Because of its role in eating behavior, which is especially relevant to eating disorders, BDNF is an attractive candidate for investigation of potential biological markers of eating disorders such as bulimia nervosa (BN) and anorexia nervosa (AN) [10].

High impact information on Bulimia

• Impaired cholecystokinin secretion in bulimia nervosa [11].
• Effect of decreasing afferent vagal activity with ondansetron on symptoms of bulimia nervosa: a randomised, double-blind trial [12].
• Since meal termination and satiety are mainly vagally mediated functions, since binge-eating and vomiting produce intense stimulation of vagal afferent fibres, and since ondansetron and other 5-HT3 antagonists decrease afferent vagal activity, the symptom improvement may result from a pharmacological correction of abnormal vagal neurotransmission [12].
• L-tryptophan as an adjunct to treatment of bulimia nervosa [13].
• A randomized, double-blind, placebo-controlled study of sibutramine in the treatment of binge-eating disorder [14].

Chemical compound and disease context of Bulimia

• Decreased serotonin function in bulimia nervosa [15].
• Association of serotonin and cortisol indices with childhood abuse in bulimia nervosa [16].
• RESULTS: For patients with bulimia nervosa, the fenfluramine-stimulated increase in serum prolactin concentration was significantly less than for controls [15].
• Dexamethasone suppression test and plasma dexamethasone levels in bulimia [17].
• Treatment of bulimia with phenelzine. A double-blind, placebo-controlled study [18].

Biological context of Bulimia

• Acute tryptophan depletion and increased food intake and irritability in bulimia nervosa [19].
• CONCLUSIONS: While most characteristics of males and females with eating disorders are similar, homosexuality/bisexuality appears to be a specific risk factor for males, especially for those who develop bulimia nervosa [20].
• There was a trend toward insufficient cortisol suppression in the DST in patients with bulimia, which was most pronounced in patients with signs of restricted caloric intake [21].
• These data lend support to a model in which increased gastric capacity, perhaps resulting from repeated binge eating, gives rise to delayed gastric emptying and blunted postprandial cholecystokinin release, leading to an impaired satiety response, which tends to perpetuate the illness [22].
• Symptom fluctuation in bulimia nervosa: relation to menstrual-cycle phase and cortisol levels [23].

Anatomical context of Bulimia

• Cerebrospinal fluid neurotransmitter metabolite levels were studied to assess whether measures of central serotonin, dopamine, or norepinephrine function are associated with severity of abnormal eating patterns in patients with bulimia nervosa [24].
• RESULTS: Drug-free bulimia nervosa patients showed a 17% reduced brain serotonin transporter availability in the hypothalamus and thalamus, as compared with healthy control subjects (2.4 +/- 0.4 vs. 2.9 +/- 0.4, p =.026), and a similar reduction in striatal dopamine transporter availability [25].
• Plasma ghrelin in anorexia, bulimia, and binge-eating disorder: relations with eating patterns and circulating concentrations of cortisol and thyroid hormones [26].
• Blood platelet monoamine oxidase activity, serotonin uptake and release rates in anorexia and bulimia patients and in healthy controls [27].
• Beta 2-adrenergic receptor regulation in circulating mononuclear leukocytes in anorexia nervosa and bulimia [28].

Gene context of Bulimia

• In particular, we found no evidence for an increased rate of binge-eating behavior in obese carriers of MC4R variants [29].
• RESULTS: A highly significant association was observed between the IGF2 ApaI G allele and scores on the Eating Attitudes Test overall and each of its subscales (bulimia, dieting, and oral control) [30].
• METHODS: Plasma leptin and cerebrospinal fluid leptin, NPY, and PYY concentrations were measured in women who were recovered from anorexia or bulimia nervosa to determine whether alterations persisted after recovery [31].
• We compared rates of binge eating behavior in the two genotypic groups defined by the presence or absence of the seven-repeat allele of DRD4 [32].
• Alterations in neuropeptide Y and/or peptide YY are suggested to play a role in the pathophysiology of bulimia [33].

Analytical, diagnostic and therapeutic context of Bulimia

• Pharmacotherapy of bulimia nervosa with fluoxetine: assessment of clinically significant attitudinal change [34].
• METHOD: After 4 days of a low monoamine diet and overnight bed rest, CSF was obtained (12-26 cc) from 11 women with bulimia and 17 normal comparison subjects (eight women and nine men) [35].
• Eight women with bulimia and eight age- and sex-matched normal control subjects were studied with positron emission tomography using [18F]-fluorodeoxyglucose (FDG) as a tracer of brain metabolic rate [36].
• Polymorphism of the serotonin 5-HT1B receptor gene (HTR1B) associated with minimum lifetime body mass index in women with bulimia nervosa [37].
• [123I] beta-CIT and single photon emission computed tomography reveal reduced brain serotonin transporter availability in bulimia nervosa [25].

References