Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fluoxetine selectively inhibits serotonin uptake in vitro and in vivo and thus enhances serotonergic function, leading to a decrease in food intake beginning with the first dose and a decrease in body weight or in weight gain after multiple doses of fluoxetine. Fluoxetine and other drugs that increase serotonergic function decrease food intake with characteristics that make them attractive for use in weight reduction. In rats, for instance, fluoxetine and other serotonergic drugs suppress stress-induced eating, suppress carbohydrate consumption selectively, and suppress insulin-induced hyperphagia. Fluoxetine and other serotonergic drugs do not cause amphetamine-like behavioral stimulation in animals and have no known abuse or addiction liability. In obese yellow mice and in normal mice, as in rats, fluoxetine causes a sustained decrease in food intake and body weight. The pharmacologic effects of fluoxetine in animals suggest its potential use in weight-reduction programs in obese humans.
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PMID:Preclinical pharmacology of fluoxetine, a serotonergic drug for weight loss. 172 30

A technique for prehepatic infusion of parenteral nutrients is described. Portal vein hyperalimentation allows hepatic modification and control of the infused nutrients before delivery of these substances into the general circulation and theoretically should reduce the incidence of metabolic complications of hyperalimentation. The clinical experience with prehepatic infusions is reported and the metabolic investigations are described. Transumbilical catheters provided prehepatic delivery of parenteral nutrients for 1 month after esophagogastrectomy for esophageal malignancy without serious infection or portal vein thrombosis. Close surveillance of blood glucose and serum osmolarity demonstrated metabolic stability during the infusion period. Nitrogen balance studies showed better nitrogen economy than is achieved by infusion of similar solutions into the central systemic circulation. Indirect calorimetry indicated that the nitrogen used for production of energy was less than the amount supplied by prehepatic infusions. The same basic liver function abnormalities encountered with systemic infusion of hyperalimentation solutions were noted. The patients gained weight after esophagogastrectomy and did not experience the attrition from malnutrition which usually occurs in the first several months after esophageal resection.
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PMID:Prehepatic hyperalimentation. 676 87

Prader-Willi syndrome (PWS) is characterized by hypotonia at birth, hypogonadism, early childhood obesity, and mental deficiency. Hypogonadotropic hypogonadism is a major characteristic of patients with PWS, and it is speculated to be due to hypothalamic insufficiency. Two adult female patients with PWS and no prior history of menses are presented. Both of these patients were treated with fluoxetine for psychopharmacologic management of obsessive features in the form of food preoccupation and hyperphagia or for compulsive behaviors in the form of severe self-injurious behaviors. The two female patients with PWS who had primary amenorrhea developed vaginal bleeding believed to be menses following at least 6 months of treatment with fluoxetine. Mature hypothalamic function is characterized by pulsatile release of gonadotropin-releasing hormone (GnRH) in a critical range of frequency and amplitude. Central nervous system neurotransmitters may modify GnRH secretion. Fluoxetine specifically inhibits the reuptake of serotonin which may impact the hypothalamic-pituitary-ovarian system in female patients with PWS.
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PMID:Onset of menses in two adult patients with Prader-Willi syndrome treated with fluoxetine. 749 74

Sleep-related eating disorders distinct from daytime eating disorders have recently been shown to be associated with sleepwalking (SW), periodic limb movement (PLM) disorder and triazolam abuse in a series of 19 adults. We now report eight other primary or combined etiologies identified by clinical evaluations and polysomnographic monitoring of 19 additional adults (mean age 40 years; 58% female): i) obstructive sleep apnea (OSA), with eating during apnea-induced confusional arousals (n = 3); ii) OSA-PLM disorder (n = 1); iii) familial SW and sleep-related eating (n = 2); iv) SW-PLM disorder (n = 1); v) SW-irregular sleep/wake pattern disorder (n = 1); vi) familial restless legs syndrome and sleep-related eating (n = 2); vii) anorexia nervosa with nocturnal bulimia (n = 2) and viii) amitriptyline treatment of migraines (n = 1). In our cumulative series of 38 patients (excluding six with simple obesity from daytime overeating), 44% were overweight (i.e. > 20% excess weight) from sleep-related eating. Nightly sleep-related binge eating (without hunger or purging) had occurred in 84% of patients. Onset of sleep-related eating was also closely linked with i) acute stress involving reality-based concerns about the safety of family members or about relationship problems (n = 6), ii) abstinence from alcohol and opiate/cocaine abuse (n = 2) and iii) cessation of cigarette smoking (n = 2). Current treatment data indicate a primary role of dopaminergic agents (carbidopa/L-dopa; bromocriptine), often combined with codeine and clonazepam, in controlling most cases involving SW and/or PLM disorder. Fluoxetine was effective in two of three patients. Nasal continuous positive airway pressure therapy controlled sleep-related eating in two OSA patients.
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PMID:Additional categories of sleep-related eating disorders and the current status of treatment. 810 56

This study examined mechanisms by which fluoxetine may reduce energy consumption and body weight. Women with binge-eating disorder (BED; n = 38) and age- and weight-matched women without BED (n = 32) monitored their dietary intake and concurrently recorded mood variables on a hand-held computer for 6 d of baseline and for 6 d after being randomly assigned to receive placebo or fluoxetine (60 mg). Fluoxetine reduced eating more than did the placebo on days 4-6 of treatment. The frequency of episodes was not affected, suggesting that fluoxetine affects satiety, not hunger. Fluoxetine did not preferentially reduce carbohydrate intake, did not affect snack consumption as compared with meal consumption, and did not affect negative-mood eating more than positive-mood eating, nor did fluoxetine affect subjects' mood ratings. Benefits of fluoxetine were of approximately equal magnitude for women with and without BED. However, women who reported higher energy consumption at baseline were more responsive to fluoxetine than were women who reported lower energy consumption at baseline, and binge-eating status was associated with greater energy consumption at all time points, including baseline. Fluoxetine affects dietary intake within 4 d of its consumption, and if future research shows that this remains true on repeated applications, this drug may be useful for short periods when difficulty with overeating is anticipated, such as during vacations.
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PMID:A double-blind, placebo-controlled trial of the effect of fluoxetine on dietary intake in overweight women with and without binge-eating disorder. 878 Mar 33

We have analysed some behavioral, neuroendocrine and serotonergic consequences of a single (30-min) social defeat followed by 14-18 h of sensory contact with the aggressor, in Lewis rats, an inbred strain highly sensitive to chronic social stressors [Berton O. et al. (1998) Neuroscience 82, 147-159]. In addition, we have investigated how the aforementioned consequences are affected by pretreatment with the selective serotonin reuptake inhibitor, fluoxetine (7.5 mg/kg/day for 21 days). A single social defeat triggered hypophagia and body weight loss, and increased anxiety in the elevated plus-maze. It did not affect baseline plasma adrenocorticotropic hormone levels and renin activity, but decreased plasma corticosterone levels. On the other hand, the responses of the latter variables to subsequent acute forced swim stress were blunted (corticosterone) or amplified (adrenocorticotropic hormone, renin activity) by prior defeat. The density of hippocampal serotonin transporters, but not that of hippocampal serotonin-1A and cortical serotonin-2A receptors, was decreased by a single social defeat; in addition, neither tryptophan availability and serotonin synthesis/metabolism, nor serotonin-1A autoreceptor-mediated functions (inhibition of serotonin synthesis, hyperphagia) were affected. Fluoxetine pretreatment diminished social defeat-induced hypophagia, body weight loss and anxiety without affecting these variables in control animals. This pretreatment increased plasma corticosterone levels in resting and acutely stressed rats, but abolished social defeat-elicited corticosterone hyporesponsiveness to acute forced swim stress. Except for a decrease in midbrain serotonin transporter density, fluoxetine did not affect the other serotonergic indices analysed herein, i.e. serotonin-1A and serotonin-2A receptor densities, serotonin synthesis/metabolism. A single social defeat in Lewis rats produces behavioral and endocrine alterations that may model some aspects of human anxiety disorders. In this paradigm, prior fluoxetine treatment is endowed with adaptive behavioral, and possibly neuroendocrine, effects without affecting the key elements of central serotonergic systems analysed herein.
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PMID:Behavioral, neuroendocrine and serotonergic consequences of single social defeat and repeated fluoxetine pretreatment in the Lewis rat strain. 1039 54

Hypericum extract (HE) might be favourably active in depressed patients with reversed vegetative signs (RVS). Therefore, we performed an exploratory subgroup analysis of a three-armed study to compare HE, fluoxetine, and placebo in patients with major depressive disorder (MDD) in a 12 wk trial. A total of 135 patients were randomized to 12 wk treatment with HE LI 160 (900 mg/d), fluoxetine (20 mg/d), or placebo. Patients with RVS were defined in two steps, according to DSM-IV. First, patients with melancholy-related vegetative signs were excluded. Secondly, patients had to have at least one score of 2 for the items 22-26 of the HAMD-28 scale, which are related to hypersomnia and hyperphagia. Twenty-seven patients remained in the group. Analysis of covariance (ANCOVA) was applied using the HAMD-17 score. Secondly a chi2 test for response was performed, using the same and further an adapted criterium as in recently published studies. ANCOVA revealed a trend to a global difference. Post-hoc analysis showed a trend to superiority of HE compared to placebo and to fluoxetine, but a very large effect size for both differences. Fluoxetine was not different from placebo. The adapted response criterium showed a significant global difference as well as a significant superiority of HE over placebo and over fluoxetine. These data are based on a small sample size and must be considered tentative. A characterization of vegetative features of patients with depression could lead to an overall increased effect size in the treatment with HE.
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PMID:Hypericum extract in patients with MDD and reversed vegetative signs: re-analysis from data of a double-blind, randomized trial of hypericum extract, fluoxetine, and placebo. 1545 12