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)

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

Anorexia Nervosa (AN) is an eating disorder of puberty or adolescence. It is characterized by self-induced weight loss; various psychological disturbances including distorted body image, fear of obesity, active pursuit of thinness and loss of recognition of a number of body enteroreceptive sensations; and secondary physiological abnormalities. The treatment of AN includes individual psychotherapy, family therapy, and nutritional rehabilitation. Hospital treatment is required when the patient's medical condition is in danger due to hypovolemia or hypotension. If cardiac arrhythmias occur without electrolyte disturbances or if oral therapy fails, nutrition should be repleted by the safest method available. This can be done by nasogastric tube or intravenous hyperalimentation. The management of AN is challenging, because the treatment process and anticipated outcome is in direct conflict with the sufferer's own wishes. A comprehensive treatment plan including both psychiatric and medical approaches is necessary. We report a severe AN case, who has refeeding problems after a three months' hospitalisation period. She was admitted to the child intensive care unit due to deterioration of her vital signs. We tried to solve her problems as a team, and believe that AN has a number of crucial problems thus requiring a multi-faceted treatment approach.
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PMID:Refeeding problems in a severe anorexia nervosa case. 1514 59

In treating patients with severe anorexia nervosa, it is important to improve their physical condition first. Patients who had lost close to 60% standard bodyweight (SBW) were candidates for inpatient treatment due to the mortality risk. With 80% SBW as the target for therapy, they were given both intravenous hyperalimentation and food by oral intake in order to improve their physical condition. In total, 51 patients were admitted. One died and four patients dropped out in the course of treatment. Forty-six patients who completed the inpatient treatment were reviewed. Although admitted with an average weight of approximately 60% SBW, they were discharged with a weight of approximately 80% SBW after approximately 60 days. An average follow up of 25.0 months was conducted, and two patients were found to have died. The mean weight, percentage resuming menstruation, and rehospitalization rate of the 44 survivors were 79% SBW, 23%, and 32%, respectively. The patients with the restricting type of anorexia had an earlier onset of the disorder and a better social outcome. Patients in whom onset occurred at a younger age had a better social outcome. After being discharged, the majority of the patients continued treatment as outpatients. Although the results were similar to those of conventional studies in terms of outcome, the shorter hospitalization was significant. Overall, in the treatment of patients with severe anorexia nervosa, it is important to begin psychotherapy while trying to improve their physical condition.
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PMID:Treatment with intravenous hyperalimentation for severely anorectic patients and its outcome. 1514 86

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

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

Eating disorders (ED), such as anorexia nervosa (AN) and bulimia nervosa (BN), are complex psychiatric disorders where different genetic and environmental factors are involved. Several lines of evidence support that brain-derived neurotrophic factor (BDNF) plays an essential role in eating behaviour and that alterations on this neurotrophic system participates in the susceptibility to both AN and BN. Accordingly, intraventricular administration of BDNF in rats determines food starvation and body weight loss, while BDNF or its specific receptor NTRK2 knockout mice develop obesity and hyperphagia. Case-control studies also suggest a BDNF contribution in the aetiology of ED: we have previously reported a strong association between the Met66 variant within the BDNF gene, restricting AN (ANR) and minimum body mass index (minBMI) in a Spanish sample, and a positive association between the Val66Met and -270C/T BDNF SNPs and ED in six different European populations. To replicate these results, avoiding population stratification effects, we recruited 453 ED trios from eight European centres and performed a family-based association study. Both haplotype relative risk (HRR) and haplotype-based haplotype relative risk (HHRR) methods showed a positive association between the Met66 allele and ANR. Consistently, we also observed an effect of the Met66 variant on low minBMI and a preferential transmission of the -270C/Met66 haplotype to the affected ANR offspring. These results support the involvement of BDNF in eating behaviour and further suggest its participation in the genetic susceptibility to ED, mainly ANR and low minBMI.
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PMID:Association of BDNF with restricting anorexia nervosa and minimum body mass index: a family-based association study of eight European populations. 1565 4

We experienced a case of anorexia nervosa (AN) associated with refeeding syndrome (RS). The patient was a 24-year-old woman who was taken to the hospital emergency room in a hypoglycemic coma as a result of aggravated emaciation due to AN. On the admission day, she had severe emaciation (BW, 27kg; BMI, 11.4), malnutritional hepatitis, bradycardia, hypotension, hypothermia and hypophosphatemia. After she was intravenously administered glucose, her level of consciousness rapidly improved. On the 7th day, we started intravenous hyperalimentation (IVH). On the 13th day, she developed delirium. Because the delirium appeared after administration of IVH, we diagnosed her with RS. An EEG study disclosed frequent high-amplitude generalized slow waves. SPECT (99mTc ethyl cysteinate dimer) showed a bilateral decrease in the average blood flow. Regional blood flow was decreased bilaterally in the frontal and temporal lobes, and in the thalamus. After she recovered from the delirium and her state of nutrition improved, follow-up EEG and SPECT studies showed a decreased frequency of generalized slow waves and improved blood flow, respectively. Her serum values of P, K, and Mg had been within the normal ranges in the course of the delirium. Thus, before giving more calories to a severely malnourished patient, a physician should consider the possibility that RS will occur, even when serum electrolytes are within the normal ranges.
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PMID:[A case of anorexia nervosa associated with delirium because of refeeding syndrome]. 1570 May 34

Based on the results of the clinical follow-up study of 41 female patients, diagnostic criteria of bulimia nervosa that should be used in clinical studies are suggested as follows: (1) presence of anorexia nervosa or transitory amenorrhea in the premorbid period; (2) eating attacks with losing of the control over food consumption not less than twice a week during 3 months; (3) compensatory behavior in the form of spontaneous vomiting, abuse of purgative and diuretic medications etc; (4) fear of obesity; (5) cycloid affective changes with higher impulsivity, reduction of the control over primitive drives and/or expressed anxiety disorders; inclination to alcohol and drug abuse and nicotine dependence; (6) changes of the body mass index; (7) absence of amenorrhea. The disease dynamics is characterized by formation of the pathological cycle "diet--overeating--compensatory behavior" on the background of cyclothymic affective disorders. Two types of bulimia nervosa--with and without other drive disorders--have been singled out.
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PMID:[Clinical features and diagnostic criteria of bulimia nervosa]. 1684 79

Dmbx1 is a paired-class homeodomain transcription factor. We show here that mice deficient in Dmbx1 exhibit severe leanness associated with hypophagia and hyperactivity and that isolation of a Dmbx1(-/-) mouse from its cohabitants induces self-starvation, sometimes leading to death, features similar to those of anorexia nervosa in humans. Interestingly, overexpression of agouti in Dmbx1(-/-) mice failed to induce aspects of the A(y)/a phenotype, including hyperphagia, obesity, and diabetes mellitus. In Dmbx1(-/-) mice, administration of agouti-related protein increased cumulative food intake for the initial 6 h but significantly decreased it over 24- and 48-h periods. In addition, Dmbx1 was shown to be expressed at embryonic day 15.5 in the lateral parabrachial nucleus, the rostral nucleus of the tractus solitarius, the dorsal motor nucleus of the vagus, and the reticular nucleus in the brainstem, all of which receive melanocortin signaling, indicating involvement of Dmbx1 in the development of the neural network for the signaling. Thus, Dmbx1 is essential for various actions of agouti-related protein and plays a role in normal regulation of energy homeostasis and behavior.
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PMID:Dmbx1 is essential in agouti-related protein action. 1787 59

Anorexia nervosa is a growing concern in mental health, often inducing death. The potential neuronal deficits that may underlie abnormal inhibitions of food intake, however, remain largely unexplored. We hypothesized that anorexia may involve altered signaling events within the nucleus accumbens (NAc), a brain structure involved in reward. We show here that direct stimulation of serotonin (5-hydroxytryptamine, 5-HT) 4 receptors (5-HT(4)R) in the NAc reduces the physiological drive to eat and increases CART (cocaine- and amphetamine-regulated transcript) mRNA levels in fed and food-deprived mice. It further shows that injecting 5-HT(4)R antagonist or siRNA-mediated 5-HT(4)R knockdown into the NAc induced hyperphagia only in fed mice. This hyperphagia was not associated with changes in CART mRNA expression in the NAc in fed and food-deprived mice. Results include that 5-HT(4)R control CART mRNA expression into the NAc via a cAMP/PKA signaling pathway. Considering that CART may interfere with food- and drug-related rewards, we tested whether the appetite suppressant properties of 3,4-N-methylenedioxymethamphetamine (MDMA, ecstasy) involve the 5-HT(4)R. Using 5-HT(4)R knockout mice, we demonstrate that 5-HT(4)R are required for the anorectic effect of MDMA as well as for the MDMA-induced enhancement of CART mRNA expression in the NAc. Directly injecting CART peptide or CART siRNA into the NAc reduces or increases food consumption, respectively. Finally, stimulating 5-HT(4)R- and MDMA-induced anorexia were both reduced by injecting CART siRNA into the NAc. Collectively, these results demonstrate that 5-HT(4)R-mediated up-regulation of CART in the NAc triggers the appetite-suppressant effects of ecstasy.
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PMID:Anorexia induced by activation of serotonin 5-HT4 receptors is mediated by increases in CART in the nucleus accumbens. 1791 92


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