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)

In abuse dwarfism the behavioral signs include some or all of the following: (1) a history of unusual eating and drinking behavior, reversible on change of domicile, such as eating from a garbage can and drinking from a toilet bowl, stealing food, alleged picky eating and rejecting food at the table, polydipsia and polyphagia, possibly alternating with vomiting and possibly also with self-starvation; (2) a history of such behavioral symptoms as enuresis, encopresis, social apathy or inertia, defiant aggressiveness, sudden tantrums, crying spasms, insomnia, eccentric sleeping and waking schedule, pain agnosia, and self-injury, all occurring only in the growth-retarding environment; (3) retarded motor development, with improvement on removal of the child from the domiclle of abuse; (4) retarded intellectual growht, reversible on change of domicile by as much as 30 to 50 IQ points; and (5) a history of pathologic family relationships, including unusual cruelty and neglect, either somatic or psychic or both.
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PMID:The syndrome of abuse dwarfism (psychosocial dwarfism or reversible hyposomatotropism). 85 51

University students (N = 208) completed a questionnaire on four aspects of eating: behavior, goals, imagery, and health status. A principal components analysis of the 18 self-report variables identified six factors: Weight Control Failure, Sensory Awareness of Food and Eating, Stable Eating Pattern, Unrestrained Overeating, "Home Cooking and Good Digestion," and Environmental Indifference. Sex differences in self-reporting were statistically significant on 10 of the 18 variables, with 6 of those significant variables heavily loaded on the first factor: Weight Control Failure. Analysis of these variables suggests that women report eating to be more problematic than do men. Several of the aspects of self-reports are discussed, including the apparent independence of sensory awareness of food and eating from self-reports of behavior, goals, and health status.
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PMID:Self-reports of eating behavior, goals, imagery, and health status: principal components and sex differences. 357 33

Two types of bilateral amygdalar lesions were performed successively. The first operation, involving the dorsomedial part, produced aphagia and subsequent hypophagia, vomiting and apathy. Consequently the body weight was reduced. After a few weeks partial recovery occurred. The second operation, involving the lateral part of the amygdaloid complex, produced hyperphagia, increase of body weight and restoration of general arousal. These results indicate the existence of two antagonistic systems: excitatory in the dorsomedial amygdala and inhibitory in the lateral amygdala. Damage of the inhibitory system reverses almost completely the syndrome produced by an initial lesion of the excitatory system.
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PMID:The normalizing effect of lateral amygdalar lesions upon the dorsomedial amygdalar syndrome in dogs. 451 16

A young man developed pathological thirst and hyperdipsia, hyperphagia, disordered temperature regulation, a lowered threshold for aggressive behavior, apathy, impaired memory, and seizures following encephalitis. He had marked hyponatremia. Bouts of water drinking produced water intoxication and precipitated status epilepticus. Studies of water handling with measurements of plasma osmolality and arginine vasopressin (AVP) revealed a very low thirst threshold (below 242 mOsm/kg) with resetting of the osmostat to a new level (255 mOsm/kg) but normal control of plasma osmolality at that level with adequate AVP release.
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PMID:Thirst, resetting of the osmostat, and water intoxication following encephalitis. 683 Jan 80

The cardinal clinical manifestations of major depression with melancholic features include sustained anxiety and dread for the future as well as evidence of physiological hyperarousal (e.g., sustained hyperactivity of the two principal effectors of the stress response, the corticotropin-releasing-hormone, or CRH, system, and the locus ceruleus-norepinephrine, or LC-NE, system). Sustained stress system activation in melancholic depression is thought to confer both behavioral arousal as well as the hypercortisolism, sympathetic nervous system activation, and inhibition of programs for growth and reproduction that consistently occur in this disorder. Data also suggest that activation of the CRH and LC systems in melancholia are involved in the long-term medical consequences of depression such as premature coronary artery disease and osteoporosis, the two-three-fold preponderance of females in the incidence of major depression, and the mechanism of action of antidepressant drugs. In addition, recent data reveal important bidirectional interactions between stress-system hormonal factors in depression and neural substrates implicated in many discrete behavioral alterations in depression (e.g., the medial prefrontal cortex, important in shifting affect based on internal and external cues, the mesolimbic dopaminergic reward system, and the amygdala fear system). We have also advanced data indicating that the hypersomnia, hyperphagia, lethargy, fatigue, and relative apathy of the syndrome of atypical depression are associated with concomitant hypofunctioning of the CRH and LC-NE systems. These data indicate the need for an entirely different therapeutic strategy than that used in melancholia for the treatment of atypical depression, and they suggest that this subtype of major depression will be associated with its own unique repertoire of long-term medical consequences.
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PMID:The endocrinology of melancholic and atypical depression: relation to neurocircuitry and somatic consequences. 989 54

Exonic and intronic mutations in Tau cause familial neurodegenerative syndromes characterized by frontotemporal dementia and dysfunction of multiple cortical and subcortical circuits. Here we describe a G389R mutation in exon 13 of Tau. When 38 years old, the proband presented with progressive aphasia and memory disturbance, followed by apathy, indifference, and hyperphagia. Repeated magnetic resonance imaging showed the dramatic progression of cerebral atrophy. Positron emission tomography revealed marked glucose hypometabolism that was most severe in left frontal, temporal, and parietal cortical regions. Rigidity, pyramidal signs and profound dementia progressed until death at 43 years of age. A paternal uncle, who had died at 43 years of age, had presented with similar symptoms. The proband's brain showed numerous tau-immunoreactive Pick body-like inclusions in the neocortex and the fascia dentata of the hippocampus. In addition, large numbers of tau-positive filamentous inclusions were present in axons in the frontal, temporal, and parietal lobes. Immunoblot analysis of sarkosyl-insoluble tau showed 2 major bands of 60 and 64 kDa. Upon dephosphorylation, these bands resolved into 4 bands consisting of three- and four-repeat tau isoforms. Most isolated tau filaments were straight and resembled filaments found in Alzheimer disease and some frontotemporal dementias with tau mutations. A smaller number of twisted filaments was also observed. Biochemically, recombinant tau proteins with the G389R mutation showed a reduced ability to promote microtubule assembly, suggesting that this may be the primary effect of the mutation. Taken together, the present findings indicate that the G389R mutation in Tau can cause a dementing condition that closely resembles Pick's disease.
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PMID:Tau gene mutation G389R causes a tauopathy with abundant pick body-like inclusions and axonal deposits. 1060 46

Hirsutism was the most often observed symptom in horses with a pituitary gland tumor and was present in all 13 examined horses. Other symptoms were atrophy of muscles (n = 10), hyperhidrosis (n = 8), polyuria/polydipsia (n = 5), bulging or supraorbital fat (n = 3), polyphagia (n = 2), apathy (n = 2) and seizures (n = 2). Laminitis was the most frequently observed concurrent disease (n = 8). Hyperglycaemia (mean, 9.9 +/- 3.71 mmol/l) in 13 horses and glucosuria (median, 55 [range, 2-55] mmol/l) in 7 horses were the most important laboratory results. The dexamethasone suppression test was positive in all tested horses (n = 9) 20 h after administration of dexamethasone. The pituitary gland tumor was visible in every case underwent computed tomography (n = 7). From these results it can be concluded that a pituitary gland tumor can be suspected based on typical clinical signs. Hyperglycaemia and glucosuria support the preliminary diagnosis and a positive dexamethasone suppression test allows a final diagnosis.
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PMID:[Clinical symptoms of and diagnostic possibilities for hypophyseal adenoma in horses]. 1069 98

We describe the clinical and pathologic phenotypes of the G389R mutation in exon 13 of the Tau gene. Progressive aphasia and memory disturbance are the initial signs and begin in the fourth or fifth decade of life, followed by apathy, indifference, hyperphagia, rigidity, pyramidal signs and dementia. Death occurs after two to five years. Magnetic resonance imaging and neuropathologic studies show frontal and temporal atrophy. Pick body-like and axonal filamentous inclusions found in the neocortex and subcortical white matter, respectively, are tau immunoreactive. Immunoblot analysis of sarkosyl-insoluble tau shows two major bands of 60 and 64 kDa that, upon dephosphorylation, resolve into four bands of three- and four-repeat isoforms. Isolated tau filaments are often straight and occasionally twisted. Recombinant mutant tau protein shows a reduced ability to promote microtubule assembly, suggesting that this may be the primary effect of the mutation. The present findings indicate that the G389R mutation in Tau can cause a dementia similar to that in Pick's disease.
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PMID:Progress in hereditary tauopathies: a mutation in the Tau gene (G389R) causes a Pick disease-like syndrome. 1119 77

A 22 year-old woman suffered from recurrent episodes of hypersomnia, apathy, and hyperphagia. The symptoms occurred 3 to 4 times per year, and each attack lasted 2 to 3 weeks. 99mTc-ethylcysteinate dimer brain single photon emission computed tomography (SPECT) was performed during symptomatic and asymptomatic periods. To localize brain regions with perfusion changes during symptomatic period, asymptomatic SPECT was subtracted from symptomatic SPECT. The subtracted SPECT showed significant hypoperfusion in the left hypothalamus, bilateral thalami, basal ganglia, bilateral medial and dorsolateral frontal regions, and left temporal lobe during the symptomatic period. These cerebral hypoperfusion areas support the diencephalic hypothesis and clinical symptoms of Kleine-Levin syndrome.
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PMID:Episodic diencephalic hypoperfusion in Kleine-Levin syndrome. 1694 79

If rational individuals pay the full costs of their decisions about food intake and exercise, economists, policy makers, and public health officials should treat the obesity epidemic as a matter of indifference. In this paper, we show that, as long as insurance premiums are not risk rated for obesity, health insurance coverage systematically shields those covered from the full costs of physical inactivity and overeating. Since the obese consume significantly more medical resources than the non-obese, but pay the same health insurance premiums, they impose a negative externality on normal weight individuals in their insurance pool. To estimate the size of this externality, we develop a model of weight loss and health insurance under two regimes--(1) underwriting on weight is allowed and (2) underwriting on weight is not allowed. We show that under regime (1), there is no obesity externality. Under regime (2), where there is an obesity externality, all plan participants face inefficient incentives to undertake unpleasant dieting and exercise. These reduced incentives lead to inefficient increases in bodyweight, and reduced social welfare. Using data on medical expenditures and bodyweight from the National Health and Interview Survey and the Medical Expenditure Panel Survey, we estimate that, in a health plan with a coinsurance rate of 17.5%, the obesity externality imposes a welfare cost of about $150 per capita. Our results also indicate that the welfare loss can be reduced by technological change that lowers the pecuniary and non-pecuniary costs of losing weight, and also by increasing the coinsurance rate.
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PMID:Health insurance and the obesity externality. 1954 56


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