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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three experiments contrasted the effects of 6-hydroxydopamine-induced lesions of the ventral noradrenergic and dorsal noradrenergic projections, predominantly to hypothalamus and cortex, respectively, upon body weight changes and food-related behaviour in the rat. In general, ventral noradrenergic bundle lesions enhanced weight gain and these effects were exaggerated by the provision of palatable cheese to the standard chow diet. In contrast, lesions of the dorsal noradrenergic bundle produced minor changes in body weight. Associated with the effects of ventral noradrenergic bundle lesions were hyperphagia, enhanced suppression of intake of food adulterated with quinine, (at high concentration), a small attenuation of food neophobia, and enhanced acquisition, but not performance, of the eating response to tail-pinch stimulation. These ventral noradrenergic bundle lesions failed to alter basal activity levels, amphetamine anorexia or the diurnal pattern of eating or activity. In contrast, lesions of the dorsal noradrenergic bundle did not produce either hyperphagia or enhanced rejection of food adulterated with quinine. However, there was a strong attenuation of food neophobia and a retarded acquisition (but unimpaired performance) of eating in response to tail-pinch stimulation. The results are discussed in connection with previous studies of ventral and dorsal noradrenergic bundle lesions, with the effects of ventromedial hypothalamic lesions and with the underlying behavioural and physiological processes that mediate these contrasting effects of different neuroanatomical patterns of central noradrenaline depletion.
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PMID:Changes in body weight and food-related behaviour induced by destruction of the ventral or dorsal noradrenergic bundle in the rat. 660 27

Past literature is reviewed briefly which suggests that variations in brain GABA metabolism may be involved in the control of food intake in rats. Recent experiments from the author's laboratory are summarized in which brain GABA has been elevated in adult female rats by intracisternal injection of the GABA-transaminase inhibitor, ethanolamine-O-sulfate (EOS). Central EOS pretreatment produced dose-dependent anorexia in normal subjects and prevented acute overeating in response to systemic insulin (12 U/kg) or 2-deoxyglucose (750 mg/kg). Similar EOS pretreatment essentially reversed the chronic overeating induced by diet palatability, bilateral medial hypothalamic lesions or genetic predisposition (in Zucker fatty rats). The ubiquity of these anorexic effects in the absence of clear motor debilitation suggests that drugs which elevate brain GABA deserve further investigation for their potential utility in the clinical treatment of overeating.
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PMID:GABA and feeding: reversal of overeating by central GABA-transaminase inhibition. 668 89

We studied a patient with lung cancer, who exhibited severe systemic derangements of metabolism causing cachexia preceding the appearance of a large bulky tumor. The data described herein left no doubt that lung cancer growing in the patient acted as a powerful hypoglycemic factor, setting in motion widespread metabolic disorders. Inappropriate secretion of insulin may be involved in the manifestation of hypoglycemia. However, no ectopic secretion of insulin, glucagon, ACTH and aldosterone appeared to be associated with the carcinoma in the patient. From the present and previous observations, it is stressed that progressive energy loss from the patient occurs by virtue of a combination of severe anorexia and the establishment of a systemic energy-losing cycle dependent on an interplay of glycolysis in the cancer cells and stimulated gluconeogenesis in the host tissues, which in turn results in derangements of protein, lipid and electrolyte metabolism. Attempts to ameliorate the patient's distress and counterbalance the effect of the tumor by parenteral hyperalimentation were not satisfactory and resulted in only a temporary improvement. This study also demonstrated that marked granulocytosis was the result of production of an excess granulopoietic colony stimulating activity by the cancer cells.
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PMID:Hypoglycemia, hypopotassemia and hyperleukocytosis associated with squamous cell carcinoma of the lung. 697 22

Concurrent diabetes mellitus and hyperadrenocorticism were diagnosed in 30 dogs over a 2-year period. Clinical signs included polyuria, hepatomegaly, polyphagia, abdominal distension, truncal alopecia, anorexia, and vomiting. Because of the similar clinical and laboratory findings for hyperadrenocorticism and diabetes mellitus, hyperadrenocorticism was initially overlooked in some dogs. Insulin resistance, characterized by high daily insulin requirements, developed in the diabetic dogs with untreated hyperadrenocorticism. Therapy with o,p'-DDD resulted in precipitous declines in insulin requirements. By lowering the dosage of o,p'-DDD and supplementing with glucocorticoids during the o,p'-DDD loading period, serious hypoglycemia was avoided. Control of coexisting hyperadrenocorticism lessened the severity of the diabetes mellitus, but insulin therapy remained a necessity in all dogs.
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PMID:Diagnosis and management of concurrent diabetes mellitus and hyperadrenocorticism in thirty dogs. 700 30

The case is recounted of a child who was admitted to hospitals several times over a period of 8 years on account of fictitious illnesses invented by his mother. The first occurred when he was 3.5 years old in January 1984. His mother, a nurse, gave a history of intermittent fever for 3 months, loss of appetite and weight. He had been treated with ampicillin, chloramphenicol, and procaine penicillin. No abnormality was detected and his weight at 15.5 kg was appropriate for his age. No fever was recorded throughout 2 weeks in hospital, but he was given chloroquine for possible malaria and then discharged. At follow-up 6 months later, the mother complained of his wheezing. On examination he was normal and had gained 3.8 kg since discharge. The possibility of vernal conjunctivitis plus asthma was entertained and he was then placed on ketotiphen prophylaxis. There was an uneventful follow-up for 6 months. 5 years later in March 1990, his mother related that he had been treated from 22 January 1988 to 21 November 1989 for tuberculosis with streptomycin, isoniazid, rifampicin, and ethambutol. He was also treated with digoxin and Esidrex-K for suspected rheumatic carditis, after which at the University Teaching Hospital, Enugu, he was investigated from 11 April 1989 to 10 August 1989 and found to be normal. One year later in August 1991 she went to one of the authors complaining about polydypsia, polyphagia, and polyuria. Examination had revealed nothing of note. A clinical assessment for diabetes mellitus found the urine specific gravity persistently at 1.010. He was therefore put on carbamazepine (Tegretol) 100 mg t.i.d. After review by a pediatric nephrologist, the child was declared normal. During this visit, the mother and child were interviewed separately. He believed he was ill because his mother said so. A diagnosis of Munchausen syndrome by proxy was made. The mother was referred back to her doctor to arrange for psychiatric care. In Munchausen syndrome, patients fabricate a variety of symptoms and evidence of illness that have no organic basis. Munchausen syndrome by proxy is a form of child abuse, difficult to diagnose, that could result in death. It is more prevalent in affluent countries with sophisticated medical facilities. Its rarity in developing countries may contribute to the difficulty of detection.
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PMID:Munchausen syndrome by proxy: an experience from Nigeria. 750 55

Protein and calorie malnutrition often starts before initiation of dialysis, and reflects the anorexia and the catabolic state of chronic renal failure. In the face of inadequate dialysis, which perpetuates the uremic state, malnutrition often worsens. Several studies, though not all, suggest that optimal dialysis improves nutritional status of dialysis patients. Such optimal dialysis now must include the use of biocompatible membranes to deliver Kt/V > 1.4 (urea reduction ratio > 65%). Additional interventions can include the use of enteral or intravenous hyperalimentation, and recombinant growth factors such as growth hormone or insulin-like growth factor-1. Importantly, studies to document the improvement in the morbidity and mortality of patients with these interventions are still needed and require large multicenter trials.
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PMID:Interventions to treat malnutrition in dialysis patients: the role of the dose of dialysis, intradialytic parenteral nutrition, and growth hormone. 761 Dec 60

This study evaluated the impact on family relations of behavioral family systems therapy (BFST) versus ego-oriented individual therapy (EOIT) as treatments for adolescents with anorexia nervosa. Twenty-two adolescents meeting DSM-III-R anorexia nervosa criteria were randomly assigned to receive approximately 16 months of either BFST or EOIT along with a common medical and dietary regimen. BFST emphasized parental control over eating, cognitive restructuring, and problem-solving communication training. EOIT emphasized building ego strength, adolescent autonomy, and insight. Measures including body mass index, self-reported general and eating-related conflict, and observed general and eating-related communication. Both treatments produced significant reductions in negative communication and parent-adolescent conflict, with some differences between condition and between eating and non-eating related measures; the improvements in eating-related conflict were maintained at a 1-year follow-up. The study demonstrated that structured therapies for adolescent anorexia do impact family relations, even when the family is never seen as a unit during the therapy.
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PMID:Family versus individual therapy for anorexia: impact on family conflict. 762 Apr 70

In Laron-type dwarfism, a basal growth rate independent of GH and insulin-like growth factor-I (IGF-I) is maintained. This represents a unique model to further assess the relationship between growth and nutritional status. In a child aged 3 yr, 7 months with severe anorexia, growth was followed in relation to his caloric intake. While receiving 496 Cal/day with 11.6 g/day protein, he grew at a rate of 2 cm/yr (period I). The mean plasma IGF-I level was below 0.07 U/mL, insulin was 3.8 +/- 0.2 microU/mL, and blood glucose was 2.9 +/- 0.3 mM/L. During moderate hyperalimentation with 1280 Cal/day and 38.3 g/day protein (period II) for 7 months, growth rate increased to 9 cm/yr with no significant change in plasma IGF-I and persistence of relative hypoinsulinemia (low response to oral glucose tolerance test). IGF-binding proteins, analyzed by Western ligand blotting, showed that 41.5- and 38.5-kilodalton forms, which were initially low, increased to form a pattern similar to that observed in hypopituitarism. These results suggest that catch-up growth did not require normal circulating GH and/or IGF-I activity. Therefore, nutrition contributes to catch-up growth and achievement of potential statural growth by a distinct cellular effect.
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PMID:Effects of nutrient intake on growth, insulin-like growth factors, and their binding proteins in a Laron-type dwarf. 767 25

Cancer anorexia/cachexia is a common clinical problem that substantially impacts upon the quality of life and survival of affected patients. Extensive investigations have not supported the use of either enteral or paternal hyperalimentation for such patients. Despite positive pilot trial reports, large randomized studies have been unable to demonstrate a clinically defensible role for either pentoxifylline, cyproheptadine, or hydrazine sulfate for patients with anorexia. Multiple placebo-controlled, randomized, double-blind, clinical trials have demonstrated that corticosteroids do have appetite-enhancing properties in patients suffering from cancer anorexia/cachexia, but none of these studies has demonstrated weight gain. In comparison, multiple studies have demonstrated that the progestational agent, megestrol acetate, has both appetite-enhancing and weight-promoting properties.
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PMID:Management of cancer anorexia/cachexia. 777 79

Terfenadine (5 mg/kg body weight, q12h) and placebo (0.5 grain/dog q12h) were both administered orally as individual agents to 18 dogs with atopy in a double-blinded study. No dog improved. Hyperactivity, polyphagia, lethargy, anorexia, increased pruritus, or ocular discharge were seen in three dogs treated with terfenadine. Under the conditions of the study, terfenadine was not a useful antipruritic agent for the atopic dog.
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PMID:Failure of terfenadine as an antipruritic agent in atopic dogs: results of a double-blinded, placebo-controlled study. 805 74


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