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

The urinary excretions by young healthy men of histamine and its metabolites, N tau-methylhistamine, imidazole acetic acid, and imidazole acetic acid conjugate(s), increased 1-3 h after food intake. The increase was seen even after the intake of konnyaku (mannan) as a protein-deficient food, suggesting that physical stimulation of the gastric mucosa by food is the main cause of histamine release. This suggestion was confirmed by the following findings in patients and mice. In patients with stomach diseases, gastrectomy resulted in decreases in the excretion of histamine and its metabolites in the urine, and patients subjected to intravenous hyperalimentation excreted less histamine and its metabolites in the urine than normal subjects. In mice, a correlation of histamine excretion with food intake was demonstrated experimentally. Namely, mice fed only during the night (21:00-0:00) showed increased excretions of histamine and its metabolites at 23:00-3:00, whereas those fed in the morning (9:00-12:00) showed increased excretions of those compounds at 11:00-15:00. All these results are consistent with the idea that urinary histamine and its metabolites mainly originate from the stomach.
J Biochem 1984 Dec
PMID:Effect of food intake on urinary excretions of histamine, N tau-methylhistamine, imidazole acetic acid and its conjugate(s) in humans and mice. 644 93

Rats treated with a sublethal dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 15 micrograms/kg) exhibited reduced feed intake and loss of body weight for the first 3 weeks after treatment. During the next 10 weeks, TCDD-treated rats maintained their body weight at a lower nearly constant percentage of that of control rats fed ad libitum. At no time did rats treated with TCDD exhibit hyperphagia which would have returned their weight to a normal level. Control rats pair-fed to TCDD-treated rats for more than 7 weeks displayed compensatory hyperphagia when permitted to feed ad libitum and their weight recovered to a near-normal level. The lower level of body weight in TCDD-treated animals was apparently due to a reduction in the regulation level or "set-point" for body weight. The following findings in TCDD-treated and control rats fed ad libitum supported this idea. First, when the reduced weight of the TCDD group was challenged by changes in the caloric density or palatability of the diet, TCDD-treated rats exhibited adjustments in feed intake and body weight that were essentially identical to those of control rats. Second, when body weight was manipulated by feeding a high-calorie diet or by restricting feed intake, both TCDD-treated and control rats quickly returned to weight levels from which they had been displaced. Third, carcass analyses conducted 7 weeks after treatment revealed that TCDD-treated rats had lower absolute amounts of body fat, protein, and water. However, when these constituents were expressed as percentages of total body weight no remarkable differences from the control were observed. Fourth, when TCDD-treated rats were induced to overeat and restore body weight to the same level as control rats fed ad libitum. TCDD-treated animals did not reassume a normal body composition but became obese. Obesity was also observed when control rats were induced to overeat. Thus, TCDD-treated rats regulate their body weight in the same fashion as control rats but at a weight regulation level or set-point that is markedly reduced.
Toxicol Appl Pharmacol 1984 Dec
PMID:Body weight regulation in rats treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin. 650 77

During the early months of life, gains in length and weight are more rapid by formula-fed than by breast-fed infants and we and others have speculated that the greater gains of the formula-fed infants are the result of greater food intake. If overfeeding during early infancy resulted in establishment of habits of overeating, or if, for any other reason, diet-induced fatness in infancy persisted into childhood, we might be able to demonstrate differences in fatness in childhood related to mode of feeding (breast or bottle) during infancy. We therefore examined at age 8 years 469 children born in 1966-1971 who had been studied intensely in our unit from 8 to 112 days of age. At age 8 years there were no differences in indices of fatness related to mode of feeding during infancy. Serum concentrations of cholesterol at age 8 years were also of interest because of reports from animal studies that differences in feeding during early life may be responsible for subsequent differences in cholesterol homeostasis. Cholesterol concentrations at age 8 years did not demonstrate significant differences related to mode of feeding during infancy. It is possible, however, that age 8 years is too early for an effect to be demonstrated.
Pediatr Res 1984 Dec
PMID:Indices of fatness and serum cholesterol at age eight years in relation to feeding and growth during early infancy. 652 35

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.
Neuroscience 1983 Dec
PMID:Changes in body weight and food-related behaviour induced by destruction of the ventral or dorsal noradrenergic bundle in the rat. 660 27

Over the past 28 years, one of us (W. E. N.) has reconstructed the esophagus with the right colon for congenital and benign disease in 84 patients. The first patient in the series, who was operated on in 1955, remains asymptomatic. Nine patients had congenital tracheoesophageal fistula with atresia; 4, esophageal varices; 30, advanced obliterative esophagitis; and 23, corrosive destruction. In 7, severe esophagitis followed esophagogastrectomy; 4 had unsuccessful operations for achalasia; and 7 had colon bypass following esophageal perforation. Eleven early nonfatal complications occurred. Late nonfatal complications were seen in 6 patients. There were 4 early deaths (4%): following dehiscence of an intrathoracic esophagocolic anastomosis and 1 due to peritonitis. Four individuals died over the years, and 5 patients were lost to follow-up. The late results in 71 patients show that 60 (84.5%) believe they have a satisfactory result. Nine (13%) individuals are symptomatic, and 2 (2.8%) must be classified as failures. Early complications have been minimized by using preoperative intestinal angiography, anastomotic stapling techniques, and the Doppler study intraoperatively to prognosticate colon blood flow. Several important observations have been made: anastomosis in the neck is preferable; the transplanted colon dilates from loss of motor activity but is functionally adequate; an isoperistaltic segment is preferable, but an antiperistaltic implant suffices; colonic mucosa is relatively resistant to acid-peptic digestion; and hyperalimentation is mandatory in very ill and debilitated patients.
Ann Thorac Surg 1983 Dec
PMID:Colon replacement of the esophagus for congenital and benign disease. 665 76

The hyperphagia/obesity syndrome produced by paraventricular hypothalamic (PVH) lesions and that produced by medial hypothalamic (MH) knife cuts were compared in adult female rats. Each treatment produced hyperphagia and overweight on a chow diet, although the PVH effect was less than the knife-cut effect. Each treatment also produced qualitatively similar ingestive responses to unpalatable quinine- and sucrose octaacetate-adulterated diets and to palatable dextrose and fat diets during the dynamic and static weight-gain phases. The PVH lesions and MH cuts disrupted day/night feeding patterns and elevated water intakes but not water/food intake ratios. However, PVH lesions, unlike MH cuts, did not increase emotional reactivity. The relation of the PVH syndrome to the classic hypothalamic hyperphagia syndrome is discussed. Also considered is the neuroanatomical substrate responsible for the PVH hyperphagic effect.
Behav Neurosci 1983 Dec
PMID:Paraventricular hypothalamic lesions and medial hypothalamic knife cuts produce similar hyperphagia syndromes. 665 67

The mechanisms by which fat feeding suppresses the hyperphagia of diabetic rats were examined. Rats that were allowed to consume a small amount (1.5 ml) of corn oil decreased subsequent food intake within 6 hr after ingesting. Diabetic rats decreased food intake much more than normal rats. Similar results were obtained when oil was given intragastrically. Analysis of blood samples revealed that diabetic rats showed greater increases in plasma ketones and triglycerides and smaller increases in plasma glycerol than normal rats following consumption of 1.5 ml corn oil. This difference between diabetic and normal rats appeared when rats were allowed to eat after oil ingestion as well as when they were fasted. Brief periods of food deprivation (2.5-4.5 hr) substantially increased plasma ketones and glycerol and decreased plasma triglycerides in both diabetic and normal rats. The results indicate that diabetic rats decrease food intake more than normal rats after fat feeding because they oxidize more of the ingested fat.
Physiol Behav 1983 Dec
PMID:Food intake and blood fuels after oil consumption: differential effects in normal and diabetic rats. 666 74

Acute feeding responses to 2-deoxyglucose (750 mg/kg) or insulin (12 U/kg) were examined 24 hr after intracisternal injection of the GABA-transaminase inhibitor ethanolamine-O-sulfate (EOS, 400 micrograms) in female rats. EOS pretreatment completely abolished acute feeding responses to both challenges. These findings complement recent research showing that central EOS can reverse chronic overeating in several experimental preparations. The present results are consistent with previous indications that EOS treatment may induce a metabolic shift away from brain glucose utilization, thus making glucoprivation irrelevant as a metabolic challenge. An alternative possibility is that EOS-induced increases of brain GABA may offset specific neural mechanisms through which these glucoprivic agents normally induce feeding.
Pharmacol Biochem Behav 1982 Dec
PMID:Inhibition of acute feeding responses to systemic 2-deoxyglucose or insulin in rats pretreated with the GABA-transaminase blocker ethanolamine-O-sulfate (EOS). 676 11

Thirty-six patients (27 with ulcerative colitis and 9 with Crohn's disease) completed a prospective controlled therapeutic trial of intravenous hyperalimentation (IVH) and total bowel rest in acute colitis. All patients received prednisone 40 mg/day which was reduced every 3 days or more depending on the response to treatment. The trial was completed either when the prednisone was reduced to 10 mg/day or when the patient came to colectomy. In the control group (5 males, 12 females; mean age 44.7 yr), 6 came to surgery and 11 responded medically in a mean time of 23.7 days. In the IVH group (8 males, 11 females; mean age 37.4 yr) 9 came to surgery and 10 responded medically in a mean time of 21.2 days. The results of this trial show that IVH with total bowel rest has no primary therapeutic effect in acute colitis.
Gastroenterology 1980 Dec
PMID:Controlled trial of intravenous hyperalimentation and total bowel rest as an adjunct to the routine therapy of acute colitis. 677 33

The increasing awareness among surgeons of overwhelming postsplenectomy sepsis has led to new and innovative procedures to save the spleen. In pancreatic transection injuries (Type II)26 the classical treatment has been distal pancreatectomy and splenectomy. The opportunity to treat several patients with pancreatic transections sustained during blunt abdominal trauma lead to the review of the literature on the subject. Particular attention was paid to treatment of these injuries during distal pancreatectomy with splenic salvage, appropriate drainage, and hyperalimentation. Associated complications were likewise investigated and reviewed.
Ann Surg 1982 Dec
PMID:Blunt transection of the pancrease treated by distal pancreatectomy, splenic salvage and hyperalimentation. Four cases and review of the literature. 681 55


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