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

The capacity of serotoninergic drugs to selectively suppress carbohydrate (CHO) intake was investigated using a procedure sensitive to drug action. The drug d-fenfluramine was administered chronically to rats whose weight had been increased by exposure to either a fat or CHO-supplemented hyperphagia-inducing diet. The drug exerted a more potent anorexic effect and weight-reducing action in rats given the dietary supplements than in control chow-fed rats. Tolerance to the drug was not apparent even after 40 days of treatment. However, there was no evidence for a selective inhibition of CHO intake, nor was the drug more potent with the CHO-supplemented diet. d-Fenfluramine was equally effective against the hyperphagia and weight gain induced by either fat or CHO supplements.
Pharmacol Biochem Behav 1988 Dec
PMID:Do serotoninergic drugs decrease energy intake by reducing fat or carbohydrate intake? Effect of d-fenfluramine with supplemented weight-increasing diets. 325 67

The effects on energy balance and brown adipose tissue thermogenesis of feeding high fat diets of differing fatty acid composition have been investigated in lean and genetically obese (ob/ob) mice. Groups of mice were fed either a low fat diet or a high fat diet based on corn oil or beef tallow for 2 wk. Energy intake and body weight gain were higher in both lean and obese animals fed the high fat diets than in respective mice fed the low fat diets. Carcass energy gain was greater for the obese than for the lean consuming each of the diets. Both lean and obese mice had a higher energy gain when fed the beef tallow diet than when fed the corn oil, despite isoenergetic intakes of the two diets. The thermogenic activity of brown adipose tissue, assessed from measurements of cytochrome oxidase activity and mitochondrial guanosine 5'-diphosphate (GDP) binding, were greater in both lean and obese mice fed the corn oil diet than in those fed the low fat diet. However, GDP binding and cytochrome oxidase activities in lean or obese mice fed the beef tallow diet were not different from those of mice of the same genotype fed the low fat diet. These results indicate that in both lean and obese (ob/ob) mice energy deposition and the stimulation of brown adipose tissue thermogenesis during the voluntary hyperphagia induced by feeding high fat diets are influenced by the fatty acid composition of the diet. A diet rich in polyunsaturated fatty acids appears to result in preferential stimulation of the thermogenic activity of brown adipose tissue, particularly in the ob/ob mouse.
J Nutr 1987 Dec
PMID:Effect of high fat diets on energy balance and thermogenesis in brown adipose tissue of lean and genetically obese ob/ob mice. 332 Feb 90

The utility of bipolar type II affective disorder subgrouping is discussed. There is low diagnostic agreement among clinicians for this putative condition. However, the clustering of cases in families and the poor response to standard treatments suggest that it is a distinct subgroup. The clinical features of the depressive phase of this condition including chronicity, intermittency, hyperphagia, hypersomnia, and reactivity relate it to the constructs of "hysteroid dysphoria," atypical depression, and seasonal affective disorder. Its association to several abnormal motivated behaviors such as alcoholism and eating disorders allows the speculation that a distinct morbid mechanism involving serotonin may underlie it and that new serotonin reuptake blocking drugs may be useful in treating it. Finally, the genetic identity of this subgroup in all likelihood will be established or rejected by genetic linkage studies utilizing the restriction fragment length polymorphism map of the genome.
J Clin Psychopharmacol 1987 Dec
PMID:Therapeutic and genetic prospects of an atypical affective disorder. 332 66

Injection (s.c.) of Na2SeO3 (SS, 20-30 mumol/kg) into male mice initiated eating, which began about 20 min after injection and continued for about 3 h. This initiation effect was observed for mice of different ages and at different times of the day. Other findings of this study were: (1) early morning injection (30 mumol/kg) caused increased food intake, as examined by gastric content 3 h after injection, compared to daytime injection; and (2) SS-induced transient hyperphagia was observed at ambient temperatures of 10 and 22 degrees C, but not at 37 degrees C. This paper discusses these results in relation to SS-induced hypothermia.
Toxicol Lett 1987 Dec
PMID:Transient hyperphagia after sodium selenite injection in mice. 347 53

Metabolic responses to 20 days of overeating were examined in five healthy volunteers. Overfeeding caused a variable increase (1-18%) in basal metabolic rate but no change in metabolic rate during light exercise. Postprandial resting metabolic rate was 8-40% higher (mean 18%) during overeating. The increase in oxygen consumption during a norepinephrine infusion was the same before (20 +/- 2%) and after (17 +/- 3%) overfeeding. Overfeeding elevated basal insulin concentrations in all subjects and increased the insulin response to intravenous glucose in four of five subjects. Overfeeding did not significantly alter mean serum T3 concentrations or erythrocyte 86Rb uptake (an index of Na+,K+-ATPase activity). These data do not confirm reports that overfeeding increases metabolic rate more during exercise than during rest. They also suggest that the increase in resting metabolic rate during overfeeding is not caused by increased responsiveness to norepinephrine or increased serum T3 concentrations.
Am J Clin Nutr 1986 Dec
PMID:Some metabolic effects of overeating in man. 353 42

Porcine insulin (2 mU/rat/day) and its saline vehicle were infused into the third cerebral ventricle of female lean or obese Zucker rats using 14-day osmotic minipumps. Lean rats receiving saline (N = 6) gained 14 +/- 3 g over the 14 days, whereas lean rats receiving insulin (N = 7) lost 12 +/- 4 g over the same interval (p less than 0.01). The average total food intake of the insulin-infused group was decreased by 14% (p less than 0.05) as compared with that of the saline-infused group. The decreased caloric consumption was adequate to account for the body weight loss. Insulin infusion had no effect on food intake or body weight of the obese rats relative to their saline-infused controls (change in body weight: saline (N = 5), -14 +/- 23 g; insulin (N = 7), +3 +/- 14 g). These results suggest that genetically obese Zucker rats have reduced sensitivity to insulin in the central nervous system. We propose that this phenomenon may participate in the development and maintenance of hyperphagia and obesity in these animals.
Appetite 1986 Dec
PMID:Intraventricular insulin reduces food intake and body weight of lean but not obese Zucker rats. 353 15

The function of the entero-insular axis and abnormalities of circulating gastric inhibitory polypeptide (GIP) were examined in mice for 40 days after induction of streptozotocin diabetes. Compared with untreated controls, streptozotocin diabetic mice exhibited marked hyperglycaemia and hypoinsulinaemia, with impaired body weight gain, lipoatrophy, hyperphagia, intestinal hypertrophy, polydipsia and renal hypertrophy. Plasma GIP concentrations were elevated in fed but not fasted streptozotocin diabetic mice, and oral fat evoked a greater GIP response than control mice. In spite of marked hyperglycaemia, fat-stimulated GIP release did not raise plasma insulin in streptozotocin diabetic mice. Neither oral nor intraperitoneal glucose produced a significant insulin response in streptozotocin diabetic mice, although oral glucose resulted in a smaller change in glycaemia. The results indicate that streptozotocin diabetes in mice is associated with ineffectiveness of the entero-insular axis, despite elevated GIP concentrations, which are probably mediated through hyperphagia and defective feedback inhibition by insulin on intestinal K cells.
Diabete Metab 1986 Dec
PMID:Gastric inhibitory polypeptide and the entero-insular axis in streptozotocin diabetic mice. 354 33

Diet plays no direct role in neutralizing the effects of the basic defect in cystic fibrosis, but it can prevent some of the acquired damage caused by complications. Adequate caloric intake provides the energy needed for exercise and cell metabolism, a strong diaphragm, normal cellular immunity, and a positive psychological outlook. Clinical management is aimed at achieving good nutrition. Patient education about nutrition and use of dietary supplements should be started immediately upon diagnosis. Careful clinical examinations and regular follow-up are necessary to detect complications that will interfere with good nutrition. Complications must be treated aggressively. Psychological and social stresses need to be recognized, and psychological referral may be necessary. The clinician's best tools to achieve these goals are the patient's dietary and gastrointestinal history, the anthropometric measurements taken at each office visit, regular patient assessment, and constant attention to detail in monitoring and charting the course of disease. Extraordinary measures, such as nighttime feedings by nasogastric or gastrostomy tube and intravenous hyperalimentation, may be necessary. For best results, these measures must be started before pulmonary complications threaten survival.
Postgrad Med 1987 Dec
PMID:Diet for cystic fibrosis. Nutritional requirements and prescriptions. 368 18

A 16-year-old boy with Prader-Labhart-Willi syndrome (PLWS) had hypotonia, feeding difficulties, failure to thrive, strabismus and bilateral inguinal hernias with cryptorchidism during infancy followed by hyperphagia, marked early-onset obesity with insulin-dependent diabetes mellitus and necrobiosis lipoidica diabeticorum, short stature, hypogonadotropic hypogonadism and some of the facial characteristics of the individuals with the PLWS. IQ is estimated around 90. Cytogenetic studies showed mosaicism: 45,X, t(Y;15) with partial deletion 15 (15pter----15q12); 46,X, t(Y;15), dic (15)(15pter----15q12::15q12----15pter) and 47, X, t(Y;15), dic(15), dic(15). The dic(15) was bisatellited, NOR-positive on both arms and represented inv dup(15). Thus, the 2 lines with the dic(15) showed partial trisomy 15 (15pter----15q12) and partial pentasomy 15 (15pter----15q12), respectively. The cell line ratios were different in lymphocyte and fibroblast cultures. The unique cytogenetic findings in this patient, the reports of a variety of chromosome 15 aberrations in PLWS, as well as aberrations of other chromosomes, suggest that the condition is a contiguous gene syndrome rather than an aneuploidy syndrome.
Am J Med Genet 1987 Dec
PMID:Unique mosaicism in Prader-Labhart-Willi syndrome--a contiguous gene or aneuploidy syndrome? 368 18

Although Prader-Willi syndrome (PWS) patients usually first present with neonatal hypotonia and feeding difficulty, they later show hyperphagia, obesity and mental retardation. Since deletions of chromosomes 15q11-q13 are noted in most PWS patients cytogenetic analysis allows one to diagnose infants suspected of PWS with a greater certainty. We report on 5 hypotonic infants clinically suspected of PWS in the first 3 months of life, whose diagnosis was confirmed by cytogenetic studies showing monosomy of 15q11-q13. Early diagnosis of PWS can lead to prevention of obesity, but counseling of parents has been difficult. Although there are significant benefits to the early diagnosis of PWS, the cost-effectiveness and practicality of screening all hypotonic infants using high resolution cytogenetic analysis has been addressed systematically.
Am J Med Genet 1987 Dec
PMID:Neonatal diagnosis of Prader-Willi syndrome and its implications. 368 23


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