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

In this study, dietary intervention before and after weaning was used to produce body fatness in adult rats ranging from severe obesity (61% body fat) to the lean condition (18% body fat). To produce severe obesity, rats were programmed for a high caloric intake during suckling. After weaning, they were provided unrestricted access to a diet in which approximately 40% of the calories were derived from fat (high-fat diet). The high-fat diet appeared to cause hyperphagia such that appetites were highly stimulated between 29 and 58 wk of age. Body weight in these rats stabilized at 1,213 +/- 62 g. Severe obesity was also observed in rats programmed for a low caloric intake if, after weaning, they ate the high-fat diet (59% body fat). These results provide evidence that the fat content of the diet may play a regulatory role in the development of severe obesity.
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PMID:Dietary-induced severe obesity: a rat model. 719 27

Several new developments promise to improve the lot of the morbidly obese. Perhaps the most important of these is the gradual recognition that morbid obesity is a serious illness that is not the result of immorality or gluttony but is, in most cases, a disabling genetically determined handicap. The second advance was the agreement at the National Institutes of Health Consensus Conference, March 25-27, 1991 that medical therapies generally fail to control severe obesity and that surgery should be considered for those individuals who have a body mass index over 40 and, if the comorbidities of obesity, such as diabetes or sleep apnea, are present, to consider surgical intervention when the body mass index is greater than 35. The third development has been the improvement of bariatric surgery, ie, the surgery for morbid obesity, with better operations, better quality controls, and rigorous follow-up. This article reviews the newer concepts of morbid obesity as a disease, delineates the indications for surgery, describes the currently recommended operations, and presents the risks and benefits of these procedures.
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PMID:The surgical treatment of morbid obesity. 758 66

Prader-Willi syndrome is characterized by dramatic hyperphagia and morbid obesity, and is associated with a deficiency in basal and meal-stimulated serum pancreatic polypeptide (PP) levels. Intravenous infusions of pancreatic polypeptide (90 min, 50 pmol/kg/h) restored normal serum PP levels, and a regimen of morning and afternoon PP infusions was found to significantly reduce food intake in Prader-Willi subjects. Food intake was evaluated in a 60-min free-feeding test that shows high reliability and validity. Basal food intake during saline infusions was striking (approximately 60 chicken sandwich quarters), and this intake was reduced overall by approximately 12% during PP infusions. This reduction was apparent only for female subjects, and may have reflected enhanced satiation rather than an overall suppression of food intake. No differences were apparent across subjects, in either basal food intake or the PP-related decrease in food intake, in the presence or absence of the widely recognized chromosomal marker for this syndrome [deletion of 15(q11-q13)]. More specific gene defects as recently reported in these subjects, however, suggest that the Prader-Willi syndrome may represent an important model for the study of food intake regulation.
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PMID:Pancreatic polypeptide infusions reduce food intake in Prader-Willi syndrome. 833 50

Although obesity is difficult to treat, the only effective long-term strategy is an emphasis on adoption of a healthy lifestyle, including exercise, and prudent control over eating habits. Such modifications in behavior can be implemented by some patients with the help and encouragement of their physician, whereas other patients need professional, psychological intervention. VLCDs are useful to attain initial weight loss, but are not (nor were ever intended to be) a substitute for the development of a prudent lifestyle. Thus, for patients with major obesity (BMI > 30), the combination of a VLCD with behavior modification offers the best medical approach to obesity. Surgery has a role in the treatment of obesity, but only in patients with morbid obesity that have repeatedly failed other treatments, including treatments involving a serious effort at behavior modification.
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PMID:A prudent and practical approach to the treatment of obesity. 934 68

Benzodiazepine receptor (BZR) agonists, used extensively for their anxiolytic effects, have been shown to increase food intake in many mammalian species. Little information, however, is available on the effects of BZR agonists on feeding behaviors of humans. Food intake was evaluated in a 60-minute free-feeding standardized test after the acute administration of the BZR agonist chlordiazepoxide (CDP, Librium; 5 mg or 20 mg) or placebo. Subjects were 12 individuals with the Prader-Willi syndrome (PWS), a disorder characterized by extreme hyperphagia and morbid obesity, and 11 controls with obesity. PWS subjects showed the characteristic hyperphagia associated with the appetite disorder, consuming more than six times as many sandwiches as controls with obesity. Results revealed no significant effect of either dose of CDP on the food intake of either group. Serum assays revealed that dose-dependent, clinically effective levels of CDP and active metabolites were achieved. These results suggest that acute administration of the BZR agonist CDP, at the therapeutic levels used, may not increase food intake in populations with obesity. However, the chronic effects of CDP on appetite in human populations still need to be explored.
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PMID:Food intake in Prader-Willi syndrome and controls with obesity after administration of a benzodiazepine receptor agonist. 952 67

The adipocyte-specific hormone leptin, the product of the obese (ob) gene, regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure. Leptin acts through the leptin receptor, a single-transmembrane-domain receptor of the cytokine-receptor family. In rodents, homozygous mutations in genes encoding leptin or the leptin receptor cause early-onset morbid obesity, hyperphagia and reduced energy expenditure. These rodents also show hypercortisolaemia, alterations in glucose homeostasis, dyslipidaemia, and infertility due to hypogonadotropic hypogonadisms. In humans, leptin deficiency due to a mutation in the leptin gene is associated with early-onset obesity. Here we describe a homozygous mutation in the human leptin receptor gene that results in a truncated leptin receptor lacking both the transmembrane and the intracellular domains. In addition to their early-onset morbid obesity, patients homozygous for this mutation have no pubertal development and their secretion of growth hormone and thyrotropin is reduced. These results indicate that leptin is an important physiological regulator of several endocrine functions in humans.
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PMID:A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. 953 16

Diabetes mellitus is not a diagnostic criterion for Prader-Willi syndrome (PWS), but it is often found in PWS patients. The etiology for diabetes mellitus in PWS may be related to the morbid obesity and consequent insulin resistance, because a decrease of oxytocin neurons and leptin resistance in PWS may cause hyperphagia, inducing obesity. However, treatment with growth hormone (GH) is beneficial for the majority of GH-deficient PWS children, because relative decreased fat mass and increased fat-free mass could prevent obesity and concomitant insulin resistance. Hypogonadism is thought to be due to hypogonadotrophic hypogonadism in a majority of PWS patients. Hypergonadotrophic hypogonadism secondary to cryptorchidism and its treatment is shown in other cases. Low luteinizing hormone and high follicle-stimulating hormone levels in PWS cases in young men with idiopathic oligospermia or in the early stages of puberty is less frequently reported.
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PMID:Prader-Willi syndrome, diabetes mellitus and hypogonadism. 1066 37

The Prader-Willi Syndrome shortens the life of patients due to the morbid obesity which it entails. The compulsive hyperphagia associated with it makes a dietetic treatment or a gastroplasty difficult. This study presents the case histories of three patients suffering from the Prader-Willi syndrome who were operated on by means of a Scopinaro's bilio-pancreatic diversion. Following a marked reduction the first year, the weight loss stabilized and then tended to diminish. The observation of three cases which continued for two and a half to six years did not reveal any considerable metabolic problems. The deficiency of iron, vitamins D and B12 as well as folic acid had to be made up by supplementation. These results are comparable with the most favorable ones in the literature. Even if the effect on the weight loss is not spectacular, the operation manages to hold off the development of the obesity, inexorable for those with the Prader-Willi syndrome, and prevents lethal complications, without having notable side effects. Lifting coercive dietary measures improves the quality of life.
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PMID:Long-term Result of Treatment of Prader-Willi Syndrome by Scopinaro's Bilio-pancreatic Diversion. Study of Three Cases and the Effect of Dextrofenfluramine on the Postoperative Evolution. 1071 67

A triple-lumen Moss(c) gastrostomy tube was advanced into the proximal duodenum as an adjunct to the postoperative management of patients who underwent vertical banded gastroplasty (VBG) for the treatment of morbid obesity. The tube efficiently aspirated the proximal duodenum and stomach to prevent postoperative ileus and allow maximum immediate postoperative absorption of an elemental diet fed simultaneously into the distal duodenum. Decompression and feeding were started as soon as the patient arrived in the recovery room. Both were continued for at least the first 48 h after surgery. Patients seemed to improve better clinically on this postoperative regimen than with only the traditional i.v. infusion of fluids, carbohydrates, and electrolytes. The length of stay also was shorter than that allowed in the Diagnosis Related Group (DRG) for the; surgical management of morbid obesity: with the average of 3.0 days (range 2-6 days) versus the general mean length of stay of 7.4 days. Immediate enteral decompression and hyperalimentation through a gastroduodenostomy tube is a useful adjunct to the post-VBG treatment of morbidly obese patients.
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PMID:Efficient Decompression and Immediate Enteral Hyperalimentation via Gastrostomy as an Adjunct to Gastroplasty. 1071 70

Obesity is a common feature of pseudohypoparathyroidism (PHP) type 1a, but is usually associated with short stature. We describe two children referred because of hyperphagia and excessive weight gain from early infancy. Tall stature in both children initially confounded the diagnosis of PHP, but on follow-up both children developed the typical hormonal abnormalities and Case 2 developed typical skeletal features of Albright hereditary osteodystrophy. PHP type 1a is caused by germline loss of function mutations in the alpha subunit of GS, the ubiquitously expressed G protein that couples many hormone receptors to the adenylate cyclase second messenger system. Recent evidence suggest that the hypothalamic GS protein coupled melanocortin-4 receptor (MC4R) may mediate the central effects of leptin on inhibition of satiety. Similar patterns of infancy onset hyperphagia, excessive weight gain and tall stature are seen in subjects with congenital leptin deficiency and in subjects with MC4R mutations. We suggest that the genetic mutations in GSalpha which underlie PHP type 1a may also directly result in severe obesity. This diagnosis should be considered in any child with a history of hyperphagia and early onset morbid obesity.
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PMID:Pseudohypoparathyroidism--another monogenic obesity syndrome. 1071 39


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