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

Obesity occurs in both clinical and animal forms in a variety of specific models which allow study of its underlining endocrine and mechanistic features. Among the neuroendocrine varieties of obesity, polycystic ovaries are probably the most common. The importance of the gonadal feedback system for regulation of food intake and obesity is indicated by the effects of castration in experimental animals which is a widely used mechanism for producing experimental obesity. Cushing syndrome and hypothalamic obesity are rare clinical syndromes. The current evidence suggests that there are two types of hypothalamic obesity from a mechanistic point of view--one associated with hyperphagia as a necessary and sufficient cause and a disturbance of the autonomic nervous system without hyperphagia as a second mechanism. Although genetic factors underlie most types of human obesity, there are several dymorphic forms of obesity including the Prader-Willy syndrome, Cohen's syndrome, Carpenter's syndrome, Ahlstrom's syndrome and the Bardet-Biedel syndrome. The Prader-Willi syndrome is characterized by obesity hypotonia hypogonadism and mental retardation. In animals, a dominant form of inheritance of obesity is seen in the yellow mouse. Current evidence suggests that this syndrome can be explained by reduced acetylation of MSH in the pituitary and/or hypothalamus. Several recessively inherited forms of obesity exist including the obese mouse, the diabetes mouse, fatty rat, the fat mouse, tubby mouse and the corpulent rat. In addition, there are a number of polygenic types of experimental obesity. The final mechanistic classification of obesity are those due to dietary manipulation. For both human beings and animals, a highly fat diet appears to be particularly problematic for the development of obesity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Genetic, hypothalamic and endocrine features of clinical and experimental obesity. 148 Jul 57

Children with Prader-Willi syndrome (PWS) are characterized by obesity, hyperphagia, hypogonadism, and mental retardation with underlying hypothalamic dysfunction and are known to have blunted or absent pancreatic polypeptide (PP) secretion in response to protein meals. In this communication, adults (26 +/- 3 years of age) with PWS were compared with age-matched normal obese and normal weight controls in regards to plasma glucose, insulin, PP, cholecystokinin (CCK), cholesterol, and triglyceride after a high protein meal. Compared with normal weight controls, adults with PWS showed a smaller and delayed rise in plasma insulin, and relatively smaller and delayed PP elevation whereas obese controls revealed hyperglycemia, markedly higher insulin, and moderately higher PP, cholesterol, and triglyceride levels than those with PWS. There was a small increment of CCK levels after a protein meal in all groups of adults. After a protein meal, the molar ratio of PP to CCK doubled in normal weight and PWS groups, and this ratio tripled in the normal obese group, suggesting no reduced PP secretion in PWS in response to CCK stimulation. PP hyposecretion in PWS thus appears to be a part of multiple endocrinopathy associated with hypothalamic dysfunction.
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PMID:Protein meal-stimulated pancreatic polypeptide secretion in Prader-Willi syndrome of adults. 266 31

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.
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PMID:Neonatal diagnosis of Prader-Willi syndrome and its implications. 368 23

Prader-Willi syndrome (PWS) is characterized by hypotonia at birth, hypogonadism, early childhood obesity, and mental deficiency. Hypogonadotropic hypogonadism is a major characteristic of patients with PWS, and it is speculated to be due to hypothalamic insufficiency. Two adult female patients with PWS and no prior history of menses are presented. Both of these patients were treated with fluoxetine for psychopharmacologic management of obsessive features in the form of food preoccupation and hyperphagia or for compulsive behaviors in the form of severe self-injurious behaviors. The two female patients with PWS who had primary amenorrhea developed vaginal bleeding believed to be menses following at least 6 months of treatment with fluoxetine. Mature hypothalamic function is characterized by pulsatile release of gonadotropin-releasing hormone (GnRH) in a critical range of frequency and amplitude. Central nervous system neurotransmitters may modify GnRH secretion. Fluoxetine specifically inhibits the reuptake of serotonin which may impact the hypothalamic-pituitary-ovarian system in female patients with PWS.
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PMID:Onset of menses in two adult patients with Prader-Willi syndrome treated with fluoxetine. 749 74

Characteristics are hypotonia, problems with feeding and thriving in the neonate and infant, later hyperphagia and severe obesity. Other findings are dysmorphic traits, hypogonadism, short stature, developmental delay, mental retardation and behavioural problems. Diabetes mellitus (NIDDM) is frequent in adults. Treatment is symptomatic. Prognosis is determined by obesity. PWS occurs almost always sporadically and is found in all ethnic groups and in both sexes. The epidemiology of PWS in Denmark is unknown. In 95% of cases with PWS cytogenetic and molecular genetic investigations show either deletion of the paternal chromosome 15q11q13 or uniparental maternal disomy of chromosome 15. Since 1992 150 bloodsamples of patients suspected for PWS have been investigated by cytogenetic and molecular genetic techniques at the John F. Kennedy Institute, DK-2600 Glostrup; deletion of the paternal chromosome 15 was found in 15 and uniparental maternal disomy of chromosome 15 in eight cases.
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PMID:[Prader-Willi syndrome--clinical picture and genetics]. 772 49

We report a classical case of Prader-Willi syndrome (PWS) in an adult with typical interstitial deletion of chromosome 15, and emphasize the study of hormonal change. This 21-year-old female had PWS face characteristics, small hands and feet, marked obesity, mental retardation, growth retardation, absence of puberty and amenorrhea. She also had the characteristic history of infantile hypotonia, poor feeding, failure to thrive and then improved appetite, followed by obesity from the age of four years. She had compulsive hyperphagia, to the extent of stealing and lying to take food. Chromosome study with high resolution banding technique revealed a small interstitial deletion at band q12 of chromosome 15, which is characteristically found in a majority of patients with PWS. Hormonal study revealed hypogonadism and growth hormone deficiency of supposed hypothalamic origin. She also had non-insulin-dependent diabetes mellitus with decreased pancreatic insulin reserve.
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PMID:Hormonal change in an adult with Prader-Willi syndrome: report of a case. 791 75

Eleven individuals with Prader-Willi syndrome and 10 control subjects who had mental retardation due to other causes (with and without overeating histories) participated in two experiments on food preferences. They gave preference rankings for various foods, then chose between a small amount of their most preferred food and an alternative choice of a larger amount of mixed-preference foods (Experiment 1) or an alternative choice of a larger amount of their least preferred food (Experiment 2). Unlike overweight-prone control subjects who selected sweet food over a larger quantity of unpreferred food, subjects with Prader-Willi syndrome selected preferred items only over least-preferred items (Experiment 2) but not over mixed-preference items (Experiment 1). Implications for treatment were discussed.
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PMID:Food preferences among individuals with and without Prader-Willi syndrome. 888 73

Prader-Willi syndrome is a multi system disorder characterized by neonatal hypotonia, later obesity, hyperphagia and mental retardation. It occurs sporadically, either as a result of microdeletion of chromosome 15p (70%) or as a result of maternal disomy of chromosome 15 (30%). The major problems encountered by parents are those of hyperphagia, food-seeking and obesity, and conduct disorder, particularly tantrums or oppositional behaviour.
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PMID:Prader-Willi syndrome. 1045 84

BACKGROUND: Prader-Willi Syndrome (PRWS) is an uncommon neuroendocrine disorder of genetic origin, described in 1956 by Prader, Labhart and Willi. The main clinical manifestations in the adult are mental retardation, hyperphagia with gross obesity, hypogonadismcriptorhismus and short stature. The life expectancy of the affected individual ranges between 20 and 30 years rarely beyond - due to complications related to excessive obesity. Sustained dieting combined with behavior modification programs, as well as gastric restrictive surgery for obesity, proved to have a high failure rate in PRWS, due to the patients' inability to cooperate in changing their eating habits. METHODS: Biliopancreatic Diversion (BPD), which does not require the patient's cooperation in changing eating habits after surgery, was performed in two PRWS patients (13- and 22-years-old), both with excessive obesity, severe respiratory distress, day sleepiness and limited mobility. RESULTS: Two years after surgery, the 13-year-old had lost 80% of her overweight, while the 22-year-old, after 1 year, had lost 34%. Recent laboratory tests showed normal data in both patients. Their respiratory distress had subsided completely, their mobility improved dramatically, and their self-image and alertness enhanced. CONCLUSION: BPD resulted in an improved quality of life in these patients.
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PMID:Biliopancreatic Diversion in Prader-Willi Syndrome Associated with Obesity. 1073 Dec 52

Although hyperphagia is a salient feature of Prader-Willi syndrome, researchers have yet to move beyond food preference and taste studies to examine more troublesome food-seeking behaviors in this population (e.g., eating food from the trash, eating inappropriate or unpalatable food combinations). Visually based tasks were used to examine willingness to eat contaminated food and various odd food combinations in 50 adolescents and adults with Prader-Willi syndrome, 42 IQ-matched participants with mental retardation, and 50 control participants without mental retardation. Although participants with Prader-Willi syndrome showed understandings similar to those of control participants about the purpose and fate of food, they endorsed eating contaminated food as well as highly unusual edible and inedible food combinations. Findings suggest novel adjuncts to traditional dietary approaches in the Prader-Willi syndrome population. Implications are also discussed for future research on food ideation in this population.
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PMID:Contaminated and unusual food combinations: what do people with Prader-Willi syndrome choose? 1080 6


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