Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Food intake was studied in 339 French children, aged 7-12 years. Daily energy consumption and distribution of intake over the waking hours estimated from dietary histories were compared in children of five corpulence categories. The categories (lean, slim, average, fat, obese) were defined on the basis of the weight/height2 index. No difference in estimated daily energy intake was observed between corpulence groups; however, the reported distribution of intake over the waking hours varied. Obese and fat children ate less at breakfast and more at dinner than leaner peers. The traditionally larger meals of the day (lunch and dinner) represented higher proportions of daily intake in fat and obese children; the energy value of breakfast and afternoon snack was inversely related to corpulence. Although these effects do not rule out hyperphagia or increased 'externality' in some overweight subjects, the results suggest a possible contribution of disturbed metabolic and/or behavioral daily cycles in the development of overweight. This hypothesis, which should be investigated further, suggests prevention strategies.
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PMID:Obesity and food intake in children: evidence for a role of metabolic and/or behavioral daily rhythms. 323 62

The studies based on candidate genes and encoded proteins known to cause severe obesity in rodents, have shown that these genes also contribute to human early-onset obesity especially for those involved in the leptin pathway: the leptin (LEP) and leptin receptor (LEPR) genes. Since 1997, less than 20 individuals carrying a LEP gene mutation have been identified. Patients are mostly characterized by severe early-onset obesity with severe hyperphagia and associated phenotype such hypogonadotrophic hypogonadism, high rate of infection associated with a deficiency in T cell and abnormalities of sympathetic nerve function. Therapeutic option (subcutaneous daily injection of leptin) is available for patients with LEP deficiency. It results in weight loss, mainly of fat mass, with a major effect on reducing food intake and on other dysfunctions including immunity and induction of puberty even in adults. In LEPR deficient subjects, phenotypic similarities with the LEP-deficient subjects were noticed, especially the exhibited rapid weight gain in the first few months of life, with severe hyperphagia and the endocrine abnormalities (hypogonadotrophic hypogonadism, insufficient somatotrophic or thyreotropic secretion). Leptin treatment is useless in the LEPR deficient subjects. Factors that could possibly bypass normal leptin delivery systems are being developed but are not yet currently available for the treatment of these patients. Measurement of circulating leptin may help for the diagnosis of such obesity: it is undetectable in LEP mutation carriers or extremely elevated in LEPR mutation carriers. Thus, LEPR gene screening might be also considered in subjects with the association of severe obesity with endocrine dysfunctions such as hypogonadism and with leptin related to corpulence level.
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PMID:Leptin and leptin receptor-related monogenic obesity. 2262 81