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)

1. Over- or undernutrition of newborn mice was caused by suckling in litters consisting initially of four or eighteen pups. After weaning mice were fed ad lib. At 13 weeks of age some mice from large litters received gold thioglucose (GTG: 600 mg/kg intraperitoneally) to induce hyperphagia, and mice were killed at 13, 19.5, 26, 39 and 52 weeks. 2. Total carcass lipid and the size and number of adipocytes in the inguinal subcutaneous, genital, perirenal and mesenteric depots were determined. 3. Mice, both male and female, raised in small litters were heavier and had more carcass fat at all ages than mice raised in large litters. After GTG-treatment mice from large litters were heavier and fatter than mice raised in small litters. 4. Fat distribution between the depots was related to carcass lipid content and not to treatment. The order of depot development was subcutaneous, parametrial, perirenal and mesenteric in females and epididymal, subcutaneous, perirenal and mesenteric in males. At 13 weeks the depots in males were more developed than those in females. 5. Litter size had no effect on adipocyte volume in female mice at 13 weeks but by 52 weeks small-litter mice had larger cells in all depots and more cells in the parametrial and perirenal depots. 6. Male mice from small litters had bigger cells at 13 weeks in all depots compared with males from large litters but by 52 weeks no significant differences remained. Greater numbers of cells were present only in the perirenal and mesenteric depots of small-litter males at some ages. 7. Depots of GTG-treated large-litter female mice had larger cells than those of small-litter females, while a similar number of cells was found by 52 weeks in all but the perirenal depot, which had significantly more cells. 8. GTG treatment of male mice from large litters also caused bigger cells than in small-litter mice, and an increased depot cell number at earlier ages in all but the epididymal depot. By 52 weeks cell numbers were similar in depots from small-litter and GTG-treated large-litter mice, except for the epididymal depot from the latter which had fewer cells. 9. Increases in cell numbers with age in different depots occurred independently of existing cell mean volume and even of tissue growth, suggesting the presence of an in-built chronology, at least in older mice.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of litter size and subsequent gold-thioglucose-induced obesity on adipose tissue weight, distribution and cellularity in male and female mice: an age study. 313 38

Twenty-seven patients with the presumed diagnosis of Prader-Willi syndrome (PWS) were studied clinically and cytogenetically. The patients were classified into three study groups on the basis of their clinical pictures: group 1 with 12 children meeting the strict diagnostic criteria for PWS; group 2 with nine floppy infants and young children, aged 3 years or less, without obesity and hyperphagia; and group 3 with six older children in whom some characteristic features of the syndrome were absent. High-resolution GTG banding of prometaphase chromosomes revealed del(15)(q11.1;q12) in eleven and t(15;15)(qter----p11.2::q12----qter) in one of the twelve group 1 patients. In group 2, four patients had del(15)(q11.1; q12), one had t(15;15)(qter----p11.1::q13----qter), and the remaining four had normal karyotypes. The deleted segment common to the 17 patients with the chromosome aberrations was confined to subband 15q11.2. On the other hand, all six group 3 patients had normal karyotypes. These findings indicated that when strictly defined PWS is absolutely correlated with chromosome 15 aberrations, i.e., there is a positive phenotype-karyotype correlation, and that the aberrations are etiologically related to the syndrome. Parental origin of the deleted chromosome was determined in seven patients, with QFQ-heteromorphisms being used as hereditary markers. The deleted chromosome originated from the paternal chromosome 15 in six patients and from the maternal 15 in one.
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PMID:Clinical and cytogenetic studies of the Prader-Willi syndrome: evidence of phenotype-karyotype correlation. 790 98

1. Over- or undernutrition of newborn mice was caused by suckling in litters consisting initially of four or eighteen pups. After weaning, mice were fed ad lib. At 13 weeks some mice received gold thioglucose (GTG, 600 mg/kg, intraperitoneally) to induce hyperphagia, and all were killed at 39 weeks. 2. Mice suckled in small litters were heavier, with more body fat and protein. GTG treatment induced rapid weight gain and treated mice from large litters were heavier than untreated mice from small litters. However, the effect of litter size was not totally removed since GTG-treated small-litter mice were heavier than GTG-treated large-litter mice and had more fat, although body protein was not different. 3. Fat distribution between the depots was related to total body fatness and not to the treatment. 4. In male mice, preweaning undernutrition resulted in smaller fat depots containing smaller cells. GTG treatment of large-litter mice restored both to the levels found in small-litter mice: the depots of the latter mice were not significantly different after treatment. 5. In female mice, preweaning undernutrition resulted not only in smaller depots and cells but also fewer cells in all depots except mesenteric. GTG-treatment caused larger depots and cells in all mice with no difference in cell size whether mice were from large or small litters. The number of cells in the perirenal and mesenteric depots was greater in GTG-treated mice and was the same whether mice were from large or small litters. 6. We conclude that the level of preweaning nutrition does not affect the ability of adipose tissue to develop subsequently through hypertrophy or hyperplasia of the adipocytes or both, given a sufficient energy surplus consisting of normal pelleted feed, low in lipid.
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PMID:Effect of gold thioglucose-induced obesity on adipose tissue weight and cellularity in male and female mice suckled in large and small litters: investigations into sex differences and site differences. 393 90

Defective BAT thermogenesis is associated with obesity in all the different types of obese animal so far studied. The deficit in normal energy expenditure may be presumed to contribute to the high metabolic efficiency and, together with the hyperphagia, to the obesity of these animals. In two types of obese animal (the ob/ob mouse, the db/db mouse) an increased propensity to become torpid provides an additional energy conserving mechanism that contributes to the high metabolic efficiency. In all these animals an abnormality of hypothalamic function appears likely. Obviously animals with induced hypothalamic lesions (the VMH-lesioned rat, the GTG-obese mouse) have an interruption in the normal pathway that links diet and the sympathetic innervation of BAT. The fa/fa rat resembles these animals in failing to activate BAT thermogenesis in response to diet: the lesion may lie in the hypothalamus itself or elsewhere in the food-intestine-hypothalamus-BAT axis, for example in intestinal peptide hormones. The ob/ob mouse has a peculiar hypothalamic defect that interferes with control of thermogenesis in BAT as well as impairing or exaggerating some aspects of thermoregulation. The db/db mouse resembles the ob/ob mouse but, since the defect is genetically distinct, presumably has a different lesion at the molecular level.
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PMID:Defective brown adipose tissue thermogenesis in obese mice. 406 36