Prader-Willi Syndrome as a Model for Obesity : International Symposium, Zurich, October 2002 (2003. 237 p. w. 38 figs. 25 cm)

Prader-Willi Syndrome as a Model for Obesity : International Symposium, Zurich, October 2002 (2003. 237 p. w. 38 figs. 25 cm)

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  • 製本 Hardcover:ハードカバー版
  • 商品コード 9783805575744

Full Description

Almost fifty years ago, in 1956, three researchers of the University of Zurich, Andrea Prader, Alexis Labhart and Heinrich Willi, first described what is now called the Prader-Willi Syndrome (PWS). The study and the therapy of this syndrome have progressed so rapidly in the past years that the decision was made to share recent advances with the scientific community and to address topics of future research at an international meeting. The results of this meeting are presented in this book. PWS results from a paternally derived deletion or an imprinting defect on chromosome 15. During their first two years of life patients with PWS suffer from muscle weakness, feeding problems and developmental delay. From the age of two years onwards they develop an almost insatiable appetite and suffer from obesity, short stature, hypogonadism and behavior problems. As it is becoming increasingly obvious that PWS is a multisystemic disorder, improving the quality of life of patients and their families requires broad professional support. While growth hormone therapy influences growth and body composition, many other problems such as insufficient satiation, hypoactivity, behavioral difficulties, speech problems and mental retardation remain to be addressed. Parents need psychological support in their daily battle against the eating disorder and the behavioral problems of their child. A comprehensive team approach will yield the best results for both patients and their parents. PWS research may also contribute to basic medical research by providing new insights into the metabolism of obese patients, whose obesity is caused by factors other than PWS. In this way, PWS may be used as a model for obesity.

Contents

Prader-Willi syndrome as a model for obesity, Eiholzer, U.; central nervous system and body weight homeostasis obesity due to mutations in the anorexigenic melanocortin pathway, a paradigm for obesity in Prader-Willi syndrome?, Krude, H., Gr ters, A.; signals that control central appetite regulation, Woods, S.C., Clegg, D.J.; hypothalamic neuropeptides and regulation of fat mass in Prader-Willi syndrome, Goldstone, A.P., Unmehopa, U.A., Thomas, E.L., Brynes, A.E., Bell, J.D., Frost, G.; Ghatei, M.A., Holland, A., Bloom, S.R., Swaab, D.F.; energy balance in prader-willi syndrome compared to simple obesity; assessment of body composition in children with Prader-Willi syndrome or simple obesity, Ellis, K.J.; physical activity and obesity, Westerterp, K.R.; model for a peripheral signaling defect in Prader-Willi syndrome, Lee, P.D.K.; comorbidities or fundamental defects of obesity; characterization of hyperphagia in Prader-Willi Syndrome, Lindgren, A.C.; consequences of impaired growth hormone secretion for body composition and metabolism in obesity and Prader-Willi syndrome, Wabitsch, M.; glucose homeostasis in Prader-Willi syndrome, Zipf, W.B., Schuster, D., Osei, K.; sleep-disordered breathing in children with common obesity, Trang, H.; Dysregulation of Respiration and Sleep in Prader-Willi Syndrome, Schl ter, B.; gonadal function and its disorders in simple obesity and Prader-Willi syndrome, Grugni, G., Morabito, F., Crin , A.