Prader-Willi syndrome: advances in genetics, pathophysiology and treatment

Trends Endocrinol Metab. 2004 Jan-Feb;15(1):12-20. doi: 10.1016/j.tem.2003.11.003.

Abstract

Prader-Willi syndrome (PWS) is a complex human genetic disease that arises from lack of expression of paternally inherited imprinted genes on chromosome 15q11-q13. Identification of the imprinting control centre, novel imprinted genes and distinct phenotypes in PWS patients and mouse models has increased interest in this human obesity syndrome. In this review I focus on: (i) the chromosomal region and candidate genes associated with PWS, and the possible links with individual PWS phenotypes identified using mouse models; (ii) the metabolic and hormonal phenotypes in PWS; (iii) postmortem studies of human PWS hypothalami; and (iv) current and potential advances in the management of PWS and its complications. This could have benefits for a wide spectrum of endocrine, paediatric and neuropsychiatric diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Chromosomes, Human, Pair 15*
  • Gastrointestinal Hormones / metabolism
  • Gene Expression Regulation
  • Genomic Imprinting / genetics*
  • Ghrelin
  • Humans
  • Hyperphagia / complications
  • Hyperphagia / genetics
  • Hypothalamus / physiopathology*
  • Leptin / metabolism
  • Obesity / genetics
  • Peptide Hormones / metabolism
  • Phenotype
  • Prader-Willi Syndrome* / genetics
  • Prader-Willi Syndrome* / physiopathology
  • Prader-Willi Syndrome* / therapy
  • Serotonin / metabolism

Substances

  • Gastrointestinal Hormones
  • Ghrelin
  • Leptin
  • Peptide Hormones
  • Serotonin