|
| Magel2-null mice exhibit neonatal growth retardation, excessive weight gain after weaning, and increased adiposity with altered metabolism in adulthood as seen in PWS patients | |
mice lacking Magel2 display increased weight gain with excess adiposity and other defects suggestive of hypothalamic deficiency  |
|
paternally Magel2-null mice have reduced embryonic viability but otherwise normal embryonic growth in survivors, followed by post-natal growth retardation and excessive weight gain, recapitulating aspects of the PWS phenotype |