Magel2 is required for leptin-mediated depolarization of POMC neurons in the hypothalamic arcuate nucleus in mice.
Prader-Willi Syndrome is the most common syndromic form of human obesity and is caused by the loss of function of several genes, including MAGEL2.Mice lacking Magel2 display increased weight gain with excess adiposity and other defects suggestive of hypothalamic deficiency.We demonstrate Magel2-null mice are insensitive to the anorexic effect of pe