Obesogenic diet can affect behavior and body weight in MeCP2 Knockout Mice
Prader-Willi syndrome is characterized by morbid obesity in children and has been linked to a disruption in Methyl-CP-G binding Protein 2 (MeCP2) gene function. Understanding how the disruption of MeCP2 affects behavior and body weight is still not completely understood. In order to examine this, MeCP2 was knocked out in mice. These MeCP2 knockout (KO) mice were subjected to a conditioned place preference test and operant conditioning. These tests assess food preferences and evaluate the impact of food reward. Body weight and high fat (HF) food intakes were also recorded to examine the effects of MeCP2 KO after exposure to an obesogenic diet. Our current data suggest that MeCP2 KO mice have a substantial preference for high fat food but showed less motivation to work for their food reward. MeCP2 KO mice also displayed higher body weight than WT mice even though they ate nearly the same amount of HF food. This indicated that MeCP2 disruption may phenotypically make KO mice more sensitive to obesogenic diets and increase preference for high fat food.
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