Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross physical or behavioral abnormalities. By 1 month of age, mutant mice exhibit mild obesity. High-fat (Western) diet enhances the weight increase in female mutants. Northern blot analysis of hypothalamus detects mRNA encoding beta-galactosidase and not the endogenous mRNA. Beta galactosidase activity pattern mimic the endogenous gene expression pattern. Y2 receptor binding experiments confirm loss of activity. Mice homozygous for the mutation have increased night time basal heart rate compared to wildtype and exhibit reduced activity levels. Increased food intake is observed. Short term leptin administration elicits a decreased response of 15.2% food intake reduction compared to the 30.5% reduction seen in wildtype controls. Mutant mice are more sensitive to sodium Phenobarbital-induced sedation. Treatment with neuropeptide Y does not induce angiogenesis in the cornea. Wound healing in the skin is delayed with reduced neovascularization. This mutant mouse strain may be useful in studies of the role of the neuropeptide Y receptor and the physiological effects of neuropeptide Y.

These <i> Npy2r</i> knock-out mice exhibit increased night time basal heart rate , reduced activity levels, increased food intake, and delayed wound healing in the skin.

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