Bone abnormalities and unilateral eye deterioration in aspartate-glutamate carrier deficient mice

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Aspartate-glutamate carrier deficient mice (citrin^<-/->, aralar^<+/-> mice) demonstrated growth retarded rate and bone abnomalities compared with their citrin-KO (citrin^<-/->, aralar^<+/+> mice) littermates. Citrin^<-/->, aralar^<+/-> mice fail to display hyperammonemia after oral administration of sucrose which is one of features of human type II citrullinemia model mice, citrin^<-/->, mGPDH^<-/-> mice. No citrin^<-/->, aralar^<+/-> mice which is suffer from unilateral eye deterioration demonstrated both eye aberrations up to 1 year.