Alternatively, our data suggest that the absence of glucose, during OLLT, might explain the decrease of hepatic GLUT2 expression, and as reported, in liver-specific GLUT2 knockout mice [38], this would not affect the normal glucose output capacity, since gene expression of Glu6Pase was raised and normoglycemia was maintained in the 7mAL/7mFR rats and in the 24mFR rats, and hyperglycemia occurred in the 24mAL rats. This evidence concerns the gene SLC2A2 and Hyperglycemia.