Previously documented glucose intolerance and enhanced glucose-stimulated insulin secretion in vivo in BN.GK-Nidd/gk1 congenics [18] have validated the most significant phenotypic features of the QTLs originally detected in the (GKxBN) F2 cross [12] and further confirmed in an F2 cross derived from BN.GK-Nidd/gk1 congenic rats [18]. Here, GK is linked to Glucose intolerance.