In sum, pancreas-wide deletion of GluN1 in young adult mice resulted in several indicators of glucose intolerance, and some trends in male mice consistent with insulin hyposecretion, although the potential influence of glucose-regulating NMDAR activity in the hypothalamus [46], where Cre expression has been demonstrated for both our promoter constructs [47,48], cannot be ruled out. The gene discussed is GRIN1; the disease is Glucose intolerance.