Further studies are required to examine if administration of ADM to pregnant mice could induce GDM symptoms with impaired β-cell functions, whether reduced number of β-cells in pancreas islets and lowered circulating insulin concentration in non-obese GDM mice are associated with increased ADM and its receptor expression in pancreatic islets, and if administration of ADM antagonist could mitigate impaired insulin production and glucose intolerance in vivo. This evidence concerns the gene ADM and Glucose intolerance.