GDM results in reduced fetoplacental vascular dilation in response to insulin or adenosine (an endogenous vasodilator nucleoside) via mechanisms including altered expression of adenosine receptors (ARs) and/or insulin receptors forms A (IR-A) and B (IR-B), L-arginine and adenosine membrane transport and transporters expression in the human fetoplacental macrovascular and microvascular endothelium. This evidence concerns the gene INSR and gestational diabetes.