Figure 4: Recycling of nucleoside transporters in cells from gestational diabetes mellitus Normal subcellular distribution of human equilibrative nucleoside transporters 1 (ENT1) in cells from normal pregnancies results in a physiological expression of the gen SLC29A1 (coding for hENT1) leading to synthesis of these proteins which are then targeted to the plasma membrane. Once in the plasma membrane hENT1 function is to take up adenosine (Ado). In gestational diabetes mellitus (GDM) the recycling of hENT1 is reduced, thus limiting its availability at the plasma membrane. This phenomenon leads to reduced hENT1-mediated uptake of adenosine (dotted arrow). It is proposed that GDM associated increased (↑) nitric oxide (NO) synthesis could be responsible of this phenomenon via a mechanism that includes activation of transcription factors acting as down-regulators of SLC29A1 promoter activity and expression. From data in references [83,84,96,97].