Insulin requires A1 XXXX receptors expression to reverse gestational diabetes-increased @entity8561 transport in @entity1 umbilical vein endothelium.

@entity1 @entity8561 @entity859 @entity6 @entity35107 @entity8742 @entity3689
UNASSIGNED: @entity6 ( @entity6 ) associates with increased @entity8561 transport and extracellular concentration of @entity859 in @entity1 umbilical vein endothelial cells (HUVECs). In this study we aim to determine whether insulin reverses @entity6 -increased @entity8561 transport requiring @entity859 receptors expression in HUVECs. Primary cultured HUVECs from full-term normal (n   =   38) and diet-treated @entity6 (n   =   38) pregnancies were used. Insulin effect was assayed on @entity1 cationic @entity3689 transporter 1 ( @entity35107 ) expression (protein, mRNA, @entity35107 promoter activity) and activity (initial rates of @entity8561 transport) in the absence or presence of @entity859 receptors agonists or antagonists. A1 @entity859 receptors (A1AR) and A2AAR expression (Western blot, quantitative PCR) was determined. Experiments were done in cells expressing or siRNA-suppressed expression of A1AR or A2AAR. HUVECs from @entity6 exhibit higher maximal transport capacity (maximal velocity (V max)/apparent Michaelis Menten constant (K m), V max/K m), which is blocked by insulin by reducing the V max to values in cells from normal pregnancies. Insulin also reversed the @entity6 -associated increase in @entity35107 protein abundance and mRNA expression, and @entity35107 promoter activity for the fragment -606  bp from the transcription start point. Insulin effects required A1AR, but not A2AAR expression and activity in this cell type. In the absence of insulin, @entity6 -increased @entity35107 expression and activity required A2AAR expression and activity. HUVECs from @entity6 pregnancies exhibit a differential requirement of A1AR or A2AAR depending on the level of insulin, a phenomenon that represent a condition where @entity859 or analogues of this @entity8742 could be acting as helpers of insulin biological effects in @entity6 .
