| The kidney is one of the most important organs in charge of the osmoregulation as well as homeostasis of water, electrolyte, and acid-base homeostasis in the body. Na+-coupled HCO3- transporters(NCBTs) play vital roles in the kidney. In the kidney, the NCBTs are involved in the reabsorption of the Na+ and HCO3–. Diabetes is a complex systemic disease that often results in kidney dysfunction, which in turn could cause disturbance in the global homeostasis of water, electrolyte and acid-base balance disorders in the body. Studies have shown that in the renal tubular Na+-coupled HCO3- transporters activity can be regulated by the insulin. High salt diet could also affect the renal function. Increasing salt intake might cause chronic kidney disease and increase the risk of hypertension. Therefore, either diabetes or high salt diet for a long time may cause renal Na+-coupled HCO3- transporters functional change.In the present study, we explored the effect of diabetes on the expression of renal acid-base transporters by using mouse models. We found that diabetes had little effect on NBCe1 and NBCn1 protein abundance in the kidney. In addition, we also examined the effect of diabetes on the expression of NBCe1, NBCn1, NBCn2, and NDCBE in mouse brain. Our results showed that the expression of these NCBT proteins was not significantly different from that of the control.In rat with high salt intake, we found that the protein abundance of renal NBCe1 tended to decrease compared to the control. However, the abundance of renal NBCn1 and NBCn2 from rats with high salt intake was not significantly different from those of the control. Our data indicate that NBCe1 likely plays a role in the adaptive response of the kidney to high salt condition.Although the protein expression of NBCe1 and NBCn1 did not change significantly under the condition of diabetes, we were not sure about the changes in the activity of these transporters under the experimental conditions. Further studies are required to address the effect of diabetes and high salt intake on the function of the NCBTs. |