Endothelial cell phenotype is linked to endothelial dysfunction in individuals with a family history of type 2 diabetes.

OBJECTIVES

The patient's family history of type 2 diabetes (FH-DM2) has been negatively associated with the functionality of endothelial cells (ECs). Our objectives in this work were to use human umbilical vein endothelial cells (HUVECs) as a model, to substantiate whether FH-DM2 influences endothelial phenotype and impairs NO and ROS synthesis, cell metabolism, and mitochondrial activity of ECs from individuals with FH-DM2.

METHODS

In this study were evaluated the synthesis of reactive oxygen species (ROS) and nitric oxide (NO), mitochondrial membrane potential (MMP), mRNA of eNOS, glucose consumption, and lactate synthesis in HUVECs from newborns with FH-DM2. Furthermore, we also evaluated EC complexity and cell size through flow cytometry.

RESULTS

Our results showed significant differences in HUVECs with FH-DM2, regarding their complexity and cell size, in the synthesis of ROS (p<0.01), and NO (p<0.05); they also reflected diminished glucose consumption and slight changes in the lactate levels.

CONCLUSION

In conclusion, our results showed that HUVECs from children with FH-DM2 have a reduced capability of synthesizing ROS and NO, which might be linked to the metabolism of endothelial cells. These results are relevant since early endothelial dysfunction has been reported in individuals with FH-DM2, and could be used to establish preventive measures to reduce the risk of developing atherosclerosis or cardiovascular diseases in healthy individuals, but with this family background.