Our results show how HUVECs, isolated from healthy newborns with a strong family history of DM2, have an abnormal intracellular synthesis of NO and an impaired expression of eNOS, GLUT1 and p53 genes, all associated with NO synthesis.
Our results suggest that mitochondria and NAD(P)H-oxidase from HUVECs obtained from healthy newborns with a family history of DM have an innate deficient response to high glucose concentrations.
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