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HUVECs from newborns with a strong family history of diabetes show diminished ROS synthesis in the presence of high glucose concentrations
Author(s) -
AlvaradoVásquez Noé,
Páez Araceli,
Zapata Estrella,
AlcázarLeyva Susana,
Zenteno Edgar,
Massó Felipe,
Montaño Luis F.
Publication year - 2007
Publication title -
diabetes/metabolism research and reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.307
H-Index - 110
eISSN - 1520-7560
pISSN - 1520-7552
DOI - 10.1002/dmrr.665
Subject(s) - reactive oxygen species , umbilical vein , intracellular , mitochondrion , mitochondrial ros , cytochalasin b , nad+ kinase , oxidative phosphorylation , glucose transporter , medicine , chemistry , biology , biochemistry , endocrinology , cell , enzyme , insulin , in vitro
Abstract Background A family history of type 2 diabetes mellitus (DM) increases the probability to develop DM and endothelial dysfunction. The probable mechanism involves augmented reactive oxygen species (ROS) synthesis. The aim of this study was to evaluate the synthesis of ROS in human umbilical vein endothelial cells (HUVECs) obtained from healthy newborns with (experimental) and without (control) a strong family history of type 2 DM, exposed to different glucose concentrations. Methods HUVECs were exposed to various glucose concentrations for 24 and 48 h periods, before cell proliferation, mitochondrial activity, and mitochondrial membrane potential were determined. Intracellular ROS synthesis in the presence or absence of the mitochondrial uncoupler CCCP, cytochalasin B, or diphenyleneiodonium (DPI) was also evaluated. Results As opposed to control HUVECs, we found that experimental HUVECs exposed to 30 mmol/L glucose showed a 50% decrease in cell proliferation, a 90% reduction in mitochondrial activity, and a statistically significant inhibition of ROS synthesis in the presence of CCCP or cytochalasin B; DPI had no effect. Conclusions 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. Copyright © 2006 John Wiley & Sons, Ltd.