RT journal article
T1 Blunted Reducing Power Generation in Erythrocytes Contributes to Oxidative Stress in Prepubertal Obese Children with Insulin Resistance
A1 González-Domínguez, Álvaro
A1 Visiedo García, Francisco Manuel
A1 Domínguez Riscart, Jesús
A1 Ruiz Mateos, Beatriz
A1 Sáez-Benito Godino, Ana
A1 Lechuga Sancho, Alfonso María
A1 Mateos Bernal, Rosa María
A2 BiomedicinaBiotecnología y Salud Pública
A2 Materno-Infantil y Radiología
K1 antioxidants
K1 childhood obesity
K1 insulin resistance
K1 oxidative stress
K1 pentose phosphate pathway
K1 reducing power
AB Childhood obesity, and specifically its metabolic complications, are related to deficient antioxidant capacity and oxidative stress. Erythrocytes are constantly exposed to multiple sources of oxidative stress; hence, they are equipped with powerful antioxidant mechanisms requiring permanent reducing power generation and turnover. Glucose-6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate dehydrogenase (6PGDH) are two key enzymes on the pentose phosphate pathway. Both enzymes supply reducing power by generating NADPH, which is essential for maintaining the redox balance within the cell and the activity of other antioxidant enzymes. We hypothesized that obese children with insulin resistance would exhibit blunted G6PDH and 6PGDH activities, contributing to their erythrocytes' redox status imbalances. We studied 15 control and 24 obese prepubertal children, 12 of whom were insulin-resistant according to an oral glucose tolerance test (OGTT). We analyzed erythroid malondialdehyde (MDA) and carbonyl group levels as oxidative stress markers. NADP+/NADPH and GSH/GSSG were measured to determine redox status, and NADPH production by both G6PDH and 6PGDH was assayed spectrophotometrically to characterize pentose phosphate pathway activity. Finally, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glutathione reductase (GR) activities were also assessed. As expected, MDA and carbonyl groups levels were higher at baseline and along the OGTT in insulin-resistant children. Both redox indicators showed an imbalance in favor of the oxidized forms along the OGTT in the insulin-resistant obese group. Additionally, the NADPH synthesis, as well as GR activity, were decreased. H2O2 removing enzyme activities were depleted at baseline in both obese groups, although after sugar intake only metabolically healthy obese participants were able to maintain their catalase activity. No change was detected in SOD activity between groups. Our results show that obese children with insulin resistance present higher levels of oxidative damage, blunted capacity to generate reducing power, and hampered function of key NADPH-dependent antioxidant enzymes.
PB MDPI
SN 2076-3921
YR 2021
FD 2021-02
LK http://hdl.handle.net/10498/24699
UL http://hdl.handle.net/10498/24699
LA eng
NO This research was funded by Spanish Government through the Carlos III Health Institute (Sanitary Research Fund (FIS)), code PI18/01316. A.G.-D. is supported by an intramural grant from the Biomedical Research and Innovation Institute of Cadiz (INiBICA), code LII19/16IN-CO24.
DS Repositorio Institucional de la Universidad de Cádiz
RD 11-nov-2026