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Systemic oxidative stress is increased to a greater degree in young, obese women following consumption of a high fat meal

High fat meals induce oxidative stress, which is associated with the pathogenesis of disease. Obese individuals have elevated resting biomarkers of oxidative stress compared to non-obese. We compared blood oxidative stress biomarkers in obese (n = 14; 30 ± 2 years; BMI 35 ± 1 kg•m(−2)) and non-obese...

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Autores principales: Bloomer, Richard J, Fisher-Wellman, Kelsey H
Formato: Texto
Lenguaje:English
Publicado: Landes Bioscience 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2763227/
https://www.ncbi.nlm.nih.gov/pubmed/20046641
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author Bloomer, Richard J
Fisher-Wellman, Kelsey H
author_facet Bloomer, Richard J
Fisher-Wellman, Kelsey H
author_sort Bloomer, Richard J
collection PubMed
description High fat meals induce oxidative stress, which is associated with the pathogenesis of disease. Obese individuals have elevated resting biomarkers of oxidative stress compared to non-obese. We compared blood oxidative stress biomarkers in obese (n = 14; 30 ± 2 years; BMI 35 ± 1 kg•m(−2)) and non-obese (n = 16; 24 ± 2 years; BMI 23 ± 1 kg•m(−2)) women, in response to a high fat meal. Blood samples were collected pre-meal (fasted), and at 1, 2, 4 and 6 hours post meal, and assayed for trolox equivalent antioxidant capacity (TEAC), xanthine oxidase activity (XO), hydrogen peroxide (H(2)O(2)), malondialdehyde (MDA), triglycerides (TAG), and glucose. An obesity status effect was noted for all variables (p < 0.001; MDA p = 0.05), with obese women having higher values than non-obese, except for TEAC, for which values were lower. Time main effects were noted for all variables (p ≤ 0.01) except for TEAC and glucose, with XO, H(2)O(2), MDA and TAG increasing following feeding with a peak response at the four or six hour post feeding time point. While values tended to decline by six hours post feeding in the non-obese women (agreeing with previous studies), they were maintained (MDA) or continued to increase (XO, H(2)O(2) and TAG) in the obese women. While no interaction effects were noted (p > 0.05), contrasts revealed greater values in obese compared to non-obese women for XO, H(2)O(2), MDA, TAG and glucose, and lower values for TEAC at times from 1–6 hours post feeding (p ≤ 0.03). We conclude that young, obese women experience a similar pattern of increase in blood oxidative stress biomarkers in response to a high fat meal, as compared to non-obese women. However, the overall oxidative stress is greater in obese women, and values appear to remain elevated for longer periods of time post feeding. These data provide insight into another potential mechanism related to obesity-mediated morbidity.
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spelling pubmed-27632272010-01-01 Systemic oxidative stress is increased to a greater degree in young, obese women following consumption of a high fat meal Bloomer, Richard J Fisher-Wellman, Kelsey H Oxid Med Cell Longev Research Papers High fat meals induce oxidative stress, which is associated with the pathogenesis of disease. Obese individuals have elevated resting biomarkers of oxidative stress compared to non-obese. We compared blood oxidative stress biomarkers in obese (n = 14; 30 ± 2 years; BMI 35 ± 1 kg•m(−2)) and non-obese (n = 16; 24 ± 2 years; BMI 23 ± 1 kg•m(−2)) women, in response to a high fat meal. Blood samples were collected pre-meal (fasted), and at 1, 2, 4 and 6 hours post meal, and assayed for trolox equivalent antioxidant capacity (TEAC), xanthine oxidase activity (XO), hydrogen peroxide (H(2)O(2)), malondialdehyde (MDA), triglycerides (TAG), and glucose. An obesity status effect was noted for all variables (p < 0.001; MDA p = 0.05), with obese women having higher values than non-obese, except for TEAC, for which values were lower. Time main effects were noted for all variables (p ≤ 0.01) except for TEAC and glucose, with XO, H(2)O(2), MDA and TAG increasing following feeding with a peak response at the four or six hour post feeding time point. While values tended to decline by six hours post feeding in the non-obese women (agreeing with previous studies), they were maintained (MDA) or continued to increase (XO, H(2)O(2) and TAG) in the obese women. While no interaction effects were noted (p > 0.05), contrasts revealed greater values in obese compared to non-obese women for XO, H(2)O(2), MDA, TAG and glucose, and lower values for TEAC at times from 1–6 hours post feeding (p ≤ 0.03). We conclude that young, obese women experience a similar pattern of increase in blood oxidative stress biomarkers in response to a high fat meal, as compared to non-obese women. However, the overall oxidative stress is greater in obese women, and values appear to remain elevated for longer periods of time post feeding. These data provide insight into another potential mechanism related to obesity-mediated morbidity. Landes Bioscience 2009 /pmc/articles/PMC2763227/ /pubmed/20046641 Text en Copyright © 2009 Landes Bioscience
spellingShingle Research Papers
Bloomer, Richard J
Fisher-Wellman, Kelsey H
Systemic oxidative stress is increased to a greater degree in young, obese women following consumption of a high fat meal
title Systemic oxidative stress is increased to a greater degree in young, obese women following consumption of a high fat meal
title_full Systemic oxidative stress is increased to a greater degree in young, obese women following consumption of a high fat meal
title_fullStr Systemic oxidative stress is increased to a greater degree in young, obese women following consumption of a high fat meal
title_full_unstemmed Systemic oxidative stress is increased to a greater degree in young, obese women following consumption of a high fat meal
title_short Systemic oxidative stress is increased to a greater degree in young, obese women following consumption of a high fat meal
title_sort systemic oxidative stress is increased to a greater degree in young, obese women following consumption of a high fat meal
topic Research Papers
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2763227/
https://www.ncbi.nlm.nih.gov/pubmed/20046641
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