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

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          Abstract

          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 2O 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 2O 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 2O 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 2O 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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          Most cited references38

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          IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance.

          Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. An inhibitory form of IRS-1 was observed in muscle and fat tissues from obese rats. These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.
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            Guidelines on diabetes, pre-diabetes, and cardiovascular diseases: executive summary. The Task Force on Diabetes and Cardiovascular Diseases of the European Society of Cardiology (ESC) and of the European Association for the Study of Diabetes (EASD).

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              Oxidants in cigarette smoke. Radicals, hydrogen peroxide, peroxynitrate, and peroxynitrite.

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                Author and article information

                Journal
                Oxid Med Cell Longev
                OMCL
                Oxidative Medicine and Cellular Longevity
                Landes Bioscience
                1942-0900
                1942-0994
                Jan-Mar 2009
                : 2
                : 1
                : 19-25
                Affiliations
                Cardiorespiratory/Metabolic Laboratory; The University of Memphis; Memphis, Tennessee USA
                Author notes
                Correspondence to: Richard J. Bloomer; Cardiorespiratory/Metabolic Laboratory; 161F Elma Neal Roane Field House; The University of Memphis; Memphis, Tennessee 38152 USA; Tel.: 901.678.4341; Fax: 901.678.3591; Email: rbloomer@ 123456memphis.edu
                Article
                1942-0900-2-1-5
                10.4161/oxim.2.1.7860
                2763227
                20046641
                133e0b23-9100-43db-bde7-0bfad9725190
                Copyright © 2009 Landes Bioscience
                History
                : 19 December 2008
                : 6 January 2009
                : 15 January 2009
                Categories
                Research Papers

                Molecular medicine
                triglycerides,oxidative stress,obesity,body mass,nutrition,free radicals
                Molecular medicine
                triglycerides, oxidative stress, obesity, body mass, nutrition, free radicals

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