scholarly journals Systemic Oxidative Stress Is Increased to a Greater Degree in Young, Obese Women Following Consumption of a High Fat Meal

2009 ◽  
Vol 2 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Richard J. Bloomer ◽  
Kelsey H. Fisher-Wellman

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 (H2O2), 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, H2O2, 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, H2O2and 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, H2O2, 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.

2008 ◽  
Vol 99 (5) ◽  
pp. 1055-1060 ◽  
Author(s):  
Richard J. Bloomer ◽  
Adrienne D. Solis ◽  
Kelsey H. Fisher-Wellman ◽  
Webb A. Smith

Both cigarette smoking and high fat meals induce oxidative stress, which is associated with the pathogenesis of numerous diseases. We compared blood antioxidant status, oxidative stress biomarkers and TAG in twenty smokers and twenty non-smokers, matched for age and physical activity, in response to a high fat test meal standardized to body mass. Blood samples were collected before feeding (resting and fasted) and at 1, 2, 4 and 6 h post feeding and analysed for antioxidant capacity (trolox equivalent antioxidant capacity; TEAC), xanthine oxidase activity (XO), hydrogen peroxide (H2O2), malondialdehyde (MDA) and TAG. Smoking status (P < 0·001) and time (P ≤ 0·01) effects were noted for all variables, with smokers demonstrating higher values compared with non-smokers for all variables except for TEAC, for which values were lower for smokers. XO, H2O2, MDA and TAG increased following feeding with a peak response at the 4 h post feeding time point, with the opposite response occurring for TEAC. Although no interaction effects were noted (P>0·05), contrasts revealed greater values in smokers compared with non-smokers for XO, H2O2, MDA and TAG, and lower values for TEAC at times from 1–6 h post feeding (P ≤ 0·05). Our findings indicate that young cigarette smokers experience an exaggerated oxidative stress response to feeding, as well as hypertriacylglycerolaemia, as compared with non-smokers. These data provide insight into another possible mechanism associating cigarette smoking with ill health and disease.


2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Zhiqiang Liu ◽  
Yan Liu ◽  
Yiqing Song ◽  
Xi Zhang ◽  
Songlin Wang ◽  
...  

Oxidative stress biomarkers have been observed in peripheral blood of chronic periodontitis patients; however, their associations with periodontitis were not consistent. This meta-analysis was performed to clarify the associations between chronic periodontitis and oxidative biomarkers in systemic circulation. Electronic searches of PubMed and Embase databases were performed until October 2014 and articles were selected to meet inclusion criteria. Data of oxidative biomarkers levels in peripheral blood of periodontitis patients and periodontal healthy controls were extracted to calculate standardized mean differences (SMDs) and 95% confidence intervals (CIs) by using random-effects model. Of 31 eligible articles, 16 articles with available data were included in meta-analysis. Our results showed that periodontitis patients had significantly lower levels of total antioxidant capacity (SMD = −2.02; 95% CI: −3.08, −0.96;P=0.000) and higher levels of malondialdehyde (SMD = 0.99; 95% CI: 0.12, 1.86;P=0.026) and nitric oxide (SMD = 4.98; 95% CI: 2.33, 7.63;P=0.000) than periodontal healthy control. Superoxide dismutase levels between two groups were not significantly different (SMD = −1.72; 95% CI: −3.50, 0.07;P=0.059). In conclusion, our meta-analysis showed that chronic periodontitis is significantly associated with circulating levels of three oxidative stress biomarkers, indicating a role of chronic periodontitis in systemic diseases.


2013 ◽  
Vol 38 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Cameron G. McCarthy ◽  
Tyler M. Farney ◽  
Robert E. Canale ◽  
Michael E. Dessoulavy ◽  
Richard J. Bloomer

Two prevalent origins of oxidative stress in Western society are the ingestion of high-fat meals and the performance of strenuous exercise. The purpose of this investigation was to compare the magnitude of increase in blood oxidative stress following acute feeding and acute exercise. Twelve exercise-trained men consumed a high-fat meal or performed 1 of 3 exercise bouts (steady-state aerobic; high-intensity, moderate-duration interval sprints; maximal intensity, short-duration interval sprints) in a random order, crossover design. Blood was collected before and at times following feeding and exercise. Samples were analyzed for trigylcerides, malondialdehyde (MDA), hydrogen peroxide (H2O2), advanced oxidation protein products (AOPP), nitrate/nitrite (NOx), trolox-equivalent antioxidant capacity (TEAC), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). A significant condition effect was noted for MDA (p = 0.01), H2O2(p < 0.0001), and AOPP (p = 0.0006), with values highest for the meal condition. An increase of 88%, 247%, and 96% was noted from pre- to post-feeding for MDA, H2O2, and AOPP, respectively. A condition effect was also noted for TEAC (p = 0.04) and CAT (p = 0.05), with values lowest for the meal condition (TEAC) and the meal and aerobic exercise condition (CAT). NOx, SOD, and GPx were relatively unaffected by feeding and exercise, while MDA, H2O2, and AOPP experienced little change from pre- to postexercise (p > 0.05). These results illustrate that the magnitude of blood oxidative stress following a high-fat meal is significantly greater than that elicited by either aerobic or anaerobic exercise in a sample of exercise-trained men.


2010 ◽  
Vol 20 (5) ◽  
pp. 393-400 ◽  
Author(s):  
Kelsey H. Fisher-Wellman ◽  
Richard J. Bloomer

Background:Carbohydrate powder in the form of maltodextrin is widely used by athletes for postexercise glycogen resynthesis. There is some concern that such a practice may be associated with a postprandial rise in reactive oxygen and nitrogen species production and subsequent oxidation of macromolecules. This is largely supported by findings of increased oxidative-stress biomarkers and associated endothelial dysfunction after intake of dextrose.Purpose:To compare the effects of isocaloric dextrose and maltodextrin meals on blood glucose, triglycerides (TAG), and oxidative-stress biomarkers in a sample of young healthy men.Methods:10 men consumed isocaloric dextrose and maltodextrin powder drinks (2.25 g/kg) in a random-order, crossover design. Blood samples were collected premeal (fasting) and at 1, 2, 4, and 6 hr postmeal and assayed for glucose, TAG, malondialdehyde, hydrogen peroxide, nitrate/nitrite, and Trolox-equivalent antioxidant capacity.Results:Significant meal effects were noted for glucose total area under the curve (p = .004), with values higher for the dextrose meal. No other statistically significant meal effects were noted (p > .05). With respect to the 2 (meal) × 5 (time) ANOVA, no significant interaction, time, or meal effects were noted for any variable (p > .05), with the exception of glucose, for which a main effect for both meal (p < .0001) and time (p = .0002) was noted.Conclusions:These data indicate that carbohydrate meals, consumed as either dextrose or maltodextrin, pose little postprandial oxidative insult to young, healthy men. As such, there should be minimal concern over such feedings, even at high dosages, assuming adequate glucose metabolism.


2017 ◽  
Vol 95 (4) ◽  
pp. 427-436 ◽  
Author(s):  
Nehal A. Afifi ◽  
Amer Ramadan ◽  
Emad Y. Erian ◽  
Dalia O. Saleh ◽  
Ahmed A. Sedik ◽  
...  

The present study aimed to evaluate the effect of trigonelline (TRG) on the hepatic complications associated with high-fat high-fructose (HFHF) diet-induced insulin resistance (IR) in rats. IR was induced by giving a saturated fat diet and 10% fructose in drinking water to rats for 8 weeks. Insulin-resistant rats were orally treated with TRG (50 and 100 mg/kg), sitagliptin (SIT; 5 mg/kg), or a combination of TRG (50 mg/kg) and SIT (5 mg/kg) for 14 days. Liver homogenates were used for assessment of hepatic lipids, oxidative stress biomarkers, and inflammatory cytokines. Histopathological and DNA cytometry examinations were carried out for hepatic and pancreatic tissues. Hepatic tissues were examined using Fourier-transform infrared spectroscopy for assessment of any molecular changes. Results of the present study revealed that oral treatment of insulin-resistant rats with TRG or TRG in combination with SIT significantly decreased homeostatic model assessment of IR, hepatic lipids, oxidative stress biomarkers, and the inflammatory cytokines. TRG or TRG in combination with SIT ameliorated the histopathological, DNA cytometry, and molecular alterations induced by a HFHF diet. Finally, it can be concluded that TRG has beneficial effects on the hepatic complications associated with IR due to its hypoglycemic effect and antioxidant potential.


2016 ◽  
Vol 32 (2) ◽  
pp. 503-511 ◽  
Author(s):  
Ahmad Ganji ◽  
Iraj Salehi ◽  
Abdolrahman Sarihi ◽  
Siamak Shahidi ◽  
Alireza Komaki

2010 ◽  
Vol 80 (1) ◽  
pp. 12-23 ◽  
Author(s):  
Richard J. Bloomer ◽  
Webb A. Smith ◽  
Kelsey H. Fisher-Wellman

We have recently noted a decrease in lipid peroxidation with oral intake of glycine propionyl-L-carnitine (GPLC). However, these findings were observed at rest, and in previously sedentary subjects. Methods: We determined the effect of GPLC on oxidative stress biomarkers at rest and in response to reactive hyperemia in exercise-trained men. Using a double-blind, crossover design, 15 healthy men were assigned to a placebo and GPLC (4.5 g/day) in random order, for four weeks, with a two-week washout between assignments. Blood samples were collected at rest and at 0, 3, and 10 minutes following a protocol of ischemia-reperfusion, and analyzed for lactate, malondialdehyde (MDA), F2-isoprostanes (F2-iso), hydrogen peroxide (H2O2), xanthine oxidase activity (XO), hypoxanthine (HYPO), total (TGSH) and oxidized (GSSG) glutathione, and Trolox-equivalent antioxidant capacity (TEAC). Results: No condition or condition by time interaction effects were noted (p>0.05). Time effects were noted for lactate (p<0.0001), MDA (p=0.02), H2O2 (p=0.0003), XO (p=0.03), HYPO (p<0.0001), TGSH (p=0.02), and GSSG (p<0.0001), with peak values noted at 0 minutes post for lactate, MDA, TGSH, and GSSG, at 3 minutes post for H2O2 and XO, and at 10 minutes post for HYPO. F2-iso and TEAC were unaffected by treatment or protocol (p>0.05). Conclusion: Short-term ischemia-reperfusion in trained men results in a modest and transient increase in selected blood oxidative stress biomarkers. Oral GPLC supplementation does not attenuate the increase in these biomarkers.


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