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- Genre: Academic theses
Description
Background: Evidence about the purported hypoglycemic and hypolipidemic effects of nopales (prickly pear cactus pads) is limited. Objective: To evaluate the efficacy of nopales for improving cardiometabolic risk factors and oxidative stress, compared to control, in adults with hypercholesterolemia. Design: In a randomized crossover trial, participants were assigned to a 2-wk intervention with 2 cups/day of nopales or cucumbers (control), with a 2 to 3-wk washout period. The study included 16 adults (5 male; 46±14 y; BMI = 31.4±5.7 kg/m2) with moderate hypercholesterolemia (low density lipoprotein cholesterol [LDL-c] = 137±21 mg/dL), but otherwise healthy. Main outcomes measured included: dietary intake (energy, macronutrients and micronutrients), cardiometabolic risk markers (total cholesterol, LDL-c, high density lipoprotein cholesterol [HDL-c], triglycerides, cholesterol distribution in LDL and HDL subfractions, glucose, insulin, homeostasis model assessment, and C-reactive protein), and oxidative stress markers (vitamin C, total antioxidant capacity, oxidized LDL, and LDL susceptibility to oxidation). Effects of treatment, time, or interactions were assessed using repeated measures ANOVA. Results: There was no significant treatment-by-time effect for any dietary composition data, lipid profile, cardiometabolic outcomes, or oxidative stress markers. A significant time effect was observed for energy, which was decreased in both treatments (cucumber, -8.3%; nopales, -10.1%; pTime=0.026) mostly due to lower mono and polyunsaturated fatty acids intake (pTime=0.023 and pTime=0.003, respectively). Both treatments significantly increased triglyceride concentrations (cucumber, 14.8%; nopales, 15.2%; pTime=0.020). Despite the lack of significant treatment-by-time effects, great individual response variability was observed for all outcomes. After the cucumber and nopales phases, a decrease in LDL-c was observed in 44% and 63% of the participants respectively. On average LDL-c was decreased by 2.0 mg/dL (-1.4%) after the cucumber phase and 3.9 mg/dL (-2.9%) after the nopales phase (pTime=0.176). Pro-atherogenic changes in HDL subfractions were observed in both interventions over time, by decreasing the proportion of HDL-c in large HDL (cucumber, -5.1%; nopales, -5.9%; pTime=0.021) and increasing the proportion in small HDL (cucumber, 4.1%; nopales, 7.9%; pTime=0.002). Conclusions: These data do not support the purported benefits of nopales at doses of 2 cups/day for 2-wk on markers of lipoprotein profile, cardiometabolic risk, and oxidative stress in hypercholesterolemic adults.
ContributorsPereira Pignotti, Giselle Adriana (Author) / Vega-Lopez, Sonia (Thesis advisor) / Gaesser, Glenn (Committee member) / Keller, Colleen (Committee member) / Shaibi, Gabriel (Committee member) / Sweazea, Karen (Committee member) / Arizona State University (Publisher)
Created2013
Description
Mitochondria produce most of the ATP needed for the cell as an energy source. It is well known that cellular respiration results in oxidative damage to the cell due to the production of reactive oxygen species (ROS). Mitochondrial dysfunction is believed to contribute to a number of degenerative diseases; because of this the mitochondrial respiratory chain is considered as potential drug target. A few series of idebenone analogues with quinone, pyridinol and pyrimidinol redox cores have been synthesized and evaluated as antioxidants able to protect cellular integrity and, more specifically, mitochondrial function. The compounds exhibited a range of activities. The activities observed were used for the design of analogues with enhanced properties as antioxidants. Compounds were identified which provide better protection against oxidative stress than idebenone, and it is thought that they do so catalytically.
ContributorsArce Amezquita, Pablo M (Author) / Hecht, Sidney M. (Thesis advisor) / Moore, Ana (Committee member) / Rose, Seth (Committee member) / Arizona State University (Publisher)
Created2012
Description
Reactive oxygen species (ROS) are a series of molecules, ions, and radicals derived from oxygen that possess remarkable reactivity. They act as signaling molecules when their concentration in cells is within a normal range. When the levels of ROS increase, reaching a concentration in which the antioxidants cannot readily quench them, oxidative stress will affect the cells. These excessive levels of ROS result in direct or indirect ROS-mediated damage of proteins, nucleic acids, and lipids. Excessive oxidative stress, particularly in chronic inflammation, has been linked with mutations and carcinogenesis. One of the main targets of ROS in severe oxidative stress is mitochondrial DNA (mtDNA). The synthesis of analogues of alpha-tocopherol is described as potential compounds with the ability to remediate defective mitochondria. An interesting possibility for eradicating cancer cells is to selectively target them with oxidative species while avoiding any deleterious effects on healthy cells. To accomplish this, analogues of the beta-hydroxyhistidine moiety of the antitumor agent bleomycin (BLM) were synthesized. The first part of this thesis focuses on the synthesis of simplified analogues of alpha-tocopherol. These analogues possess a bicyclic pyridinol as the antioxidant core and an alkyl group as the lipophilic chain to mimic alpha-tocopherol. Additionally, analogues with a completely oxidized pyridinol core were synthesized. Some of these analogues showed promising properties against ROS production and lipid peroxidation. The protection they conferred was shown to be tightly regulated by their concentration. The second part of this thesis focuses on the synthesis of analogues of beta-hydroxyhistidine. BLMs are glycopeptides that possess anticancer activity and have been used to treat testicular carcinomas, Hodgkin's lymphoma, and squamous cell carcinomas. The activity of BLM is based on the degradation of DNA, or possibly RNA, caused by a Fe(II)-BLM complex in the presence of O2. The beta-hydroxyhistidine moiety of BLM contributes to metal coordination via two ligands: the N-3 nitrogen atom of imidazole and possibly the nitrogen atom of the amide. A series of beta-hydroxyhistidine analogues has successfully been synthesized.
ContributorsArmendáriz Guajardo, José Israel (Author) / Hecht, Sidney M. (Thesis advisor) / Moore, Ana (Committee member) / Gould, Ian (Committee member) / Arizona State University (Publisher)
Created2014
Description
Mitochondria are crucial intracellular organelles which play a pivotal role in providing energy to living organisms in the form of adenosine triphosphate (ATP). The mitochondrial electron transport chain (ETC) coupled with oxidative phosphorylation (OX-PHOS) transforms the chemical energy of amino acids, fatty acids and sugars to ATP. The mitochondrial electron transport system consumes nearly 90% of the oxygen used by the cell. Reactive oxygen species (ROS) in the form of superoxide anions (O2*-) are generated as byproduct of cellular metabolism due to leakage of electrons from complex I and complex III to oxygen. Under normal conditions, the effects of ROS are offset by a variety of antioxidants (enzymatic and non-enzymatic).
Mitochondrial dysfunction has been proposed in the etiology of various pathologies, including cardiovascular and neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, ischemia-reperfusion (IR) injury, diabetes and aging. To treat these disorders, it is imperative to target mitochondria, especially the electron transport chain. One of the methodologies currently used for the treatment of mitochondrial and neurodegenerative diseases where endogenous antioxidant defenses are inadequate for protecting against ROS involves the administration of exogenous antioxidants.
As part of our pursuit of effective neuroprotective drugs, a series of pyridinol and pyrimidinol analogues have been rationally designed and synthesized. All the analogues were evaluated for their ability to quench lipid peroxidation and reactive oxygen species (ROS), and preserve mitochondrial membrane potential (Δm) and support ATP synthesis. These studies are summarized in Chapter 2.
Drug discovery and lead identification can be reinforced by assessing the metabolic fate of orally administered drugs using simple microsomal incubation experiments. Accordingly, in vitro microsomal studies were designed and carried out using bovine liver microsomes to screen available pyridinol and pyrimidinol analogues for their metabolic lability. The data obtained was utilized for an initial assessment of potential bioavailability of the compounds screened and is summarized fully in Chapter 3.
Mitochondrial dysfunction has been proposed in the etiology of various pathologies, including cardiovascular and neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, ischemia-reperfusion (IR) injury, diabetes and aging. To treat these disorders, it is imperative to target mitochondria, especially the electron transport chain. One of the methodologies currently used for the treatment of mitochondrial and neurodegenerative diseases where endogenous antioxidant defenses are inadequate for protecting against ROS involves the administration of exogenous antioxidants.
As part of our pursuit of effective neuroprotective drugs, a series of pyridinol and pyrimidinol analogues have been rationally designed and synthesized. All the analogues were evaluated for their ability to quench lipid peroxidation and reactive oxygen species (ROS), and preserve mitochondrial membrane potential (Δm) and support ATP synthesis. These studies are summarized in Chapter 2.
Drug discovery and lead identification can be reinforced by assessing the metabolic fate of orally administered drugs using simple microsomal incubation experiments. Accordingly, in vitro microsomal studies were designed and carried out using bovine liver microsomes to screen available pyridinol and pyrimidinol analogues for their metabolic lability. The data obtained was utilized for an initial assessment of potential bioavailability of the compounds screened and is summarized fully in Chapter 3.
ContributorsAlam, Mohammad Parvez (Author) / Hecht, Sidney M. (Thesis advisor) / Gould, Ian R (Committee member) / Moore, Ana (Committee member) / Arizona State University (Publisher)
Created2014
Description
Birds have plasma glucose levels that are 1.5-2 times greater than mammals of similar body mass in addition to higher free fatty acid concentrations, both of which would typically impair endothelium-dependent vasodilation if observed in mammals. Endothelium-dependent vasodilation can be stimulated in mammals through the use of acetylcholine (ACh), which primarily acts through nitric oxide (NO) and cyclooxygenase (COX)-mediated pathways, with varying reliance on endothelial-derived hyperpolarizing factors (EDHFs). Very few studies have been conducted on small resistance systemic arteries from birds. The hypothesis was that because birds have naturally high glucose and free fatty acid concentrations, ACh-induced vasodilation of isolated arteries from mourning doves (Zenaida macroura) would be independent of endothelial-derived factors and resistant to high glucose-mediated vascular dysfunction. Small resistance mesenteric and cranial tibial (c. tibial) arteries were pre-constricted to 50% of resting inner diameter with phenyleprine then exposed to increasing doses of ACh (10-9 to 10-5 μM) or the NO donor, sodium nitroprusside (SNP; 10-12 to 10-3 μM). For both vessel beds, ACh-induced vasodilation occurred mainly through the activation of potassium channels, whereas vasodilation of mesenteric arteries additionally occurred through COX. Although arteries from both vessel beds fully dilated with exposure to sodium nitroprusside, ACh-mediated vasodilation was independent of NO. To examine the effect of high glucose on endothelium-dependent vasodilation, ACh dose response curves were conducted following exposure of isolated c. tibial arteries to either a control solution (20mM glucose) or high glucose (30mM). ACh-induced vasodilation was significantly impaired (p = 0.013) when exposed to high glucose, but normalized in subsequent vessels with pre-exposure to the superoxide dismutase mimetic tiron (10 mM). Superoxide concentrations were likewise significantly increased (p = 0.0072) following exposure to high glucose. These findings indicate that dove arteries do not appear to have endogenous mechanisms to counteract the deleterious effects of oxidative stress. Additional studies are required to assess whether endogenous mechanisms exist to protect avian vascular reactivity from systemic hyperglycemia.
ContributorsJarrett, Catherine Lee (Author) / Sweazea, Karen L (Thesis advisor) / Johnston, Carol (Committee member) / Gaesser, Glenn (Committee member) / Arizona State University (Publisher)
Created2012
Description
It has been well established that mitochondria play a critical role in the pathology of Friedreich's Ataxia. This disease is believed to be caused by a deficiency of frataxin, which research suggests is responsible for iron sulfur cluster assembly. This incomplete assembly of iron sulfur clusters is believed to be linked with dysfunctional complexes in the mitochondrial respiratory chain, increased oxidative stress, and potential cell death. Increased understanding of the pathophysiology of this disease has enabled the development of various therapeutic strategies aimed at restoring mitochondrial respiration. This thesis contains an analysis of the biological activity of several classes of antioxidants against oxidative stress induced by diethyl maleate in Friedreich's Ataxia lymphocytes and CEM leukemia cells. Analogues of vitamin E α-tocopherol have been shown to protect cells under oxidative stress. However, these same analogues show various levels of inhibition towards the electron transport chain complex I. Bicyclic pyridinols containing a ten carbon substituent provided favorable cytoprotection. N-hydroxy-4-pyridone compounds were observed to provide little protection. Similarly, analogues of CoQ10 in the form of pyridinol and pyrimidinol compounds also preserved cell viability at low concentrations.
ContributorsJaruvangsanti, Jennifer (Author) / Hecht, Sidney (Thesis advisor) / Woodbury, Neal (Committee member) / Skibo, Edward (Committee member) / Arizona State University (Publisher)
Created2012
Description
Background. Effects of lifestyle interventions on early biomarkers of oxidative stress and CVD risk in youth with prediabetes are unknown. Objective. To evaluate the effects of a lifestyle intervention to prevent type 2 diabetes among obese prediabetic Latino adolescents on oxidized lipoproteins. Design: In a quasi-experimental design, 35 adolescents (51.4% male, age 15.5(1.0) y, body mass index (BMI) percentile 98.5(1.2), and glucose 2 hours after an oral glucose tolerance test-OGTT 141.2(12.2) mg/dL) participated in a 12-week intervention that included weekly exercise (three 60 min-sessions) and nutrition education (one 60 min-session). Outcomes measured at baseline and post-intervention were: fasting oxidized LDL and oxidized HDL (oxLDL and oxHDL) as oxidative stress variables; dietary intake of fresh fruit and vegetable (F&V) and fitness (VO2max) as behavioral variables; weight, BMI, body fat, and waist circumference as anthropometric variables; fasting glucose and insulin, 2hour glucose and insulin after an OGTT, insulin resistance (HOMA-IR), and lipid panel (triglycerides, total cholesterol, VLDL-c, LDL-c, HDL-c, and Non-HDL) as cardiometabolic variables. Results. Comparing baseline to post-intervention, significant decreases in oxLDL concentration were shown (51.0(14.0) and 48.7(12.8) U/L, p=0.022); however, the intervention did not decrease oxHDL (395.2(94.6) and 416.1(98.4) ng/mL, p=0.944). F&V dietary intake (116.4(97.0) and 165.8(91.0) g/d, p=0.025) and VO2max (29.7(5.0) and 31.6(4.7) ml*kg-1*min-1, p<0.001) significantly increased. Within-subjects correlations between changes in F&V intake and oxidized lipoproteins, adjusted for VO2max changes, were non-significant (R=-0.15, p=0.52 for oxLDL; R=0.22, p=0.25 for oxHDL). Anthropometric variables were significantly reduced (weight -1.3% p=0.042; BMI -2.2% and BMI percentile -0.4%, p=0.001; body fat -6.6% and waist circumference -1.8%, p=0.025). Cardiometabolic variables significantly improved, including reductions in glucose 2hour (-19.3% p<0.001), fasting insulin (-12.9% p=0.008), insulin 2hour (-53.5% p<0.001), and HOMA-IR (-12.5% p=0.015), with 23 participants (66%) that reverted toward a normal glucose tolerance status. Most lipid panel significantly changed (triglycerides -10.2% p=0.032; total cholesterol -5.4% p=0.002; VLDL-c -10.4% p=0.029; HDL-c -3.2% p=0.022; and Non-HDL -5.5% p=0.0007). Conclusion. The intervention resulted in differential effects on oxidized lipoproteins and significant improvements in behavioral, anthropometric and cardiometabolic variables, reducing the high metabolic risk of obese prediabetic kids.
ContributorsRenteria Mexia, Ana Maria (Author) / Shaibi, Gabriel Q (Thesis advisor) / Vega-Lopez, Sonia (Committee member) / Swan, Pamela D (Committee member) / Olson, Micah L (Committee member) / Lee, Chong (Committee member) / Arizona State University (Publisher)
Created2017
Description
Cardiovascular disease has reached epidemic proportions resulting in its ranking as the number one cause of mortality in the Western world. A key player in the pathophysiology of vascular disease is oxidative stress due to free radical accumulation. This intervention study was conducted to evaluate any potential mediation of oxidative stress using a soil-derived organometallic compound (OMC) with suspected antioxidant properties. A 10-week study was conducted in male Sprague-Dawley rats (n = 42) fed either a high-fat diet (HFD) consisting of 60% kcal from fat or a standard Chow diet containing only 6% kcals from fat. Rats from each diet group were then subdivided into 3 subgroups (n = 6-10 each) that received 0.0 mg/mL, 0.6 mg/mL or 3.0 mg/mL OMC. Neither the diet nor OMC significantly changed protein expression of inducible nitric oxide synthase (iNOS) in isolated aortas. Plasma levels of the inflammatory marker, tumor necrosis factor alpha (TNFα) were below detection after the 10-week trial. Superoxide dismutase (SOD), a scavenger of the free radical, superoxide, was not significantly different following HFD although levels of SOD were significantly higher in Chow rats treated with 0.6 mg/mL OMC compared to HFD rats treated with the same dose (p < 0.05). Lipopolysaccharides (LPS) were significantly increased following 10 weeks of high fat intake (p < 0.05). This increase in endotoxicity was prevented by the high dose of OMC. HFD significantly increased fasting serum glucose levels at both 6 weeks (p < 0.001) and 10 weeks (p < 0.025) compared to Chow controls. The high dose of OMC significantly prevented the hyperglycemic effects of the HFD in rats at 10 weeks (p = 0.021). HFD-fed rats developed hyperinsulinemia after 10 weeks of feeding (p = 0.009), which was not prevented by OMC. The results of this study indicate that OMC may be an effective strategy to help manage diet-induced hyperglycemia and endotoxemia. However, further research is needed to determine the mechanism by which OMC helps prevent hyperglycemia as measures of inflammation (TNFα) and vascular damage (iNOS) were inconclusive.
ContributorsWatson, Deborah F (Author) / Sweazea, Karen L (Thesis advisor) / Johnston, Carol (Committee member) / Mayol-Kreiser, Sandra (Committee member) / Arizona State University (Publisher)
Created2018
Description
Environmental stressors can perturb cellular homeostasis. Cells activate an integrated stress response that will alleviate the effects of the ongoing stress. Stress-activated protein kinases function to phosphorylate the eukaryotic translation initiation factor, eIF2α, which results in inhibition of translation of house-keeping genes. Following these events, formation of cytoplasmic messenger ribonucleoprotein complexes, known as stress granules, will take place. Stress granules typically have a pro-survival function. These studies demonstrate that assembly of stress granules can also lead to necroptosis. Necroptosis is a caspase-independent, receptor-interacting protein kinase 3 (RIPK3)-dependent cell death pathway executed by mixed lineage kinase domain-like (MLKL) protein. Cellular stress is induced using arsenite (oxidative stress) or by infection with vaccinia virus (VACV) E3 protein Z-DNA-binding domain mutant, VACV-E3LΔ83N. In both cases, RIPK3-dependent death was observed in interferon (IFN)-primed L929 cells. This death led to phosphorylation and trimerization of MLKL, indicative of necroptosis. Necroptosis induced by oxidative stress and VACV-E3LΔ83N infection was dependent on the host Z-form nucleic acid sensor, DNA-dependent activator of IFN-regulatory factors (DAI), as it was inhibited in DAI-deficient L929 cells. Under both cellular stresses, DAI associated with RIPK3 and formed high-molecular-weight complexes, consistent with formation of the necrosomes. DAI localized into stress granules during necroptosis induced by arsenite and the mutant virus, and the necrosomes formed only in presence of stress granule assembly. The significance of stress granules for cellular stress-induced necroptosis was demonstrated using knock-out (KO) cell lines unable to form granules: T cell-restricted intracellular antigen 1 (TIA-1) KO MEF cells and Ras GTPase-activating protein-binding proteins 1 and 2 (G3BP1/2) KO U2OS cells. Necroptosis was inhibited in absence of stress granule formation as no cell death or activation of MLKL was observed in the knock-out cell lines following arsenite treatment or VACV-E3LΔ83N infection. Furthermore, wild-type VACV was able to inhibit stress granule assembly, which coincided with the virus ability to inhibit necroptosis. These studies have led to a model of Z-form nucleic acids being involved in activation of the stress granule-mediated necroptosis following induction by environmental stressors. These results have significance for understanding the etiology of human diseases and the antiviral innate immunity.
ContributorsSzczerba, Mateusz Bartlomiej (Author) / Jacobs, Bertram L (Thesis advisor) / Langland, Jeffrey (Committee member) / Lake, Douglas (Committee member) / Chen, Qiang (Committee member) / Arizona State University (Publisher)
Created2021
Description
Background: Postprandial hyperglycemia can increase levels of oxidative stress and is an independent risk factor for complications associated with type 2 diabetes.
Purpose: To evaluate the acute effects of a 15-min postmeal walk on glucose control and markers of oxidative stress following a high-carbohydrate meal.
Methods: Ten obese subjects (55.0 ± 10.0 yrs) with impaired fasting glucose (107.1 ± 9.0 mg/dL) participated in this repeated measures trial. Subjects arrived at the laboratory following an overnight fast and underwent one of three conditions: 1) Test meal with no walking or fiber (CON), 2) Test meal with 10g fiber and no walking (FIB), 3) Test meal with no fiber followed by a 15-min treadmill walk at preferred walking speed (WALK). Blood samples were taken over four hours and assayed for glucose, insulin, thiobarbituric reactive substances (TBARS), catalase, uric acid, and total antioxidant capacity (TAC). A repeated measures ANOVA was used to compare mean differences for all outcome variables.
Results: The 2hr and 4hr incremental area under the curve (iAUC) for glucose was lower in both FIB (2hr: -93.59 mmol∙120 min∙L-1, p = 0.006; 4hr: -92.59 mmol∙240 min∙L-1; p = 0.041) and WALK (2hr: -77.21 mmol∙120 min∙L-1, p = 0.002; 4hr: -102.94 mmol∙240 min∙L-1; p = 0.005) conditions respectively, compared with CON. There were no differences in 2hr or 4hr iAUC for glucose between FIB and WALK (2hr: p = 0.493; 4hr: p = 0.783). The 2hr iAUC for insulin was significantly lower in both FIB (-37.15 μU ∙h/mL; p = 0.021) and WALK (-66.35 μU ∙h/mL; p < 0.001) conditions, compared with CON, and was significantly lower in the WALK (-29.2 μU ∙h/mL; p = 0.049) condition, compared with FIB. The 4hr iAUC for insulin in the WALK condition was significantly lower than both CON (-104.51 μU ∙h/mL; p = 0.001) and FIB (-77.12 μU ∙h/mL; p = 0.006) conditions. Markers of oxidative stress were not significantly different between conditions.
Conclusion: A moderate 15-minute postmeal walk is an effective strategy to reduce postprandial hyperglycemia. However, it is unclear if this attenuation could lead to improvements in postprandial oxidative stress.
Purpose: To evaluate the acute effects of a 15-min postmeal walk on glucose control and markers of oxidative stress following a high-carbohydrate meal.
Methods: Ten obese subjects (55.0 ± 10.0 yrs) with impaired fasting glucose (107.1 ± 9.0 mg/dL) participated in this repeated measures trial. Subjects arrived at the laboratory following an overnight fast and underwent one of three conditions: 1) Test meal with no walking or fiber (CON), 2) Test meal with 10g fiber and no walking (FIB), 3) Test meal with no fiber followed by a 15-min treadmill walk at preferred walking speed (WALK). Blood samples were taken over four hours and assayed for glucose, insulin, thiobarbituric reactive substances (TBARS), catalase, uric acid, and total antioxidant capacity (TAC). A repeated measures ANOVA was used to compare mean differences for all outcome variables.
Results: The 2hr and 4hr incremental area under the curve (iAUC) for glucose was lower in both FIB (2hr: -93.59 mmol∙120 min∙L-1, p = 0.006; 4hr: -92.59 mmol∙240 min∙L-1; p = 0.041) and WALK (2hr: -77.21 mmol∙120 min∙L-1, p = 0.002; 4hr: -102.94 mmol∙240 min∙L-1; p = 0.005) conditions respectively, compared with CON. There were no differences in 2hr or 4hr iAUC for glucose between FIB and WALK (2hr: p = 0.493; 4hr: p = 0.783). The 2hr iAUC for insulin was significantly lower in both FIB (-37.15 μU ∙h/mL; p = 0.021) and WALK (-66.35 μU ∙h/mL; p < 0.001) conditions, compared with CON, and was significantly lower in the WALK (-29.2 μU ∙h/mL; p = 0.049) condition, compared with FIB. The 4hr iAUC for insulin in the WALK condition was significantly lower than both CON (-104.51 μU ∙h/mL; p = 0.001) and FIB (-77.12 μU ∙h/mL; p = 0.006) conditions. Markers of oxidative stress were not significantly different between conditions.
Conclusion: A moderate 15-minute postmeal walk is an effective strategy to reduce postprandial hyperglycemia. However, it is unclear if this attenuation could lead to improvements in postprandial oxidative stress.
ContributorsKnurick, Jessica (Author) / Johnston, Carol S (Thesis advisor) / Sweazea, Karen L (Committee member) / Gaesser, Glenn A (Committee member) / Shaibi, Gabriel Q (Committee member) / Lee, Chong D (Committee member) / Arizona State University (Publisher)
Created2015