Matching Items (4)
Filtering by

Clear all filters

150900-Thumbnail Image.png
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

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
193386-Thumbnail Image.png
Description
This thesis explores the potential anti-inflammatory effects of daily vinegar ingestion in healthy adults over a 4-week period, with a focus on cytokine levels, innate immunity markers, and C-reactive protein (CRP). Participants were healthy, non-smoking adults (n=28, 18-41 years of age) free of chronic disease. Participants were randomized to the

This thesis explores the potential anti-inflammatory effects of daily vinegar ingestion in healthy adults over a 4-week period, with a focus on cytokine levels, innate immunity markers, and C-reactive protein (CRP). Participants were healthy, non-smoking adults (n=28, 18-41 years of age) free of chronic disease. Participants were randomized to the active treatment group (VIN; two tablespoons liquid vinegar at mealtime twice daily; n=16) or the control group (CON; one commercial vinegar tablet daily; n=12). A fasting blood sample was collected at the start and completion of the 4-week intervention, and serum was analyzed for 15 cytokines and C-reactive protein (CRP). Fluctuations in the anti-inflammatory cytokines (e.g., IL-4, IL-10, IL-5, and IL-13) did not differ between treatment groups during the trial; however, notable reductions in two pro-inflammatory cytokines were observed at week 4 for VIN participants in comparison to CON participants. IL-1 trended lower for VIN versus CON participants (-2.7±6.0 and 1.0±6.6 pg/ml respectively, p=0.102), and IL-12p40 was reduced significantly during the trial in VIN versus CON participants (-5.7±12.5 and +1.04±9.8 pg/ml; p=0.051). The rise in CRP at week 4 for all participants, while not statistically significant, underscores the complexity of the relationship between inflammatory markers. These findings suggest that daily vinegar ingestion may afford greater resilience to inflammatory conditions (as indicated by increasing CRP concentrations). Recommendations for future research include expanding participant pools, extending intervention periods, and conducting more comprehensive studies to unravel the intricate dynamics of vinegar's impact on inflammatory processes.
ContributorsCoven, Hannah (Author) / Johnston, Carol (Thesis advisor) / Shepard, Tina (Committee member) / Mayol-Kreiser, Sandra (Committee member) / Arizona State University (Publisher)
Created2024
153650-Thumbnail Image.png
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

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.
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
156509-Thumbnail Image.png
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

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