Theses and Dissertations
This collection includes both ASU Theses and Dissertations, submitted by graduate students, and the Barrett, Honors College theses submitted by undergraduate students.
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- Creators: Johnston, Carol
Description
High fat diets (HFD) are known to cause hepatic non-alcoholic steatosis in rats in as few as four weeks. Accumulation of triglycerides in liver and skeletal muscle is associated with insulin resistance and obesity. However, studies of fat accumulation in cardiac muscle are not as prevalent. Therefore, the first hypothesis of this study was that HFD would lead to hepatic steatosis as well as lipid accumulation in pectoralis and cardiac muscles, tissues responsible for the majority of postprandial glucose disposal. Prior studies also indicated that HFD leads to increased inflammation and oxidative stress within the vasculature resulting in impaired endothelium-dependent vasodilation, however biomarkers of immune system reactivity were not assessed. Therefore, the second aim of this study was to explore additional pathways of immune system reactivity and stress (natural antibodies; heat shock protein 60 (HSP60)) in rats fed either a control (chow) or high fat (HFD) diet. HSP60 has also recently been recognized as an early marker of vascular dysfunction in humans. The hypothesis was that immune system reactivity and early vascular dysfunction would be heightened in rats fed a HFD compared to chow-fed controls. Young male Sprague-Dawley rats (140-160g) were maintained on a chow diet (5% fat, 57.33% carbohydrate, 3.4kcal/g) or HFD (60% fat, 20% carbohydrate, 5.24 kcal/g) for 6 weeks. HFD rats developed hepatic steatosis with significantly elevated liver triglyceride concentrations compared to chow-fed controls (20.73±2.09 vs.9.75±0.52 mg triglycerides/g tissue, respectively; p=0.001). While lipid accumulation appeared to be evident in the pectoralis muscle from HFD rats, triglyceride concentrations were not significantly different from controls. Likewise, there was no evidence of lipid infiltration in cardiac muscles of HFD rats. Lipid accumulation in the liver of overweight HFD rats may contribute to the observed insulin resistance in these animals. Contrary to the second hypothesis, there were no significant differences in plasma HSP60 expression between HFD and chow rats (p>0.05). Likewise, hemagglutination and hemolysis responses were similar between HFD and chow-fed rats (p>0.05). These findings suggest that immune system responses may not be affected by 6 weeks of high fat intake and that HSP60 is not an early marker of vascular dysfunction in this rodent model.
ContributorsLiss, Tyler Jessee (Author) / Sweazea, Karen (Thesis director) / Shaibi, Gabriel (Committee member) / Johnston, Carol (Committee member) / Barrett, The Honors College (Contributor) / School of Nutrition and Health Promotion (Contributor) / School of Historical, Philosophical and Religious Studies (Contributor)
Created2013-05
Description
Background: Effective glucose management using exercise modalities in older patients with type 2 diabetes and activities of daily living (ADL) disabilities are unknown.
Purpose: The study investigated the acute effects of motor-assisted cycling and functional electrical stimulation (FES) cycling on the 2-h postprandial glucose responses compared with sitting control in older adults with type 2 diabetes and ADL disabilities.
Methods: The study used a 3×3 crossover study design. Nine participants were randomly assigned to one of the three treatment sequences: ABC, BCA, and CAB. (A, motor-assisted cycling; B, FES cycling; C, sitting control). Linear mixed models (LMM) with Bonferroni post-hoc tests were used to test the mean differences for the 2-h postprandial glucose, estimated by the area under the curve (AUC) and incremental AUC (iAUC), between intervention and control treatments after adjustment for covariates (e.g., age, sex, and race).
Results: There were significant mean differences for iAUC (p = 0.005) and AUC (p = 0.038) across motor-assisted cycling, control, and FES cycling treatments. The FES cycling had a lower mean of 2-hour postprandial iAUC as compared with sitting control (iAUC 3.98 mmol∙h/L vs 6.92 mmol∙h/L, p = 0.006, effect size [ES] = 1.72) and the motor-assisted cycling (iAUC, 3.98 mmol∙h/L vs 6.19 mmol∙h/L , p = 0.0368, ES = 1.29), respectively. The FES cycling also had a lower mean of the 2-hour postprandial AUC as compared with sitting control (AUC, 18.29 mmol∙h/L vs 20.95 mmol∙h/L, p = 0.043, ES = 0.89), but had an AUC similar to the motor-assisted cycling (18.29 mmol∙h/L vs 20.23 mmol∙h/L , p = 0.183, ES = 0.19). There were no statistical differences in iAUC (6.19 mmol∙h/L vs 6.92 mmol∙h/L) and AUC (20.23 mmol∙h/L vs 20.95 mmol∙h/L) between the motor-assisted cycling and sitting control (all p>0.05).
Conclusion: Performing 30 minutes of FES cycling on a motor-assisted bike (40 Hz, 39 rpm, 25-29 mA) significantly decreased the 2-h postprandial glucose levels in older adults with type 2 diabetes and ADL disabilities. These findings suggested that FES cycling can be a promising exercise modality for glucose management in diabetic patients with ADL disabilities.
Purpose: The study investigated the acute effects of motor-assisted cycling and functional electrical stimulation (FES) cycling on the 2-h postprandial glucose responses compared with sitting control in older adults with type 2 diabetes and ADL disabilities.
Methods: The study used a 3×3 crossover study design. Nine participants were randomly assigned to one of the three treatment sequences: ABC, BCA, and CAB. (A, motor-assisted cycling; B, FES cycling; C, sitting control). Linear mixed models (LMM) with Bonferroni post-hoc tests were used to test the mean differences for the 2-h postprandial glucose, estimated by the area under the curve (AUC) and incremental AUC (iAUC), between intervention and control treatments after adjustment for covariates (e.g., age, sex, and race).
Results: There were significant mean differences for iAUC (p = 0.005) and AUC (p = 0.038) across motor-assisted cycling, control, and FES cycling treatments. The FES cycling had a lower mean of 2-hour postprandial iAUC as compared with sitting control (iAUC 3.98 mmol∙h/L vs 6.92 mmol∙h/L, p = 0.006, effect size [ES] = 1.72) and the motor-assisted cycling (iAUC, 3.98 mmol∙h/L vs 6.19 mmol∙h/L , p = 0.0368, ES = 1.29), respectively. The FES cycling also had a lower mean of the 2-hour postprandial AUC as compared with sitting control (AUC, 18.29 mmol∙h/L vs 20.95 mmol∙h/L, p = 0.043, ES = 0.89), but had an AUC similar to the motor-assisted cycling (18.29 mmol∙h/L vs 20.23 mmol∙h/L , p = 0.183, ES = 0.19). There were no statistical differences in iAUC (6.19 mmol∙h/L vs 6.92 mmol∙h/L) and AUC (20.23 mmol∙h/L vs 20.95 mmol∙h/L) between the motor-assisted cycling and sitting control (all p>0.05).
Conclusion: Performing 30 minutes of FES cycling on a motor-assisted bike (40 Hz, 39 rpm, 25-29 mA) significantly decreased the 2-h postprandial glucose levels in older adults with type 2 diabetes and ADL disabilities. These findings suggested that FES cycling can be a promising exercise modality for glucose management in diabetic patients with ADL disabilities.
Contributorsma, tongyu (Author) / Lee, Chong (Thesis advisor) / Hooker, Steven (Committee member) / Shaibi, Gabriel (Committee member) / Johnston, Carol (Committee member) / Ringenbach, Shannon (Committee member) / Arizona State University (Publisher)
Created2019
Description
Nonalcoholic fatty liver disease is the most common form of chronic liver disease in the United States. Diets high in saturated fats are known to promote obesity and hepatic steatosis. The consumption of a high fat diet (HFD) can increase the risk factors associated with insulin resistance, which can lead to the onset of diabetes and obesity. A prior study of a soil-derived organometallic complex (OMC) showed that supplementation reduces glucose and body mass in diabetic mice. The goal of this study was to test the efficacy of a similar OMC compound on the mitigation of hepatic steatosis induced from a HFD. Six-week-old male Sprague-Dawley rats (n=42) were divided into the following diet groups: standard rodent chow or 60% kcal from fat high fat diet (mainly lard) for 10-weeks. Rats were further divided into OMC treatment groups with OMC added to their drinking water: 0 mg/ml, 0.6 mg/ml or 3.0mg/ml OMC. At 10 weeks, study animals were euthanized with sodium pentobarbital (200 mg/kg, i.p.) and cardiac plasma as well as liver samples were collected and stored at -80° C until further analyses. Plasma ALT and AST as well as liver triglyceride and free glycerol concentrations were measured using commercially available kits. To assess cellular injury, aspartate transaminase (AST; released mainly from injured cardiac and liver cells) and alanine transaminase (ALT; released mainly from injured liver cells) were examined. Rats fed HFD had elevated plasma ALT activity, which was prevented by treatment with the high dose of OMC (p<0.05). No changes in plasma AST activity were detected. Examination of liver triglyceride and free glycerol concentrations showed increased fat accumulation in the liver of rats consuming HFD (Two-Way ANOVA, p<0.001). OMC did not prevent this increase. These findings suggest that, although OMC does not prevent the accumulation of lipids in the liver of rats fed HFD, it does mitigate liver injury resulting from excess dietary intake of saturated fats.
ContributorsWood, Courtney Ann (Author) / Sweazea, Karen (Thesis director) / Shaibi, Gabriel (Committee member) / Johnston, Carol (Committee member) / School of Art (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2019-05