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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Description
With the rising prevalence of obesity and diabetes, novel treatments to help mitigate or prevent symptoms of these conditions are warranted. Prior studies have shown that fossilized plant materials found in soil lowers blood sugar in a mouse model of diabetes. The goal of this study is to determine whether a similar organometallic complex (OMC) could prevent insulin resistance in the skeletal muscle brought on by chronic high fat intake by examining the protein expression of key enzymes in the insulin signaling pathway and examining glucoregulatory measures. Six-week-old periadolescent male Sprague-Dawley rats (n=42) were randomly chosen to be fed either a high fat diet (HFD) (20% protein, 20% carbohydrates [6.8% sucrose], 60% fat) or a standard chow diet (18.9% protein, 57.33% carbohydrates, 5% fat) for 10 weeks. Rats from each diet group were then randomly assigned to one of three doses of OMC (0, 0.6, 3.0 mg/mL), which was added to their drinking water and fasting blood glucose was measured at baseline and again at 10 weeks. After 10 weeks, rats were euthanized, and soleus muscle samples were isolated, snap-frozen, and stored at -80°C until analyses. Fasting plasma glucose was measured using a commercially available glucose oxidase kit. Following 6 and 10 weeks, HFD rats developed significant hyperglycemia (p<0.001 and p=0.025) compared to chow controls which was prevented by high dose OMC (p=0.021). After 10 weeks, there were significant differences in fasting serum insulin between diets (p=0.009) where levels were higher in HFD rats. No significant difference was seen in p-PI3K expression between groups. These results suggest that OMC could prevent insulin resistance by reducing hyperglycemia. Further studies are needed to characterize the effects of diet and OMC on the insulin signaling pathway in skeletal muscle, the main site of postprandial glucose disposal. This study was supported by a grant from Isagenix International LLC as well as funds from Barrett, the Honors College at Arizona State University, Tempe Campus.
ContributorsStarr, Ashlee (Author) / Sweazea, Karen (Thesis director) / Johnston, Carol (Committee member) / Hyatt, JP (Committee member) / Sanford School of Social and Family Dynamics (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-12
Description
Affecting nearly 1% of the world’s population, Celiac disease is an autoimmune disease that causes damage to the small intestine through the ingestion of gluten. Over time, the villi of the small intestine are destroyed which prevents nutrients from being absorbed properly leading to impaired health and growth of an individual. Currently, there is no cure for celiac disease. Those that are diagnosed with Celiac disease usually adhere to a gluten-free diet. By doing so, most manage their symptoms and minimize the damage to their small intestine. However, this diet is only effective if one is able to strictly adhere to the diet. If gluten is consumed, even on accident which is rather easy, the villi of the small intestine are damaged and individuals are at risk for a number of symptoms including chronic diarrhea, constipation, and even cognitive impairment. A cure for Celiac disease that extends beyond lifestyle changes would better help those affected and ensure their small intestine functions properly and growth of an individual is not impaired. One potential solution is medication that prevents inflammation from T cells through the blockage of cytokine signaling of interleukin-6. This thesis proposes a research project to identify a phase 3, double blind, placebo controlled trial that would test the efficacy of the potential drugs.
ContributorsRehman, Shiza (Author) / Hartwell, Leland (Thesis director) / Johnston, Carol (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2022-12
Description
Birds maintain resting plasma glucose concentrations (pGlu) nearly twice that of comparably sized mammals. Despite this, birds do not incur much of the oxidative tissue damage that might be expected from a high pGlu. Their ability to stave off oxidative damage allows birds to serve as a negative model of hyperglycemia-related complications, making them ideal for the development of new diabetes treatments with the potential for human application. Previous studies conducted by the Sweazea Lab at Arizona State University aimed to use diet as a means to raise blood glucose in mourning doves (Zenaida macroura) in order to better understand the mechanisms they utilize to stave off oxidative damage. These protocols used dietary interventions—a 60% high fat (HF) “chow” diet, and a high carbohydrate (HC) white bread diet—but were unsuccessful in inducing pathologies. Based on this research, we hypothesized that a model of an urban diet (high in fat, refined carbohydrates, and sodium) might impair vasodilation, as the effect of this diet on birds is currently unknown. We found that tibial vasodilation was significantly impaired in birds fed an urban diet compared to those fed a seed diet. Unexpectedly, vasodilation in the urban diet group was comparable to data of wild-caught birds from previous research, possibly indicating that the birds had already been eating a diet similar to this study’s urban diet before they were caught. This may constitute evidence that the seed diet improved vasodilation while the urban diet more closely mimicked the diet of the birds before the trial, suggesting that the model of the urban diet acted as the control diet in this context. This study is the first step in elucidating avian mechanisms for dealing with diabetogenic diets and has potential to aid in the development of treatments for humans with metabolic syndrome.
ContributorsRenner, Michael William (Author) / Sweazea, Karen (Thesis director) / Johnston, Carol (Committee member) / Basile, Anthony (Committee member) / Dean, W.P. Carey School of Business (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2020-05
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
Description
Oral health encompasses a wide variety of conditions with two of the primary conditions being enamel degradation and periodontal disease. These ailments are intertwined and are known to be prevented by a combination of good oral hygiene and a balanced diet. Despite this, incidence rates of oral health conditions in both high and low-and-middle income countries remain high. Periodontal disease prevention is of particular relevance due to its correlation with cardiovascular disease. One highly popular diet that could serve as an alternative strategy in combatting these oral health conditions is intermittent fasting. Intermittent fasting has shown promise in decreasing systemic inflammation and blood glucose levels, both of which are correlated with periodontal disease and enamel degradation. To explore this relationship between intermittent fasting and oral health a 9-week experimental protocol with 4 randomly established groups was completed. These groups included ad libitum high and low-fat groups, and time restricted feeding high and low-fat groups. After the 9-week protocol the mice were sacrificed, and their intact jaws and gingiva tissue were isolated. Three primary methods were used to quantify the effects of intermittent fasting on oral health: comparing the enamel density between groups, comparing the alveolar bone recession between groups, and comparing the gene expression of periodontal disease markers between groups. Body composition and fasting blood glucose levels of the mice were also quantified. We found that the fasting groups had lower average fasting blood glucose levels and maintained a more physiologically ideal body composition. Despite this, the oral health analyses did not have any consistent significant results. The results of this study suggest that despite intermittent fasting’s role in blood glucose levels and body composition regulation, it has minimal effects on enamel degradation and periodontal disease development.
ContributorsCollis, Graham (Author) / Jakiche, Michael (Co-author) / Roberts, Joseph (Thesis director) / Johnston, Carol (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2024-05