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
Doxorubicin (DOX) is a cardiotoxic, anthracycline-based, anti-neoplastic agent that causes pathological cardiac remodeling due to altered protein expression associated with cardiotoxicity. DOX cardiotoxicity causes increased Akt phosphorylation, blunted AMPK phosphorylation and upregulated mTOR phosphorylation. Akt is activated by cellular stress and damage. AMPK is activated by increases in AMP and

Doxorubicin (DOX) is a cardiotoxic, anthracycline-based, anti-neoplastic agent that causes pathological cardiac remodeling due to altered protein expression associated with cardiotoxicity. DOX cardiotoxicity causes increased Akt phosphorylation, blunted AMPK phosphorylation and upregulated mTOR phosphorylation. Akt is activated by cellular stress and damage. AMPK is activated by increases in AMP and ADP concentrations and decreased ATP concentration. mTOR is active in cellular growth and remodeling. These proteins are cellular kinases with cascades that are influenced by one another. Exercise preconditioning may diminish the cardiotoxic effects on these proteins. Female, Ovariectomized Sprague-Dawley rats (N=33) were randomized to: Exercise+DOX (EX+DOX, n=9); Exercise+Vehicle (EX+VEH, n=8); Sedentary+DOX (SED+DOX, n=8); and Sedentary+Vehicle (SED+VEH, n=8) groups. DOX (4mg/kg) or VEH (saline) intraperitoneal injections were administered bi-weekly (cumulative dose of 12mg/kg). VEH animals received body weight matched volumes of saline based on dosing in animals receiving DOX. Exercise (EX) animals underwent high intensity (85-95% VO2 peak) interval training (HIIT) (4x4 min bouts) separated by low intensity (50-60% VO2max) intervals (2 min bouts) 5 days per week. Exercise began 1 week prior to the first injection and was continued throughout the study. Rats were euthanized 5 days after the last injection. Left ventricular tissue was isolated, processed into lysate and used for western blot analyses [2x2 ANOVA; (α=0.05)]. DOX induced significant phosphorylation of Akt and mTOR (p=0.035; p=0.032) only in SED+DOX rats, but unchanged in EX+DOX rats. No significant differences (p=0.374) in AMPK phosphorylation were observed between groups. Exercise Preconditioning prevents some DOX-induced changes in the cardiac mTOR signaling pathway implicated in pathological remodeling.
ContributorsPanknin, Timothy M (Author) / Angadi, Siddhartha (Thesis director) / Sweazea, Karen (Committee member) / Dickinson, Jared (Committee member) / School of Nutrition and Health Promotion (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
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Description
Weight cycling (WC) is characterized by repeated bouts of weight loss followed by regain. WC has been associated with a number of adverse health consequences and is a risk factor for cardiovascular disease. Body weight regulation is complex. Little is known about why women who intentionally lose weight are so

Weight cycling (WC) is characterized by repeated bouts of weight loss followed by regain. WC has been associated with a number of adverse health consequences and is a risk factor for cardiovascular disease. Body weight regulation is complex. Little is known about why women who intentionally lose weight are so likely to regain their weight back. Humans are motivated by a variety of psychological pressures as well as physiological stimuli that influence eating behaviors and weight control. One of the complex factors that has been shown to predict weight regain, in weight-reduced individuals, is hunger. Ghrelin is a known gastrointestinal hormone that rises during weight loss and is a strong trigger of hunger and increased appetite. Increased ghrelin levels have been associated with disordered eating behaviors and active weight loss. The Three Factor Eating Questionnaire (TFEQ-R18) describes elements that may affect hunger and satiety. These factors are: cognitive restraint (CR, defined as regulating food intake because of weight maintenance), uncontrolled eating (UE, defined as difficulty in regulating eating), and emotional eating (EE, refers to the tendency to eat more than needed because of mood state). Objective: The purpose of this study was to explore the associations of fasting plasma ghrelin with eating behaviors and weight cycling in overweight and obese women. Methods: This is a cross-sectional observation of women aged 20-60 years who completed a Weight and Lifestyle Inventory (WALI) and the TFEQ-R18. Women provided a 12-h fasting blood sample and plasma ghrelin was measured using a commercial radioimmunoassay (ELISA kit Cat# EZGRA-88k). Intra- and inter-assay CVs were 88.4% + 13.8% and 84.4% + 8.4% respectively. Descriptive data were computed and Pearson correlations were assessed adjusting for age and body weight (SPSS, v23). Results: A WC Index (WCI) was computed as number of WC reported x the amount of weight lost per cycle. 61 women (mean age: 39.3 + 11 yr; BMI: 31.4 + 7; WCI: 70 + 60; range = 0 to 253) completed questionnaires. Ghrelin was significantly and negatively correlated to weight (R= -0.25, P = 0.03), BMI (R= -0.32, P = .006), UE (R = -0.29, p = 0.02), and EE (R = -0.29, p = 0.04). Ghrelin was not significantly related to WCI. WCI was not significantly correlated with any TFEQ-18 subscales. Conclusion: In this observational study, lower ghrelin was associated with higher UE and EE. Thus physiological hunger sensations from ghrelin secretion, is not a likely stimulus of eating behavior in these women. There are a host of psychological triggers, such as stress, loneliness, guilt, anger etc. that may enhance eating. Future research will need to explore what psychological triggers influence eating behavior and why obese women are resistant to the powerful physiological hunger cues of ghrelin.
ContributorsHearns, Joan B. (Author) / Swan, Pamela (Thesis director) / Sweazea, Karen (Committee member) / School of Nutrition and Health Promotion (Contributor) / Barrett, The Honors College (Contributor)
Created2016-05