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According to the CDC, diabetes is the 7th leading cause of death in the U.S. and rates are continuing to rise nationally and internationally. Chronically elevated blood glucose levels can lead to type 2 diabetes and other complications. Medications can be used to treat diabetes, but often have side effects.

According to the CDC, diabetes is the 7th leading cause of death in the U.S. and rates are continuing to rise nationally and internationally. Chronically elevated blood glucose levels can lead to type 2 diabetes and other complications. Medications can be used to treat diabetes, but often have side effects. Lifestyle and diet modifications can be just as effective as medications in helping to improve glycemic control, and prevent diabetes or improve the condition in those who have it. Studies have demonstrated that consuming vinegar with carbohydrates can positively impact postprandial glycemia in diabetic and healthy individuals. Continuous vinegar intake with meals may even reduce fasting blood glucose levels. Since vinegar is a primary ingredient in mustard, the purpose of this study was to determine if mustard consumption with a carbohydrate-rich meal (bagel and fruit juice) had an effect on the postprandial blood glucose levels of subjects. The results showed that mustard improved glycemia by 17% when subjects consumed the meal with mustard as opposed to the control. A wide variety of vinegars exists. The defining ingredient in all vinegars is acetic acid, behind the improvement in glycemic response observed with vinegar ingestion. Vinegar-containing foods range from mustard, to vinaigrette dressings, to pickled foods. The benefits of vinegar ingestion with carbohydrates are dose-dependent, meaning that adding even small amounts to meals can help. Making a conscious effort to incorporate these foods into meals, in addition to an overall healthy lifestyle, could provide an additional tool for diabetics and nondiabetics alike to consume carbohydrates in a healthier manner.
ContributorsJimenez, Gabriela (Author) / Johnston, Carol (Thesis director) / Lespron, Christy (Committee member) / School of Nutrition and Health Promotion (Contributor) / School of International Letters and Cultures (Contributor) / Barrett, The Honors College (Contributor)
Created2016-05
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The development of the Diabetic Physiological state is influenced by the Receptor for Advanced Glycation End Products (RAGE). This receptor was discovered in 1992, and the accumulation of research on this subject has been extensive. Structural characterization studies of the RAGE protein have shown that it is a transmembrane protein

The development of the Diabetic Physiological state is influenced by the Receptor for Advanced Glycation End Products (RAGE). This receptor was discovered in 1992, and the accumulation of research on this subject has been extensive. Structural characterization studies of the RAGE protein have shown that it is a transmembrane protein that binds a number of different motile ligands. The diversity of ligands that can attach to the binding domain is the primary factor that allows for RAGE to exhibit its wide-range effects on host cells. Two different studies were completed: one study dealt with the role of IAPP in beta cell death, and the second study was related to RAGE influence on cardiomyocytes and, more specifically, it was related to cardiac cell death. After the completion of the two studies, a comprehensive report was written for each topic. The two papers were merged into a single document. Molecular studies are important for understanding the underlying mechanisms that motivate pathophysiological presentation. In addition to a molecular understanding of the development of diabetes, a clinical research study was completed through the examination of appropriate literature sources. This clinical aspect allowed for the progression of different phases in the research process. A relationship between vinegar and lower plasma glucose was found. The exact mechanism behind this relationship will be studied in the future.
ContributorsGonzalez, Matthew Joseph (Author) / Johnston, Carol (Thesis director) / Collins, Michael (Committee member) / Barrett, The Honors College (Contributor) / School of Nutrition and Health Promotion (Contributor)
Created2015-05
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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

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
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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

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