Matching Items (12)
Filtering by
- All Subjects: Physiology
- All Subjects: Vinegar--Therapeutic use.
- Creators: Johnston, Carol
- Member of: ASU Electronic Theses and Dissertations
Description
Objective: Vinegar consumption studies have demonstrated possible therapeutic effects in reducing HbA1c and postprandial glycemia. The purpose of the study was to closely examine the effects of a commercial vinegar drink on daily fluctuations in fasting glucose concentrations and postprandial glycemia, and on HbA1c, in individuals at risk for Type 2 Diabetes Mellitus (T2D). Design: Thirteen women and one man (21-62 y; mean, 46.0±3.9 y) participated in this 12-week parallel-arm trial. Participants were recruited from a campus community and were healthy and not diabetic by self-report. Participants were not prescribed oral hypoglycemic medications or insulin; other medications were allowed if use was stable for > 3 months. Subjects were randomized to one of two groups: VIN (8 ounces vinegar drink providing 1.5 g acetic acid) or CON (1 vinegar pill providing 0.04 g acetic acid). Treatments were taken twice daily immediately prior to the lunch and dinner meals. Venous blood samples were drawn at trial weeks 0 and 12 to measure insulin, fasting glucose, and HbA1c. Subjects recorded fasting glucose and 2-h postprandial glycemia concentrations daily using a glucometer. Results: The VIN group showed significant reductions in fasting capillary blood glucose concentrations (p=0.05) that were immediate and sustained throughout the duration of the study. The VIN group had reductions in 2-h postprandial glucose (mean change of −7.6±6.8 mg/dL over the 12-week trial), but this value was not significantly different than that for the CON group (mean change of 3.3±5.3 mg/dL over the 12-week trial, p=0.232). HbA1c did not significantly change (p=0.702), but the reduction in HbA1c in the VIN group, −0.14±0.1%, may have physiological relevance. Conclusions: Significant reductions in HbA1c were not observed after daily consumption of a vinegar drink containing 1.5 g acetic acid in non-diabetic individuals. However, the vinegar drink did significantly reduce fasting capillary blood glucose concentrations in these individuals as compared to a vinegar pill containing 0.04 g acetic acid. These results support a therapeutic effect for vinegar in T2D prevention and progression, specifically in high-risk populations.
ContributorsQuagliano, Samantha (Author) / Johnston, Carol (Thesis advisor) / Appel, Christy (Committee member) / Dixon, Kathleen (Committee member) / Arizona State University (Publisher)
Created2013
Description
ABSTRACT The hormone leptin is an important regulator of body weight and energy balance, while nitric oxide (NO) produced in the blood vessels is beneficial for preventing disease-induced impaired vasodilation and hypertension. Elevations in the free radical superoxide can result in impaired vasodilation through scavenging of NO. Omega 3 is a polyunsaturated fatty acid that is beneficial at reducing body weight and in lowering many cardiovascular risk factors like atherosclerosis. The present study was designed to examine the change in plasma concentrations of leptin, nitric oxide, and the antioxidant superoxide dismutase in addition to examining the association between leptin and NO in healthy normal weight adult female subjects before and following omega 3 intakes. Participants were randomly assigned to either a fish oil group (600 mg per day) or a control group (1000 mg of coconut oil per day) for 8 weeks. Results showed no significant difference in the percent change of leptin over the 8 week supplementation period for either group (15.3±31.9 for fish oil group, 7.83±27 for control group; p=0.763). The percent change in NO was similarly not significantly altered in either group (-1.97±22 decline in fish oil group, 11.8±53.9 in control group; p=0.960). Likewise, the percent change in superoxide dismutase for each group was not significant following 8 weeks of supplementation (fish oil group: 11.94±20.94; control group: 11.8±53.9; p=0.362). The Pearson correlation co-efficient comparing the percent change of both leptin and NO was r2= -0.251 demonstrating a mildly negative, albeit insignificant, relationship between these factors. Together, these findings suggest that daily supplementation with 600 mg omega 3 in healthy females is not beneficial for improving these cardiovascular risk markers. Future studies in this area should include male subjects as well as overweight subjects with larger doses of fish oil that are equivalent to three or more servings per week. The importance of gender cannot be underestimated since estrogen has protective effects in the vasculature of females that may have masked any further protective effects of the fish oil. In addition, overweight individuals are often leptin-resistant and develop impaired vasodilation resulting from superoxide-mediated scavenging of nitric oxide. Therefore, the reported antioxidant and weight loss properties of omega 3 supplementation may greatly benefit overweight individuals.
ContributorsAlanbagy, Samer (Author) / Sweazea, Karen (Thesis advisor) / Johnston, Carol (Committee member) / Shepard, Christina (Committee member) / Lespron, Christy (Committee member) / Arizona State University (Publisher)
Created2014
Description
The omega-3 fatty acids in fatty fish and fish oil, eicosapentanoic acid (EPA) and docosahexanoic acid (DHA), have been associated with a reduction in risk for cardiovascular disease. Blood type is a known contributor to risk for cardiovascular events. This study evaluated the effect of fish oil supplements on cardiovascular risk markers in adults with blood types A or O. An 8-week parallel-arm, randomized, double-blind trial was conducted in healthy adult men and women with either blood type A (BTA) or blood type O (BTO). Participants were randomized to receive fish oil supplements (n=10 [3 BTA/7 BTO]; 2 g [containing 1.2 g EPA+DHA]/d) or a coconut oil supplement (n=7 [3 BTA/4 BTO]; 2 g/d). Markers that were examined included total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), high-sensitivity C-reactive protein (hsCRP), and hemoglobin A1C (HbA1C). Results indicated that the percent change in LDL cholesterol was significantly greater in the coconut oil group vs the fish oil group (-14.8±12.2% vs +2.8±18.9% respectively, p=0.048). There were no other significant differences between treatment groups, or between blood types A and O, for the other cardiovascular risk markers. Further research with a larger and more diverse sample may yield a more conclusive result.
ContributorsHerring, Dana (Author) / Johnston, Carol (Thesis advisor) / Vega-Lopez, Sonia (Committee member) / Shepard, Christina (Committee member) / Arizona State University (Publisher)
Created2014
Description
Long term high fat diets (HFD) are correlated with the development of diabetes
and kidney disease. However, the impact of short term high fat intake on the etiology of kidney disease has not been well-studied. Therefore, this study examined the impact of a six week HFD (60% fat) on kidney structure and function in young male Sprague-Dawley rats. Previous studies have shown that these animals develop indices of diabetes compared to rats fed a standard rodent chow (5% fat) for six weeks. The hypothesis of this study is that six weeks of HFD will lead to early stages of kidney disease as evidenced by morphological and functional changes in the kidney. Alterations in morphology were determined by measuring structural changes in the kidneys (changes in mass, fatty acid infiltration, and structural damage). Alterations in kidney function were measured by analyzing urinary biomarkers of oxidative RNA/DNA damage, renal tissue lipid peroxidation, urinary markers of impaired kidney function (urinary protein, creatinine, and hydrogen peroxide (H2O2)), markers of inflammation (tumor necrosis factor alpha (TNFα) and interleukin 6 (IL-6)), as well as cystatin C, a plasma biomarker of kidney function. The results of these studies determined that short term HFD intake is not sufficient to induce early stage kidney disease. Beyond increases in renal mass, there were no significant differences between the markers of renal structure and function in the HFD and standard rodent chow-fed rats.
and kidney disease. However, the impact of short term high fat intake on the etiology of kidney disease has not been well-studied. Therefore, this study examined the impact of a six week HFD (60% fat) on kidney structure and function in young male Sprague-Dawley rats. Previous studies have shown that these animals develop indices of diabetes compared to rats fed a standard rodent chow (5% fat) for six weeks. The hypothesis of this study is that six weeks of HFD will lead to early stages of kidney disease as evidenced by morphological and functional changes in the kidney. Alterations in morphology were determined by measuring structural changes in the kidneys (changes in mass, fatty acid infiltration, and structural damage). Alterations in kidney function were measured by analyzing urinary biomarkers of oxidative RNA/DNA damage, renal tissue lipid peroxidation, urinary markers of impaired kidney function (urinary protein, creatinine, and hydrogen peroxide (H2O2)), markers of inflammation (tumor necrosis factor alpha (TNFα) and interleukin 6 (IL-6)), as well as cystatin C, a plasma biomarker of kidney function. The results of these studies determined that short term HFD intake is not sufficient to induce early stage kidney disease. Beyond increases in renal mass, there were no significant differences between the markers of renal structure and function in the HFD and standard rodent chow-fed rats.
ContributorsCrinigan, Catherine (Author) / Sweazea, Karen (Thesis advisor) / Johnston, Carol (Committee member) / Mayol-Kreiser, Sandra (Committee member) / Arizona State University (Publisher)
Created2015
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 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
Description
Many people with or at risk for diabetes have difficulty maintaining normal postprandial blood glucose levels (120-140 mg/dl). Research has shown that vinegar decreases postprandial glycemia. The purpose of this study was to examine a possible mechanism by which vinegar decreases postprandial glycemia, particularly the effect of vinegar ingestion on gut fermentation. In this parallel arm randomized control trial, the effects of daily ingestion of vinegar on gut fermentation markers were observed among adults at risk for type 2 diabetes in Phoenix, Arizona. Subjects (n=14) were randomly assigned to treatments consisting of a vinegar drink (1.5g acetic acid) or a placebo (2 vinegar pills containing 40mg acetic acid each). All participants were required to consume the vinegar drink (16 oz) or 2 placebo pills every day for 12 weeks. At week 12, participants filled out a questionnaire to report gastrointestinal (GI) symptoms and three consecutive breath samples were taken from each subject to measure fasting breath hydrogen (BH2) with a breath analyzer. Fasting BH2 measures for the vinegar drink group (16.1+11.8 ppm) were significantly different than those from the pill group (3.6+1.4) with a partial eta squared of 0.39 (p=0.023). After adjusting for age as a confounding factor (r=0.406) and removing an outlier, fasting BH2 measures for the vinegar drink group (4.3+1.1 ppm) were still significantly different than those from the pill group (3.6+1.4) with a partial eta squared of 0.35 (p=0.045). Participants in both groups reported mild changes in GI symptoms. In conclusion, adults at risk for type 2 diabetes that consume 2 tablespoons of vinegar a day may have increased gut fermentation compared to those who do not consume vinegar.
ContributorsWhite, Serena (Author) / Johnston, Carol (Thesis advisor) / Appel, Christy (Committee member) / Martin, Keith (Committee member) / Arizona State University (Publisher)
Created2013
Description
ABSTRACT This randomized, controlled, double-blind crossover study examined the effects of a preprandial, 20g oral dose of apple cider vinegar (ACV) on colonic fermentation and glycemia in a normal population, with the ultimate intention of identifying the mechanisms by which vinegar has been shown to reduce postprandial glycemia and insulinemia. Fifteen male and female subjects were recruited, ages 20-60y, who had no prior history of gastrointestinal (GI) disease or resections impacting normal GI function, were non-smokers, were non-vegetarian/vegan, were not taking any medications known to alter (glucose) metabolism, and were free of chronic disease including diabetes. Subjects were instructed to avoid exercise, alcohol and smoking the day prior to their trials and to consume a standardized, high-carbohydrate dinner meal the eve prior. There was a one-week washout period per subject between appointments. Breath hydrogen, serum insulin and capillary glucose were assessed over 3 hours after a high-starch breakfast meal to evaluate the impact of preprandial supplementation with ACV or placebo (water). Findings confirmed the antiglycemic effects of ACV as documented in previous studies, with significantly lower mean blood glucose concentrations observed during ACV treatment compared to the placebo at 30 min (p=0.003) and 60 min (p=0.005), and significantly higher mean blood glucose concentrations at 180 min (p=0.045) postprandial. No significant differences in insulin concentrations between treatments. No significant differences were found between treatments (p>0.05) for breath hydrogen; however, a trend was observed between the treatments at 180 min postprandial where breath hydrogen concentration was visually perceived as being higher with ACV treatment compared to the placebo. Therefore, this study failed to support the hypothesis that preprandial ACV ingestion produces a higher rate of colonic fermentation within a 3 hour time period following a high-carbohydrate meal. Due to variations in experiment duration noted in other literature, an additional study of similar nature with an expanded specimen collections period, well beyond 3 hours, is warranted.
ContributorsMedved, Emily M (Author) / Johnston, Carol (Thesis advisor) / Sweazea, Karen (Committee member) / Shepard, Christina (Committee member) / Arizona State University (Publisher)
Created2012
Description
To date, there have not been any studies in a human population that explore the potential of vinegar ingestion in reducing visceral fat, a common yet serious metabolic disease risk factor. However, previous research in animal models exhibit promising findings, showing that vinegar is effective at reducing visceral fat. This is thought to be due to the activation of AMPK (adenosine monophosphate protein kinase) by acetic acid, the active ingredient in vinegar. The purpose of this study was to identify if this potentially groundbreaking relationship exists in human subjects. Healthy, nonsmoking, sedentary adults between the ages 18-45 y and a waist circumference measurement greater than or equal to 33 inches for women and 38 inches for men were recruited for this study. Twenty-three participants completed this 8-week, parallel arm, randomized control trial that tested the efficacy of red wine vinegar consumption (2 tablespoons red wine vinegar, twice per day, before a meal; providing 3.6 g acetic acid) against a placebo (1 apple cider vinegar pill, twice per day, before a meal; providing 0.0225 g acetic acid) for 8 weeks. Participants were randomized into either the vinegar (VIN) or control (CON) group after being stratified by age, gender, waist circumference, and weight. Results found that the VIN group experienced a 2% decrease in visceral fat (cm3, quantified by a DXA scan), but this change did not differ significantly from that of the CON group (p=0.256). The VIN group also experienced a slight decrease in insulin compared to the CON group, but this change was not significantly different than the control change (p=0.125). However, the change in HOMA-IR trended downward in the VIN group (-16%) as compared to the CON group (+9%) (p=0.079) with a large effect size, 0.153. Other parameters did not show statistically significant results between the groups. Further research is indicated in order to examine the potential of vinegar to reduce visceral fat.
ContributorsBaker, Olivia (Author) / Johnston, Carol (Thesis advisor) / Mayol-Kreiser, Sandra (Committee member) / Lespron, Christy (Committee member) / Arizona State University (Publisher)
Created2018
Description
Background: Acetic acid in vinegar has demonstrated antiglycemic effects in previous studies; however, the mechanism is unknown.
Objective: To determine whether acetic acid dissociates in the addition of sodium chloride and describe a flavorful vinaigrette that maintains the functional properties of acetic acid.
Design: Phase I - Ten healthy subjects (23-40 years) taste tested five homemade vinaigrette and five commercial dressings. Perceived saltiness, sweetness, tartness, and overall tasted were scored using a modified labeled affective magnitude scale. Each dressing was tested three times for pH with a calibrated meter. Phase II – Randomized crossover trial testing six dressings against a control dressing two groups of nine healthy adult subjects (18-52 years). Height, weight and calculated body mass index (BMI) were performed at baseline. Subjects participated in four test sessions each, at least seven days apart. After a 10-hour fast, participants consumed 38g of the test drink, followed by a bagel meal. Capillary blood glucose was obtained at fasting, and every 30 minutes over a 2-hour period the test meal.
Results: Dressing pH reduced as sodium content increased. In the intervention trials, no significant differences were observed between groups (p >0.05). The greatest reduction in postprandial glycemia (~21%) was observed in the dressing containing 200 mg of sodium. Effect size was large in both group 1 (η2=0.161) and group 2 (η2=0.577).
Conclusion: The inclusion of sodium into acetic acid may impair its ability to attenuate blood glucose after a meal.
Objective: To determine whether acetic acid dissociates in the addition of sodium chloride and describe a flavorful vinaigrette that maintains the functional properties of acetic acid.
Design: Phase I - Ten healthy subjects (23-40 years) taste tested five homemade vinaigrette and five commercial dressings. Perceived saltiness, sweetness, tartness, and overall tasted were scored using a modified labeled affective magnitude scale. Each dressing was tested three times for pH with a calibrated meter. Phase II – Randomized crossover trial testing six dressings against a control dressing two groups of nine healthy adult subjects (18-52 years). Height, weight and calculated body mass index (BMI) were performed at baseline. Subjects participated in four test sessions each, at least seven days apart. After a 10-hour fast, participants consumed 38g of the test drink, followed by a bagel meal. Capillary blood glucose was obtained at fasting, and every 30 minutes over a 2-hour period the test meal.
Results: Dressing pH reduced as sodium content increased. In the intervention trials, no significant differences were observed between groups (p >0.05). The greatest reduction in postprandial glycemia (~21%) was observed in the dressing containing 200 mg of sodium. Effect size was large in both group 1 (η2=0.161) and group 2 (η2=0.577).
Conclusion: The inclusion of sodium into acetic acid may impair its ability to attenuate blood glucose after a meal.
ContributorsBonsall, Amber K (Author) / Johnston, Carol (Thesis advisor) / Mayol-Kreiser, Sandra (Committee member) / Lespron, Christy (Committee member) / Arizona State University (Publisher)
Created2017
Description
The glycation of plasma proteins leading to the production of advanced glycation end products (AGEs) and subsequent damage is a driving factor in the pathophysiology of diabetic complications. The overall research objective was to elucidate the mechanisms by which birds prevent protein glycation in the presence of naturally high plasma glucose concentrations. This was accomplished through the specific purpose of examining the impact of temperature and glucose concentration on the percent glycation of chicken serum albumin (CSA) in comparison to human serum albumin (HSA). Purified CSA and HSA solutions prepared at four different glucose concentrations (0 mM, 5.56 mM, 11.11 mM, and 22.22 mM) were incubated at three different temperatures (37.0°C, 39.8°C, and 41.4°C) on separate occasions for seven days with aliquots extracted on days 0, 3, and 7. Samples were analyzed by LC-ESI-MS for percent glycation of albumin. The statistically significant interaction between glucose concentration, temperature, albumin type, and time as determined by four-way repeated measures ANOVA (p = 0.032) indicated that all independent variables interacted to affect the mean percent glycation of albumin. As glucose concentration increased, the percent glycation of both HSA and CSA increased over time at all temperatures. In addition, HSA was glycated to a greater extent than CSA at the two higher glucose concentrations examined for all temperature conditions. Temperature differentially affected percent glycation of HSA and CSA wherein glycation increased with rising temperatures for HSA but not CSA. The results of this study suggest an inherent difference between the human and chicken albumin that contributes to the observed differences in glycation. Further research is needed to characterize this inherent difference in an effort to elucidate the mechanism by which birds protect plasma proteins from glycation. Future related work has the potential to lead to the development of novel therapies to prevent or reverse protein glycation prior to the formation of AGEs in humans, thus preventing the development and devastating effects of numerous diabetic complications.
ContributorsZuck, Jessica (Author) / Sweazea, Karen (Thesis advisor) / Johnston, Carol (Committee member) / Lespron, Christy (Committee member) / Arizona State University (Publisher)
Created2016