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- All Subjects: Obesity
- Creators: Herman, Richard
- Creators: Katsanos, Christos
- Creators: Mayol-Kreiser, Sandra
Description
In adults, consuming a high-fat meal can induce endothelial dysfunction while exercise may mitigate postprandial endothelial dysfunction. Whether exercise is protective against postprandial endothelial dysfunction in obese youth is unknown. The purpose of this study was to determine if high-intensity interval exercise (HIIE) performed the evening prior to a high-fat meal protects against postprandial endothelial dysfunction in obese adolescent males. Fourteen obese adolescent males (BMI%tile=98.5±0.6; 14.3±1.0yrs) completed the study. After initial screening, participants arrived, fasted at 9:00 in the morning where brachial artery flow-mediated dilation (FMD) was measured using duplex ultrasound after 20min of supine rest (7.0±3.0%) and completed a maximal exercise test on a cycle ergometer (VO2peak=2.6±0.5 L/min). Participants were randomized and completed 2 conditions: a morning high-fat meal challenge with evening prior HIIE (EX+M) or a morning high-fat meal challenge without prior exercise (MO). The EX+M condition included a single HIIE session on a cycle ergometer (8 X 2min at ≥90%HRmax, with 2min active recovery between bouts, 42min total) which was performed at 17:00 the evening prior to the meal challenge. In both conditions, a mixed-meal was tailored to participants body weight consisting of 0.7g of fat/kg of body weight consumed (889±95kcal; 65% Fat, 30% CHO). FMD was measured at fasting (>10hrs) and subsequently measured at 2hr and 4hr after high-fat meal consumption. Exercise did not improve fasting FMD (7.5±3.0 vs. 7.4±2.8%, P=0.927; EX+M and MO, respectively). Despite consuming a high-fat meal, FMD was not reduced at 2hr (8.4±3.4 vs. 7.6±3.9%; EX+M and MO, respectively) or 4hr (8.8±3.9 vs. 8.6±4.0%; EX+M and MO, respectively) in either condition and no differences were observed between condition (p(condition*time)=0.928). These observations remained after adjusting for baseline artery diameter and shear rate. We observed that HIIE, the evening prior, had no effect on fasting or postprandial endothelial function when compared with a meal only condition. Future research should examine whether exercise training may be able to improve postprandial endothelial function rather than a single acute bout in obese youth.
ContributorsRyder, Justin Ross (Author) / Shaibi, Gabriel Q (Thesis advisor) / Gaesser, Glenn A (Committee member) / Vega-Lopez, Sonia (Committee member) / Crespo, Noe C (Committee member) / Katsanos, Christos (Committee member) / Arizona State University (Publisher)
Created2014
Description
Nut consumption, specifically almonds, have been shown to help maintain weight and influence disease risk factors in adult populations. Limited studies have been conducted examining the effect of a small dose of almonds on energy intake and body weight. The objective of this study was to determine the influence of pre-meal almond consumption on energy intake and weight in overweight and obese adults. In this study included 21, overweight or obese, participants who were considered healthy or had a controlled disease state. This 8-week parallel arm study, participants were randomized to consume an isocaloric amount of almonds, (1 oz) serving, or two (2 oz) cheese stick serving, 30 minutes before the dinner meal, 5 times per week. Anthropometric measurements including weight, waist circumference, and body fat percentage were recorded at baseline, week 1, 4, and 8. Measurement of energy intake was self-reported for two consecutive days at week 1, 4 and 8 using the ASA24 automated dietary program. The energy intake after 8 weeks of almond consumption was not significantly different when compared to the control group (p=0.965). In addition, body weight was not significantly reduced after 8 weeks of the almond intervention (p=0.562). Other parameters measured in this 8-week trial did not differ between the intervention and the control group. These data presented are underpowered and therefore inconclusive on the effects that 1 oz of almonds, in the diet, 5 per week has on energy intake and bodyweight.
ContributorsMcBride, Lindsey (Author) / Johnston, Carol (Thesis advisor) / Swan, Pamela (Committee member) / Mayol-Kreiser, Sandra (Committee member) / Arizona State University (Publisher)
Created2011
Description
Skeletal muscle (SM) mitochondria generate the majority of adenosine triphosphate (ATP) in SM, and help regulate whole-body energy expenditure. Obesity is associated with alterations in SM mitochondria, which are unique with respect to their arrangement within cells; some mitochondria are located directly beneath the sarcolemma (i.e., subsarcolemmal (SS) mitochondria), while other are nested between the myofibrils (i.e., intermyofibrillar (IMF) mitochondria). Functional and proteome differences specific to SS versus IMF mitochondria in obese individuals may contribute to reduced capacity for muscle ATP production seen in obesity. The overall goals of this work were to (1) isolate functional muscle SS and IMF mitochondria from lean and obese individuals, (2) assess enzyme activities associated with the electron transport chain and ATP production, (3) determine if elevated plasma amino acids enhance SS and IMF mitochondrial respiration and ATP production rates in SM of obese humans, and (4) determine differences in mitochondrial proteome regulating energy metabolism and key biological processes associated with SS and IMF mitochondria between lean and obese humans.
Polarography was used to determine functional differences in isolated SS and IMF mitochondria between lean (37 ± 3 yrs; n = 10) and obese (35 ± 3 yrs; n = 11) subjects during either saline (control) or amino acid (AA) infusions. AA infusion increased ADP-stimulated respiration (i.e., coupled respiration), non-ADP stimulated respiration (i.e., uncoupled respiration), and ATP production rates in SS, but not IMF mitochondria in lean (n = 10; P < 0.05). Neither infusion increased any of the above parameters in muscle SS or IMF mitochondria of the obese subjects.
Using label free quantitative mass spectrometry, we determined differences in proteomes of SM SS and IMF mitochondria between lean (33 ± 3 yrs; n = 16) and obese (32 ± 3 yrs; n = 17) subjects. Differentially-expressed mitochondrial proteins in SS versus IMF mitochondria of obese subjects were associated with biological processes that regulate: electron transport chain (P<0.0001), citric acid cycle (P<0.0001), oxidative phosphorylation (P<0.001), branched-chain amino acid degradation, (P<0.0001), and fatty acid degradation (P<0.001). Overall, these findings show that obesity is associated with redistribution of key biological processes within the mitochondrial reticulum responsible for regulating energy metabolism in human skeletal muscle.
Polarography was used to determine functional differences in isolated SS and IMF mitochondria between lean (37 ± 3 yrs; n = 10) and obese (35 ± 3 yrs; n = 11) subjects during either saline (control) or amino acid (AA) infusions. AA infusion increased ADP-stimulated respiration (i.e., coupled respiration), non-ADP stimulated respiration (i.e., uncoupled respiration), and ATP production rates in SS, but not IMF mitochondria in lean (n = 10; P < 0.05). Neither infusion increased any of the above parameters in muscle SS or IMF mitochondria of the obese subjects.
Using label free quantitative mass spectrometry, we determined differences in proteomes of SM SS and IMF mitochondria between lean (33 ± 3 yrs; n = 16) and obese (32 ± 3 yrs; n = 17) subjects. Differentially-expressed mitochondrial proteins in SS versus IMF mitochondria of obese subjects were associated with biological processes that regulate: electron transport chain (P<0.0001), citric acid cycle (P<0.0001), oxidative phosphorylation (P<0.001), branched-chain amino acid degradation, (P<0.0001), and fatty acid degradation (P<0.001). Overall, these findings show that obesity is associated with redistribution of key biological processes within the mitochondrial reticulum responsible for regulating energy metabolism in human skeletal muscle.
ContributorsKras, Katon Anthony (Author) / Katsanos, Christos (Thesis advisor) / Chandler, Douglas (Committee member) / Dinu, Valentin (Committee member) / Mor, Tsafrir S. (Committee member) / Arizona State University (Publisher)
Created2017
Description
Obesity impairs skeletal muscle maintenance and regeneration, a condition that can progressively lead to muscle loss, but the mechanisms behind it are unknown. Muscle is primarily composed of multinucleated cells called myotubes which are derived by the fusion of mononucleated myocytes. A key mediator in this process is the cellular fusion protein syncytin-1. This led to the hypothesis that syncytin-1 could be decreased in the muscle of obese/insulin resistant individuals. In contrast, it was found that obese/insulin resistant subjects had higher syncytin-1 expression in the muscle compared to that of the lean subjects. Across the subjects, syncytin-1 correlated significantly with body mass index, percent body fat, blood glucose and HbA1c levels, insulin sensitivity and muscle protein fractional synthesis rate. The concentrations of specific plasma fatty acids, such as the saturated fatty acid (palmitate) and monounsaturated fatty acid (oleate) are known to be altered in obese/insulin resistant humans, and also to influence the protein synthesis in muscle. Therefore, it was evaluated that the effects of palmitate and oleate on syncytin-1 expression, as well as 4E-BP1 phosphorylation, a key mechanism regulating muscle protein synthesis in insulin stimulated C2C12 myotubes. The results showed that treatment with 20 nM insulin, 300 µM oleate, 300 µM oleate +20 nM insulin and 300 µM palmitate + 300 µM oleate elevated 4E-BP1 phosphorylation. At the same time, 20 nM insulin, 300 µM palmitate, 300 µM oleate + 20 nM insulin and 300 µM palmitate + 300 µM oleate elevated syncytin-1 expression. Insulin stimulated muscle syncytin-1 expression and 4E-BP1 phosphorylation, and this effect was comparable to that observed in the presence of oleate alone. However, the presence of palmitate + oleate diminished the stimulatory effect of insulin on muscle syncytin-1 expression and 4E-BP1 phosphorylation. These findings indicate oleate but not palmitate increased total 4E-BP1 phosphorylation regardless of insulin and the presence of palmitate in insulin mediated C2C12 cells. The presence of palmitate inhibited the upregulation of total 4EB-P1 phosphorylation. Palmitate but not oleate increased syncytin-1 expression in insulin mediated C2C12 myotubes. It is possible that chronic hyperinsulinemia in obesity and/or elevated levels of fatty acids such as palmitate in plasma could have contributed to syncytin-1 overexpression and decreased muscle protein fractional synthesis rate in obese/insulin resistant human muscle.
ContributorsRavichandran, Jayachandran (Author) / Katsanos, Christos (Thesis advisor) / Coletta, Dawn (Committee member) / Dickinson, Jared (Committee member) / Arizona State University (Publisher)
Created2017
Description
Objectives: To investigate the potential of vinegar supplementation as a means for reducing visceral fat in healthy overweight and obese adults, and to evaluate its effects on fasting blood glucose and fasting insulin.
Subjects and Methods: Forty-five sedentary overweight and obese adult participants with a waist circumference greater than 32 inches for women and 37 inches for men were randomly assigned to one of two groups, the vinegar group (VIN, n=21) or the control group (CON, n=24), and instructed to consume either two tablespoons of liquid red wine vinegar (3.6g acetic acid) or a control pill (0.0225g acetic acid) twice daily at the beginning of a meal for 8 weeks. Participants were also instructed to maintain normal diet and physical activity levels. Anthropometric measures, dual-energy x-ray absorptiometry (DXA) scans, blood samples, and 24-hour dietary recalls were collected at baseline and at end of trial. A compliance calendar was provided for daily tracking of vinegar supplementation.
Results: Compliance to vinegar supplementation averaged 92.7 ±13.3% among the VIN group and 89.1 ±18.9% among the CON group. There were no statistically significant differences in anthropometric measurements between baseline and week 8: weight (P=0.694), BMI (P=0.879), and waist circumference (P=0.871). Similarly, DXA scan data did not show significant changes in visceral fat (P=0.339) or total fat (P=0.294) between baseline and week 8. The VIN group had significant reductions in fasting glucose (P=0.003), fasting insulin (P <0.001), and homeostatic model assessment of insulin resistance scores (P <0.001) after treatment.
Conclusions: These data do not support the findings from previous studies that indicated a link between vinegar supplementation and increased fat metabolism, specifically visceral fat reduction.
Subjects and Methods: Forty-five sedentary overweight and obese adult participants with a waist circumference greater than 32 inches for women and 37 inches for men were randomly assigned to one of two groups, the vinegar group (VIN, n=21) or the control group (CON, n=24), and instructed to consume either two tablespoons of liquid red wine vinegar (3.6g acetic acid) or a control pill (0.0225g acetic acid) twice daily at the beginning of a meal for 8 weeks. Participants were also instructed to maintain normal diet and physical activity levels. Anthropometric measures, dual-energy x-ray absorptiometry (DXA) scans, blood samples, and 24-hour dietary recalls were collected at baseline and at end of trial. A compliance calendar was provided for daily tracking of vinegar supplementation.
Results: Compliance to vinegar supplementation averaged 92.7 ±13.3% among the VIN group and 89.1 ±18.9% among the CON group. There were no statistically significant differences in anthropometric measurements between baseline and week 8: weight (P=0.694), BMI (P=0.879), and waist circumference (P=0.871). Similarly, DXA scan data did not show significant changes in visceral fat (P=0.339) or total fat (P=0.294) between baseline and week 8. The VIN group had significant reductions in fasting glucose (P=0.003), fasting insulin (P <0.001), and homeostatic model assessment of insulin resistance scores (P <0.001) after treatment.
Conclusions: These data do not support the findings from previous studies that indicated a link between vinegar supplementation and increased fat metabolism, specifically visceral fat reduction.
ContributorsGonzalez, Lisa Ann (Author) / Johnston, Carol (Thesis advisor) / Mayol-Kreiser, Sandra (Committee member) / McCoy, Maureen (Committee member) / Arizona State University (Publisher)
Created2019
Description
Brown adipose tissue (BAT) is thought to be important in combating obesity as it can expend energy in the form of heat, e.g. thermogenesis. The goal of this study was to study the effect of injected norepinephrine (NE) on the activation of BAT in rats that were fed a high fat diet (HFD). A dose of 0.25 mg/kg NE was used to elicit a temperature response that was measured using transponders inserted subcutaneously over the BAT and lower back and intraperitoneally to measure the core temperature. The results found that the thermic effect of the BAT increased after the transition from low fat diet to a high fat diet (LFD) yet, after prolonged exposure to the HFD, the effects resembled levels found with the LFD. This suggests that while a HFD may stimulate the effect of BAT, long term exposure may have adverse effects on BAT activity. This may be due to internal factors that will need to be examined further.
ContributorsSion, Paul William (Author) / Herman, Richard (Thesis director) / Borges, Chad (Committee member) / School of Molecular Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
Description
There has been an alarming rise in the prevalence of obesity which has been attributed to the paralleled rise in consumption of high-fat foods. It’s commonly accepted that high-fat diets can lead to increased weight gain, however not all fats have the same physiological action. This study primarily focuses on the effect of canola oil, a monounsaturated fat, on energy homeostasis and body composition when it’s given as a supplement to a high-fat diet composed of saturated fatty acid. Rodent models were divided into three dietary groups: 1) low-fat diet (LFD), 2) high-fat diet (HFD) and 3) canola oils supplemented HFD (HF+CAN). After 4 weeks of dietary intervention, samples of epididymal fat, perinephric fat, and liver were analyzed across the three groups to see if the changes in energy homeostasis could be explained by the cellular behavior and composition of these tissues. Interestingly, the supplement of canola oil appeared to reverse the deleterious effects of a saturated fat diet, reverting energy intake, body weight gain and adipose tissue sizes to that (if not lower than that) of the LFD group. The only exception to this effect was the liver: the livers remained larger and fattier than those of the HFD. This occurrence is possibly due to a decrease in free fatty acid uptake in the adipose tissues—resulting in smaller adipose tissue sizes—and increased fatty acid uptake in the liver. The mechanism by which this occurs has yet to be elucidated and will be the primary focus of upcoming studies on the effect of monounsaturated fat on other diets.
ContributorsZuo, Connie Wanda (Author) / Washo-Krupps, Delon (Thesis director) / Deviche, Pierre (Committee member) / Herman, Richard (Committee member) / Barrett, The Honors College (Contributor) / Department of Chemistry and Biochemistry (Contributor) / School of Life Sciences (Contributor)
Created2015-05
Description
DNA methylation, a subset of epigenetics, has been found to be a significant marker associated with variations in gene expression and activity across the entire human genome. As of now, however, there is little to no information about how DNA methylation varies between different tissues inside a singular person's body. By using research data from a preliminary study of lean and obese clinical subjects, this study attempts to put together a profile of the differences in DNA methylation that can be observed between two particular body tissues from this subject group: blood and skeletal muscle. This study allows us to start describing the changes that occur at the epigenetic level that influence how differently these two tissues operate, along with seeing how these tissues change between individuals of different weight classes, especially in the context of the development of symptoms of Type 2 Diabetes.
ContributorsRappazzo, Micah Gabriel (Author) / Coletta, Dawn (Thesis director) / Katsanos, Christos (Committee member) / Dinu, Valentin (Committee member) / Barrett, The Honors College (Contributor) / Harrington Bioengineering Program (Contributor) / Department of Psychology (Contributor)
Created2013-12
Description
It is presently believed that brown adipose tissue (BAT) is an important tissue in the control of obesity because it has the propensity to increase energy expenditure. The purpose of this study was to attempt to quantify the thermogenesis of BAT when four rats were exposed to a progression of low-fat to high-fat diet. Exogenous norepinephrine (NE) injections (dose of 0.25 mg/kg i.p.) were administered in order to elicit a temperature response, where increases in temperature indicate increased activity. Temperatures were measured via temperature sensing transponders that had been inserted at the following three sites: interscapular BAT (iBAT), the abdomen (core), and lower back (reference). Data showed increased BAT activity during acute (2-3 weeks) high fat diet (HFD) in comparison to low fat diet (LFD), but a moderate to marked decrease in BAT activity during chronic HFD (6-8 weeks) when compared to acute HFD. This suggests that while a HFD may initially stimulate BAT in the short-term, a long-term HFD diet may have negative effects on BAT activation.
ContributorsSivak, Hanna (Author) / Sweazea, Karen (Thesis director) / Herman, Richard (Committee member) / Caplan, Michael (Committee member) / School of Life Sciences (Contributor) / College of Integrative Sciences and Arts (Contributor) / Barrett, The Honors College (Contributor)
Created2016-12
Description
Obesity is a rising problem in the country today, and countless efforts have been made to achieve long-term weight loss. Recent research indicates that through the manipulation of Brown Adipose Tissue (BAT) activity within the body, weight loss can be achieved. The goal of this experiment was to understand the effects of a high-fat diet (HFD) on BAT activity and diet-induced thermogenesis in cold-stressed rats. It was predicted that the HFD would stimulate BAT activity and this would then drive up thermogenic activity to promote weight loss. Diet-induced thermogenesis was predicted to increase during the HFD phase of this experiment as the body would require more energy to digest the more calorically dense food. Upon arrival at six weeks of age, the rats were started on a low-fat diet (LFD) ad libitum for three weeks. They were then transitioned into a HFD ad libitum for the next 8 weeks. Throughout the experiment, the rats were maintained in a cold-stressed environment at 22°C. It was determined that one of the rats was identified as obesity prone, while the other three rats were obesity resistant based on the rate of weight gain and caloric intake. Obesity can decrease metabolism in the body for many reasons, yet it was not seen in this experiment that the obesity prone rat demonstrated decreased metabolism in comparison to the others. Based on the differences seen in the reference temperatures and the BAT temperatures, it was determined that the BAT was active throughout both the LFD and HFD phases. However, the BAT did not rise significantly during the HFD period as expected. More research is indicated with a larger sample size to determine if BAT activity does continue to increase during a HFD as a result of diet-induced thermogenesis.
ContributorsLubold, Jessica Marie Sarah (Author) / Morse, Lisa (Thesis director) / Herman, Richard (Committee member) / School of Nutrition and Health Promotion (Contributor) / Barrett, The Honors College (Contributor)
Created2016-12