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- All Subjects: Obesity
- Genre: Academic theses
- 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
Obesity and its underlying insulin resistance are caused by environmental and genetic factors. DNA methylation provides a mechanism by which environmental factors can regulate transcriptional activity. The overall goal of the work herein was to (1) identify alterations in DNA methylation in human skeletal muscle with obesity and its underlying insulin resistance, (2) to determine if these changes in methylation can be altered through weight-loss induced by bariatric surgery, and (3) to identify DNA methylation biomarkers in whole blood that can be used as a surrogate for skeletal muscle.
Assessment of DNA methylation was performed on human skeletal muscle and blood using reduced representation bisulfite sequencing (RRBS) for high-throughput identification and pyrosequencing for site-specific confirmation. Sorbin and SH3 homology domain 3 (SORBS3) was identified in skeletal muscle to be increased in methylation (+5.0 to +24.4 %) in the promoter and 5’untranslated region (UTR) in the obese participants (n= 10) compared to lean (n=12), and this finding corresponded with a decrease in gene expression (fold change: -1.9, P=0.0001). Furthermore, SORBS3 was demonstrated in a separate cohort of morbidly obese participants (n=7) undergoing weight-loss induced by surgery, to decrease in methylation (-5.6 to -24.2%) and increase in gene expression (fold change: +1.7; P=0.05) post-surgery. Moreover, SORBS3 promoter methylation was demonstrated in vitro to inhibit transcriptional activity (P=0.000003). The methylation and transcriptional changes for SORBS3 were significantly (P≤0.05) correlated with obesity measures and fasting insulin levels. SORBS3 was not identified in the blood methylation analysis of lean (n=10) and obese (n=10) participants suggesting that it is a muscle specific marker. However, solute carrier family 19 member 1 (SLC19A1) was identified in blood and skeletal muscle to have decreased 5’UTR methylation in obese participants, and this was significantly (P≤0.05) predicted by insulin sensitivity.
These findings suggest SLC19A1 as a potential blood-based biomarker for obese, insulin resistant states. The collective findings of SORBS3 DNA methylation and gene expression present an exciting novel target in skeletal muscle for further understanding obesity and its underlying insulin resistance. Moreover, the dynamic changes to SORBS3 in response to metabolic improvements and weight-loss induced by surgery.
Assessment of DNA methylation was performed on human skeletal muscle and blood using reduced representation bisulfite sequencing (RRBS) for high-throughput identification and pyrosequencing for site-specific confirmation. Sorbin and SH3 homology domain 3 (SORBS3) was identified in skeletal muscle to be increased in methylation (+5.0 to +24.4 %) in the promoter and 5’untranslated region (UTR) in the obese participants (n= 10) compared to lean (n=12), and this finding corresponded with a decrease in gene expression (fold change: -1.9, P=0.0001). Furthermore, SORBS3 was demonstrated in a separate cohort of morbidly obese participants (n=7) undergoing weight-loss induced by surgery, to decrease in methylation (-5.6 to -24.2%) and increase in gene expression (fold change: +1.7; P=0.05) post-surgery. Moreover, SORBS3 promoter methylation was demonstrated in vitro to inhibit transcriptional activity (P=0.000003). The methylation and transcriptional changes for SORBS3 were significantly (P≤0.05) correlated with obesity measures and fasting insulin levels. SORBS3 was not identified in the blood methylation analysis of lean (n=10) and obese (n=10) participants suggesting that it is a muscle specific marker. However, solute carrier family 19 member 1 (SLC19A1) was identified in blood and skeletal muscle to have decreased 5’UTR methylation in obese participants, and this was significantly (P≤0.05) predicted by insulin sensitivity.
These findings suggest SLC19A1 as a potential blood-based biomarker for obese, insulin resistant states. The collective findings of SORBS3 DNA methylation and gene expression present an exciting novel target in skeletal muscle for further understanding obesity and its underlying insulin resistance. Moreover, the dynamic changes to SORBS3 in response to metabolic improvements and weight-loss induced by surgery.
ContributorsDay, Samantha Elaine (Author) / Coletta, Dawn K. (Thesis advisor) / Katsanos, Christos (Committee member) / Mandarino, Lawrence J. (Committee member) / Shaibi, Gabriel Q. (Committee member) / Dinu, Valentin (Committee member) / Arizona State University (Publisher)
Created2017
Description
Obesity is currently a prevalent health concern in the United States. Essential to combating it are accurate methods of assessing individual dietary intake under ad libitum conditions. The acoustical monitoring system (AMS), consisting of a throat microphone and jaw strain sensor, has been proposed as a non-invasive method for tracking free-living eating events. This study assessed the accuracy of eating events tracked by the AMS, compared to the validated vending machine system used by the NIDDK in Phoenix. Application of AMS data toward estimation of mass and calories consumed was also considered. In this study, 10 participants wore the AMS in a clinical setting for 24 hours while all food intake was recorded by the vending machine. Results indicated a correlation of 0.76 between number of eating events by the AMS and the vending machine (p = 0.019). A dependent T-test yielded a p-value of 0.799, illustrating a lack of significant difference between these methods of tracking intake. Finally, number of seconds identified as eating by the AMS had a 0.91 correlation with mass of intake (p = 0.001) and a 0.70 correlation with calories of intake (p = 0.034). These results indicate that the AMS is a valid method of objectively recording eating events under ad libitum conditions. Additional research is required to validate this device under free-living conditions.
ContributorsSteinke, Amanda (Author) / Johnston, Carol (Thesis advisor) / Votruba, Susanne (Committee member) / Hall, Richard (Committee member) / Arizona State University (Publisher)
Created2013
Description
Obesity is one of the most challenging health conditions of our time, characterized by complex interactions between behavioral, environmental, and genetic factors. These interactions lead to a distinctive obese phenotype. Twenty years ago, the gut microbiota (GM) was postulated as a significant factor contributing to the obese phenotype and associated metabolic disturbances. Exercise had shown to improve and revert the metabolic abnormalities in obese individuals. Also, genistein has a suggested potential anti-obesogenic effect. Studying the dynamic interaction of the GM with relevant organs in metabolic homeostasis is crucial for the design of new long-term therapies to treat obesity. The purpose of this experimental study is to examine exercise (Exe), genistein (Gen), and their combined intervention (Exe + Gen) effects on GM composition and musculoskeletal mitochondrial oxidative function in diet-induced obese mice. Also, this study aims to explore the association between gut microbial diversity and mitochondrial oxidative capacity. 132 adult male (n=63) and female (n= 69) C57BL/6 mice were randomized to one of five interventions for twelve weeks: control (n= 27), high fat diet (HFD; n=26), HFD + Exe (n=28), HFD + Gen (n=27), or HFD + Exe + Gen (n=24). All HFD drinking water was supplemented with 42g sugar/L. Fecal pellets were collected, DNA extracted, and measured the microbial composition by sequencing the V4 of the 16S rRNA gene with Illumina. The mitochondrial oxidative capacity was assessed by measuring the enzymatic kinetic activity of the citrate synthase (CS) of forty-nine mice. This study found that Exe groups had a significantly higher bacterial richness compared to HFD + Gen or HFD group. Exe + Gen showed the synergistic effect to drive the GM towards the control group´s GM composition as we found Ruminococcus significantly more abundant in the HFD + Exe + Gen than the rest of the HFD groups. The study did not find preventive capacity in either of the interventions on the CS activity. Therefore, further research is needed to confirm the synergistic effect of Exe, Exe, and Gen on the gut bacterial richness and the capacity to prevent HFD-induced deleterious effect on GM and mitochondrial oxidative capacity.
ContributorsOrtega Santos, Carmen Patricia (Author) / Whisner, Corrie M (Thesis advisor) / Dickinson, Jared M (Committee member) / Katsanos, Christos (Committee member) / Gu, Haiwei (Committee member) / Liu, Li (Committee member) / Al-Nakkash, Layla (Committee member) / Arizona State University (Publisher)
Created2021