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- All Subjects: Physiology
- Creators: Johnston, Carol
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
While exercising mammalian muscle increasingly relies on carbohydrates for fuel as aerobic exercise intensity rises above the moderate range, flying birds are extraordinary endurance athletes and fuel flight, a moderate-high intensity exercise, almost exclusively with lipid. In addition, Aves have long lifespans compared to weight-matched mammals. As skeletal muscle mitochondria account for the majority of oxygen consumption during aerobic exercise, the primary goal was to investigate differences in isolated muscle mitochondria between these species and to examine to what extent factors intrinsic to mitochondria may account for the behavior observed in the intact tissue and whole organism. First, maximal enzyme activities were assessed in sparrow and rat mitochondria. Citrate synthase and aspartate aminotransferase activity were higher in sparrow compared to rat mitochondria, while glutamate dehydrogenase activity was lower. Sparrow mitochondrial NAD-linked isocitrate dehydrogenase activity was dependent on phosphate, unlike the mammalian enzyme. Next, the rate of oxygen consumption (JO), electron transport chain (ETC) activity, and reactive oxygen species (ROS) production were assessed in intact mitochondria. Maximal rates of fat oxidation were lower than for carbohydrate in rat but not sparrow mitochondria. ETC activity was higher in sparrows, but no differences were found in ROS production between species. Finally, fuel selection and control of respiration at three rates between rest and maximum were assessed. Mitochondrial fuel oxidation and selection mirrored that of the whole body; in rat mitochondria the reliance on carbohydrate increased as the rate of oxygen consumption increased, whereas fat dominated under all conditions in the sparrow. These data indicate fuel selection, at least in part, can be modulated at the level of the mitochondrial matrix when multiple substrates are present at saturating levels. As an increase in matrix oxidation-reduction potential has been linked to a suppression of fat oxidation and high ROS production, the high ETC activity relative to dehydrogenase activity in avian compared to mammalian mitochondria may result in lower matrix oxidation-reduction potential, allowing fatty acid oxidation to proceed while also resulting in low ROS production in vivo.
ContributorsKuzmiak, Sarah (Author) / Willis, Wayne T (Thesis advisor) / Mandarino, Lawrence (Committee member) / Sweazea, Karen (Committee member) / Harrison, Jon (Committee member) / Gadau, Juergen (Committee member) / Arizona State University (Publisher)
Created2012
Description
In social insect colonies, as with individual animals, the rates of biological processes scale with body size. The remarkable explanatory power of metabolic allometry in ecology and evolutionary biology derives from the great diversity of life exhibiting a nonlinear scaling pattern in which metabolic rates are not proportional to mass, but rather exhibit a hypometric relationship with body size. While one theory suggests that the supply of energy is a major physiological constraint, an alternative theory is that the demand for energy is regulated by behavior. The central hypothesis of this dissertation research is that increases in colony size reduce the proportion of individuals actively engaged in colony labor with consequences for energetic scaling at the whole-colony level of biological organization. A combination of methods from comparative physiology and animal behavior were developed to investigate scaling relationships in laboratory-reared colonies of the seed-harvester ant, Pogonomyrmex californicus. To determine metabolic rates, flow-through respirometry made it possible to directly measure the carbon dioxide production and oxygen consumption of whole colonies. By recording video of colony behavior, for which ants were individually paint-marked for identification, it was possible to reconstruct the communication networks through which information is transmitted throughout the colony. Whole colonies of P. californicus were found to exhibit a robust hypometric allometry in which mass-specific metabolic rates decrease with increasing colony size. The distribution of walking speeds also scaled with colony size so that larger colonies were composed of relatively more inactive ants than smaller colonies. If colonies were broken into random collections of workers, metabolic rates scaled isometrically, but when entire colonies were reduced in size while retaining functionality (queens, juveniles, workers), they continued to exhibit a metabolic hypometry. The communication networks in P. californicus colonies contain a high frequency of feed-forward interaction patterns consistent with those of complex regulatory systems. Furthermore, the scaling of these communication pathways with size is a plausible mechanism for the regulation of whole-colony metabolic scaling. The continued development of a network theory approach to integrating behavior and metabolism will reveal insights into the evolution of collective animal behavior, ecological dynamics, and social cohesion.
ContributorsWaters, James S., 1983- (Author) / Harrison, Jon F. (Thesis advisor) / Quinlan, Michael C. (Committee member) / Pratt, Stephen C. (Committee member) / Fewell, Jennifer H. (Committee member) / Gadau, Juergen (Committee member) / Arizona State University (Publisher)
Created2012
Description
Background: Vegan and vegetarian diets have gained in popularity in recent years. Stated reasons for this include some possible health benefits and concerns of animal welfare. Though considered to be nutritionally adequate, questions remain over whether current protein recommendations of 0.8 g/kg/d are sufficient to maintain body processes and growth. Protein is unique in that it is the only macronutrient that contains nitrogen. Its status can be determined through nitrogen balance analysis of the urine if protein content of the diet is known. Nitrogen balance is considered the gold standard for determining protein intake requirements. A negative balance indicates a catabolic state, whereas a positive nitrogen balance is seen during anabolism. In healthy people, nitrogen equilibrium is desired under normal circumstances. This equilibrium reflects the net synthesis and breakdown of proteins. While nitrogen balance techniques have been used for decades, currently, there are no known studies measuring nitrogen balance and protein intake in strict vegans. Methods: Twenty vegan, inactive, male participants were recruited and received a 5-day eucaloric diet with a known protein content held constant at 0.8 g/kg/d. On day five, 24-hour urine was collected by participants and aliquoted for future analysis. Nitrogen content of the urine was determined through photometric assay and compared to the known nitrogen content of the diet to calculate nitrogen balance status.
Results: Mean absolute nitrogen balance (-1.38 ± 1.22 g/d, effect size = -1.13) was significantly lower than zero (equilibrium) (p < .001). Mean relative nitrogen balance (-18.60 ± 16.96 mg/kg/d, effect size = -1.10) was significantly lower than zero (p < .001). There were no correlations seen between nitrogen balance and age, years as vegan, or fat- free mass.
Conclusion: Consuming 0.8 g/kg/d of protein is insufficient to produce nitrogen balance in long-term vegans.
ContributorsBartholomae, Eric (Author) / Johnston, Carol (Thesis advisor) / Sweazea, Karen (Committee member) / Wharton, Christopher (Committee member) / Lee, Chong (Committee member) / Kressler, Jochen (Committee member) / Arizona State University (Publisher)
Created2022
Description
Birds have the highest blood glucose concentrations of all vertebrates. Meanwhile, birds do not develop the same physiological complications (e.g., increased oxidative stress and glycation) that mammals do when blood glucose is elevated (i.e., diabetes). Therefore, birds may serve as a negative model animal for hyperglycemic complications. The physiological reason for high blood glucose in birds remains largely unknown although several unique characteristics of birds may contribute including a lack of the insulin responsive glucose transport protein, relatively high glucagon concentrations, as well as reliance on fatty acids to sustain the high energetic demands of flight. In breaking down triglycerides for energy, glycerol is liberated, which can be converted to glucose through a process called gluconeogenesis. In addition, the extent to which birds maintain homeostatic control over blood glucose in response to extreme dietary interventions remains unclear and few dietary studies have been conducted in wild-caught birds. Using Mourning Doves (Zenaida macroura) as a model organism, this dissertation tests four hypotheses: 1) Gluconeogenesis contributes to high circulating blood glucose concentration; 2-4) similar to mammals, a fully refined carbohydrate (i.e., white bread diet); a high saturated fat diet (60% kcal from fat); and an urban-type diet comprised of a 1:1 ratio of French fries and birds seed will increase blood glucose compared to a nutritionally-balanced diet after a four-week duration. Contrary to the hypothesis, 150 mg/kg Metformin (which inhibits glycerol gluconeogenesis) increased blood glucose, but 300 mg/kg resulted in no change. However, when 2.5 mg/kg of 1,4-dideoxy-1,4-imino-D-arabinitol (DAB; a glycogenolysis inhibitor) was given with 150 mg/kg of Metformin, blood glucose was not different from the control (50 ul water). This suggests that glycerol gluconeogenesis does not contribute to the naturally high blood glucose in birds and that a low dose of Metformin may increase the rate of glycogenolysis. In addition, all three experimental diets failed to alter blood glucose compared to control diets. Collectively, these results suggest that, in addition to a negative model for diabetes complications, birds can also serve a negative model for diet-induced hyperglycemia. Future research should further examine dietary manipulation in birds while controlling for and examining different variables (e.g., species, sex, duration, diet composition, urbanization).
ContributorsBasile, Anthony Joseph (Author) / Sweazea, Karen L (Thesis advisor) / Deviche, Pierre (Committee member) / Johnston, Carol (Committee member) / Trumble, Ben (Committee member) / Parrington, Diane J (Committee member) / Arizona State University (Publisher)
Created2022
Description
The ability to tolerate bouts of oxygen deprivation varies tremendously across the animal kingdom. Adult humans from different regions show large variation in tolerance to hypoxia; additionally, it is widely known that neonatal mammals are much more tolerant to anoxia than their adult counterparts, including in humans. Drosophila melanogaster are very anoxia-tolerant relative to mammals, with adults able to survive 12 h of anoxia, and represent a well-suited model for studying anoxia tolerance. Drosophila live in rotting, fermenting media and a result are more likely to experience environmental hypoxia; therefore, they could be expected to be more tolerant of anoxia than adults. However, adults have the capacity to survive anoxic exposure times ~8 times longer than larvae. This dissertation focuses on understanding the mechanisms responsible for variation in survival from anoxic exposure in the genetic model organism, Drosophila melanogaster, focused in particular on effects of developmental stage (larval vs. adults) and within-population variation among individuals.
Vertebrate studies suggest that surviving anoxia requires the maintenance of ATP despite the loss of aerobic metabolism in a manner that prevents a disruption of ionic homeostasis. Instead, the abilities to maintain a hypometabolic state with low ATP and tolerate large disturbances in ionic status appear to contribute to the higher anoxia tolerance of adults. Furthermore, metabolomics experiments support this notion by showing that larvae had higher metabolic rates during the initial 30 min of anoxia and that protective metabolites were upregulated in adults but not larvae. Lastly, I investigated the genetic variation in anoxia tolerance using a genome wide association study (GWAS) to identify target genes associated with anoxia tolerance. Results from the GWAS also suggest mechanisms related to protection from ionic and oxidative stress, in addition to a protective role for immune function.
Vertebrate studies suggest that surviving anoxia requires the maintenance of ATP despite the loss of aerobic metabolism in a manner that prevents a disruption of ionic homeostasis. Instead, the abilities to maintain a hypometabolic state with low ATP and tolerate large disturbances in ionic status appear to contribute to the higher anoxia tolerance of adults. Furthermore, metabolomics experiments support this notion by showing that larvae had higher metabolic rates during the initial 30 min of anoxia and that protective metabolites were upregulated in adults but not larvae. Lastly, I investigated the genetic variation in anoxia tolerance using a genome wide association study (GWAS) to identify target genes associated with anoxia tolerance. Results from the GWAS also suggest mechanisms related to protection from ionic and oxidative stress, in addition to a protective role for immune function.
ContributorsCampbell, Jacob B (Author) / Harrison, Jon F. (Thesis advisor) / Gadau, Juergen (Committee member) / Call, Gerald B (Committee member) / Sweazea, Karen L (Committee member) / Rosenberg, Michael S. (Committee member) / Arizona State University (Publisher)
Created2018
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
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
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