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- All Subjects: Diet
- All Subjects: Endocrinology
- Creators: Sweazea, Karen
- Status: Published
Description
For animals that experience annual cycles of gonad development, the seasonal timing (phenology) of gonad growth is a major adaptation to local environmental conditions. To optimally time seasonal gonad growth, animals use environmental cues that forecast future conditions. The availability of food is one such environmental cue. Although the importance of food availability has been appreciated for decades, the physiological mechanisms underlying the modulation of seasonal gonad growth by this environmental factor remain poorly understood.
Urbanization is characterized by profound environmental changes, and urban animals must adjust to an environment vastly different from that of their non-urban conspecifics. Evidence suggests that birds adjust to urban areas by advancing the timing of seasonal breeding and gonad development, compared to their non-urban conspecifics. A leading hypothesis to account for this phenomenon is that food availability is elevated in urban areas, which improves the energetic status of urban birds and enables them to initiate gonad development earlier than their non-urban conspecifics. However, this hypothesis remains largely untested.
My dissertation dovetailed comparative studies and experimental approaches conducted in field and captive settings to examine the physiological mechanisms by which food availability modulates gonad growth and to investigate whether elevated food availability in urban areas advances the phenology of gonad growth in urban birds. My captive study demonstrated that energetic status modulates reproductive hormone secretion, but not gonad growth. By contrast, free-ranging urban and non-urban birds did not differ in energetic status or plasma levels of reproductive hormones either in years in which urban birds had advanced phenology of gonad growth or in a year that had no habitat-related disparity in seasonal gonad growth. Therefore, my dissertation provides no support for the hypothesis that urban birds begin seasonal gonad growth because they are in better energetic status and increase the secretion of reproductive hormones earlier than non-urban birds. My studies do suggest, however, that the phenology of key food items and the endocrine responsiveness of the reproductive system may contribute to habitat-related disparities in the phenology of gonad growth.
Urbanization is characterized by profound environmental changes, and urban animals must adjust to an environment vastly different from that of their non-urban conspecifics. Evidence suggests that birds adjust to urban areas by advancing the timing of seasonal breeding and gonad development, compared to their non-urban conspecifics. A leading hypothesis to account for this phenomenon is that food availability is elevated in urban areas, which improves the energetic status of urban birds and enables them to initiate gonad development earlier than their non-urban conspecifics. However, this hypothesis remains largely untested.
My dissertation dovetailed comparative studies and experimental approaches conducted in field and captive settings to examine the physiological mechanisms by which food availability modulates gonad growth and to investigate whether elevated food availability in urban areas advances the phenology of gonad growth in urban birds. My captive study demonstrated that energetic status modulates reproductive hormone secretion, but not gonad growth. By contrast, free-ranging urban and non-urban birds did not differ in energetic status or plasma levels of reproductive hormones either in years in which urban birds had advanced phenology of gonad growth or in a year that had no habitat-related disparity in seasonal gonad growth. Therefore, my dissertation provides no support for the hypothesis that urban birds begin seasonal gonad growth because they are in better energetic status and increase the secretion of reproductive hormones earlier than non-urban birds. My studies do suggest, however, that the phenology of key food items and the endocrine responsiveness of the reproductive system may contribute to habitat-related disparities in the phenology of gonad growth.
ContributorsDavies, Scott (Author) / Deviche, Pierre (Thesis advisor) / Sweazea, Karen (Committee member) / McGraw, Kevin (Committee member) / Orchinik, Miles (Committee member) / Warren, Paige (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
Reproduction is energetically costly and seasonal breeding has evolved to capitalize on predictable increases in food availability. The synchronization of breeding with periods of peak food availability is especially important for small birds, most of which do not store an extensive amount of energy. The annual change in photoperiod is the primary environmental cue regulating reproductive development, but must be integrated with supplementary cues relating to local energetic conditions. Photoperiodic regulation of the reproductive neuroendocrine system is well described in seasonally breeding birds, but the mechanisms that these animals use to integrate supplementary cues remain unclear. I hypothesized that (a) environmental cues that negatively affect energy balance inhibit reproductive development by acting at multiple levels along the reproductive endocrine axis including the hypothalamus (b) that the availability of metabolic fuels conveys alterations in energy balance to the reproductive system. I investigated these hypotheses in male house finches, Haemorhous mexicanus, caught in the wild and brought into captivity. I first experimentally reduced body condition through food restriction and found that gonadal development and function are inhibited and these changes are associated with changes in hypothalamic gonadotropin-releasing hormone (GnRH). I then investigated this neuroendocrine integration and found that finches maintain reproductive flexibility through modifying the release of accumulated GnRH stores in response to energetic conditions. Lastly, I investigated the role of metabolic fuels in coordinating reproductive responses under two different models of negative energy balance, decreased energy intake (food restriction) and increased energy expenditure (high temperatures). Exposure to high temperatures lowered body condition and reduced food intake. Reproductive development was inhibited under both energy challenges, and occurred with decreased gonadal gene expression of enzymes involved in steroid synthesis. Minor changes in fuel utilization occurred under food restriction but not high temperatures. My results support the hypothesis that negative energy balance inhibits reproductive development through multilevel effects on the hypothalamus and gonads. These studies are among the first to demonstrate a negative effect of high temperatures on reproductive development in a wild bird. Overall, the above findings provide important foundations for investigations into adaptive responses of breeding in energetically variable environments.
ContributorsValle, Shelley (Author) / Deviche, Pierre (Thesis advisor) / McGraw, Kevin (Committee member) / Orchinik, Miles (Committee member) / Propper, Catherine (Committee member) / Sweazea, Karen (Committee member) / Arizona State University (Publisher)
Created2018
Description
Western diets, high in dietary fat and red meat, are associated with hyperglycemia and weight gain, symptoms that promote insulin resistance and diabetes. Previous studies have shown that elevated glucose promotes glycation of circulating proteins such as albumin, which is thought to lead to hyperglycemia complications. It was hypothesized that diets with no meat consumption (pesco-vegetarian and lacto-vegetarian) would reduce protein glycation, in comparison to a diet with meat. Forty six healthy adult omnivorous subjects were randomized into one of three groups and instructed to either consume red meat (i.e. meat) or poultry twice per day (control), eliminate meat and increase fish consumption (pesco-vegetarian), or adopt a vegetarian diet devoid of fish, meat or poultry (lacto-vegetarian) for four weeks. Fasting plasma samples were collected from participants at baseline and after 4 weeks of the dietary intervention. Plasma glucose concentrations were measured using a commercially available kit. Percent glycated albumin was measured on a separate aliquot of plasma by mass spectrometry. Plasma glucose concentrations were significantly increased following 4-weeks of pesco-vegetarian diet (P=0.002, paired t-test). Neither the lacto-vegetarian (P=0.898) or the control diet (P=0.233) affected plasma glucose concentrations. Despite the significant increase in plasma glucose following a pesco-vegetarian diet, no change in percent glycated albumin was observed (P>0.50, ANOVA). These findings may indicate a protective effect of the pesco-vegetarian diet on protein glycation in the presence of elevated plasma glucose and suggest the need for additional studies to examine the link between increased fish consumption and glucose regulation.
ContributorsRaad, Noor (Author) / Sweazea, Karen (Thesis director, Committee member) / Borges, Chad (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2015-05
Description
Birds have unusually high plasma glucose concentrations compared to mammals of similar size despite their high metabolic rate. While birds use lipids as their main source of energy, it is still unclear how and why they maintain high plasma glucose concentrations. To investigate a potential underlying mechanism, this study looks at the role of lipolysis in glucose homeostasis. The purpose of this study is to examine the effects of decreased glycerol availability (through inhibition of lipolysis) on plasma glucose concentrations in mourning doves. The hypothesis is that decreased availability of glycerol will result in decreased production of glucose through gluconeogenesis leading to reduced plasma glucose concentrations. In the morning of each experiment, mourning doves were collected at the Arizona State University Tempe campus, and randomized into either a control group (0.9% saline) or experimental group (acipimox, 50mg/kg BM). Blood samples were collected prior to treatment, and at 1, 2, and 3 hours post-treatment. At 3 hours, doves were euthanized, and tissue samples were collected for analysis. Acipimox treatment resulted in significant increases in blood glucose concentrations at 1 and 2 hours post- treatment as well as renal triglyceride concentrations at 3 hours post-treatment. Change in plasma free glycerol between 0h and 3h followed an increasing trend for the acipimox treated animals, and a decreasing trend in the saline treated animals. These results do not support the hypothesis that inhibition of lipolysis should decrease blood glycerol and blood glucose levels. Rather, the effects of acipimox in glucose homeostasis appear to differ significantly between birds and mammals suggesting differing mechanisms for glucose homeostasis.
ContributorsKouteib, Soukaina (Author) / Sweazea, Karen (Thesis director) / Deviche, Pierre (Committee member) / Chandler, Douglas (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2015-05
Description
The transition to college has been identified as a vulnerable period for weight gain and the onset of obesity. Research has shown that the gut microbiota is different in obese compared to lean individuals, but a period of weight gain has never been studied in free-living individuals. The objective of this longitudinal, observational study was to assess the association between changes in the intestinal microbiota and weight-related outcomes in healthy college students living in on-campus dormitories at Arizona State University (n=39). Anthropometric measures and fecal samples were collected at the beginning and end of the school year, and microbial relative abundance for A. muciniphila, F. prausnitzii, R. gnavus, and L. acidophilus was measured through qPCR analyses. In this population, body mass index (BMI) and waist circumference (WC) increased by 0.97 ± 1.28 kg/m2 and 2.64 ± 4.90 cm, respectively. Wilcoxon-Rank tests revealed that R. gnavus fold change was significantly different between groups of weight loss/maintenance and weight gain ≥ 5% body weight (0.14 [-0.21, 0.64], n=24 vs. -0.14 [-0.92, 0.05], n=15, respectively; p=0.028). Correlation analyses suggested a significant negative association between A. muciniphila fold change and both % WC change and % BMI change (r= -0.66; p<0.01 and r= -0.33; p=0.04, respectively). However, multivariate regression analysis controlling for sex and race/ethnicity showed a significant association between A. muciniphila and % WC change, but not % BMI change (R2= 0.53; p<0.01 and R2= 0.24; p=0.15). F. prausnitzii was not associated with weight-related outcomes in this sample. L. acidophilus was excluded from study analyses after subsequent qPCR trials revealed no amplification in participant samples. Overall, this was the first study to show a relationship between A. muciniphila fold change and weight-related outcomes over a period of weight gain. Specifically, A. muciniphila was strongly negatively associated with WC in this sample. Further research is needed to more accurately describe these associations and potential mechanisms associated with the shift in gut microbiota observed with weight gain. Findings from future research may be used to develop interventions for college students aiming to shift the gut microbiota to prevent weight gain.
ContributorsJourney, Elizabeth (Author) / Whisner, Corrie M (Thesis advisor) / Bruening, Meredith (Committee member) / Sweazea, Karen (Committee member) / Arizona State University (Publisher)
Created2017
Description
ABSTRACT
Background. College students’ modifiable health behaviors, including unhealthful eating patterns, predispose them to risk for future cardiometabolic conditions.
Purpose. This novel 8-week randomized control parallel-arm study compared the effects of a daily 18-hour Time-Restricted Feeding protocol vs. an 8-hour fast on diet quality in college students. Secondary outcomes were resting morning blood pressure, biomarkers of glucose regulation, biomarkers of lipid metabolism, and anthropometric measures.
Methods. Eighteen healthy college students (age = 23 ± 4 years; BMI = 23.2 ± 2.3 kg/m2; MET = 58.8 ± 32.9 min/wk) completed this study. Participants were randomized to a daily 18-hour fasting protocol (Intervention; n = 8) or a daily 8-hour fasting protocol (Control; n = 10) for eight weeks. One ‘cheat’ day was permitted each week. Outcomes were measured at weeks 0 (baseline), 4, and 8. A non-parametric Mann Whitney U test was used to compare the week 4 change from baseline between groups. Statistical significance was set at p≤0.05.
Results. Diet quality (p = 0.030) and body weight (p = 0.016) improved from baseline to week 4 for the INV group in comparison to the CON group. The data suggest these improvements may be related to reductions in snacking frequency and increased breakfast consumption. Fasting blood glucose and hip circumference tended to improve for the INV group in comparison to the CON group (p = 0.091 and p = 0.100). However, saturated fat intake tended to increase in the INV group in comparison to the CON group (p = 0.064). Finally, there were no treatment differences between groups (p>0.05) for the 4-week change in total calories, dietary vitamin C, added sugars, resting systolic blood pressure, resting diastolic blood pressure, insulin, homeostatic model assessment for insulin resistance (HOMA-IR), low-density lipoprotein (LDL) cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, waist circumference, or MET.
Conclusion. These data, although preliminary, suggest that the 18-hour fasting protocol was effective for improving diet quality and reducing weight in comparison to the 8-hour fasting protocol in healthy college students. Future intervention trials will need to confirm these findings and determine the long-term relevance of these improvements for health outcomes.
Background. College students’ modifiable health behaviors, including unhealthful eating patterns, predispose them to risk for future cardiometabolic conditions.
Purpose. This novel 8-week randomized control parallel-arm study compared the effects of a daily 18-hour Time-Restricted Feeding protocol vs. an 8-hour fast on diet quality in college students. Secondary outcomes were resting morning blood pressure, biomarkers of glucose regulation, biomarkers of lipid metabolism, and anthropometric measures.
Methods. Eighteen healthy college students (age = 23 ± 4 years; BMI = 23.2 ± 2.3 kg/m2; MET = 58.8 ± 32.9 min/wk) completed this study. Participants were randomized to a daily 18-hour fasting protocol (Intervention; n = 8) or a daily 8-hour fasting protocol (Control; n = 10) for eight weeks. One ‘cheat’ day was permitted each week. Outcomes were measured at weeks 0 (baseline), 4, and 8. A non-parametric Mann Whitney U test was used to compare the week 4 change from baseline between groups. Statistical significance was set at p≤0.05.
Results. Diet quality (p = 0.030) and body weight (p = 0.016) improved from baseline to week 4 for the INV group in comparison to the CON group. The data suggest these improvements may be related to reductions in snacking frequency and increased breakfast consumption. Fasting blood glucose and hip circumference tended to improve for the INV group in comparison to the CON group (p = 0.091 and p = 0.100). However, saturated fat intake tended to increase in the INV group in comparison to the CON group (p = 0.064). Finally, there were no treatment differences between groups (p>0.05) for the 4-week change in total calories, dietary vitamin C, added sugars, resting systolic blood pressure, resting diastolic blood pressure, insulin, homeostatic model assessment for insulin resistance (HOMA-IR), low-density lipoprotein (LDL) cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, waist circumference, or MET.
Conclusion. These data, although preliminary, suggest that the 18-hour fasting protocol was effective for improving diet quality and reducing weight in comparison to the 8-hour fasting protocol in healthy college students. Future intervention trials will need to confirm these findings and determine the long-term relevance of these improvements for health outcomes.
ContributorsMayra, Selicia (Author) / Johnston, Carol (Thesis advisor) / Sears, Dorothy (Committee member) / Swan, Pamela (Committee member) / Sweazea, Karen (Committee member) / Wharton, Christopher (Christopher Mack), 1977- (Committee member) / Arizona State University (Publisher)
Created2020
Description
Birds maintain resting plasma glucose concentrations (pGlu) nearly twice that of comparably sized mammals. Despite this, birds do not incur much of the oxidative tissue damage that might be expected from a high pGlu. Their ability to stave off oxidative damage allows birds to serve as a negative model of hyperglycemia-related complications, making them ideal for the development of new diabetes treatments with the potential for human application. Previous studies conducted by the Sweazea Lab at Arizona State University aimed to use diet as a means to raise blood glucose in mourning doves (Zenaida macroura) in order to better understand the mechanisms they utilize to stave off oxidative damage. These protocols used dietary interventions—a 60% high fat (HF) “chow” diet, and a high carbohydrate (HC) white bread diet—but were unsuccessful in inducing pathologies. Based on this research, we hypothesized that a model of an urban diet (high in fat, refined carbohydrates, and sodium) might impair vasodilation, as the effect of this diet on birds is currently unknown. We found that tibial vasodilation was significantly impaired in birds fed an urban diet compared to those fed a seed diet. Unexpectedly, vasodilation in the urban diet group was comparable to data of wild-caught birds from previous research, possibly indicating that the birds had already been eating a diet similar to this study’s urban diet before they were caught. This may constitute evidence that the seed diet improved vasodilation while the urban diet more closely mimicked the diet of the birds before the trial, suggesting that the model of the urban diet acted as the control diet in this context. This study is the first step in elucidating avian mechanisms for dealing with diabetogenic diets and has potential to aid in the development of treatments for humans with metabolic syndrome.
ContributorsRenner, Michael William (Author) / Sweazea, Karen (Thesis director) / Johnston, Carol (Committee member) / Basile, Anthony (Committee member) / Dean, W.P. Carey School of Business (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2020-05
Description
Glucocorticoids are a class of corticosteroids that bind to glucocorticoid receptors
within cells that result in changes in the metabolism of carbohydrates and immune functions.
Ingesting glucocorticoids has also been linked to insulin resistance, a main feature of Type 2
diabetes. Experiments including polymerase chain reaction, western blotting, and glycogen
synthase analysis were conducted to determine if exposure to higher doses of dexamethasone, a
glucocorticoid, induces insulin resistance in cultured rat skeletal muscle via interaction with
thioredoxin-interacting protein (TXNIP). Treatment with dexamethasone was shown to cause
mild increases in TXNIP while a definitive increase or decrease in insulin signaling was unable
to be determined.
within cells that result in changes in the metabolism of carbohydrates and immune functions.
Ingesting glucocorticoids has also been linked to insulin resistance, a main feature of Type 2
diabetes. Experiments including polymerase chain reaction, western blotting, and glycogen
synthase analysis were conducted to determine if exposure to higher doses of dexamethasone, a
glucocorticoid, induces insulin resistance in cultured rat skeletal muscle via interaction with
thioredoxin-interacting protein (TXNIP). Treatment with dexamethasone was shown to cause
mild increases in TXNIP while a definitive increase or decrease in insulin signaling was unable
to be determined.
ContributorsCusimano, Jason A (Author) / Sweazea, Karen (Thesis director) / Reaven, Peter (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2020-05