Understanding how energy flows through ecosystems reveals underlying ecological patterns that can drive processes such as growth and survival of organisms. To understand how energy is transferred through organisms, the energy content or energy density (ED) of both consumers and prey must be determined. To facilitate the ease of ED measurement across taxa, I developed a model to estimate the ED of organisms using percent ash-free dry weight (AFDW). Using data obtained from 11 studies with broad taxonomic, temporal and spatial coverage, I compared common predictors of ED using linear models. AFDW was determined to be the superior predictor of ED relative to previous metrics and was predictive for a broad range of taxonomic groups including aquatic invertebrates, aquatic vertebrates, aquatic plants and terrestrial invertebrates. This AFDW model enables measurement of ED with minimal cost and time investment, which allows ED to be more readily determined for diverse taxa. Next, I applied the AFDW method to the diet of a pelagic consumer, juvenile Chinook Salmon, to determine the effect of variable prey ED on growth. In 2017, I collected monthly zooplankton and fish samples of known importance in the diet of juvenile Chinook Salmon to look for fine-scale taxonomic, temporal and spatial differences in ED. Decapod zoeae and megalopae differed significantly from each other and showed family level variability in ED. Amphipods also showed significant species-level variability in ED. Temporal differences were observed, but did not reveal a consistent pattern among groups. Spatial variability was not significant. Using bioenergetics models, growth of juvenile Chinook Salmon was predicted to be greater when using fine-scale ED estimates. This difference was not substantial on average, but in some cases represented more than a two-fold difference in growth between coarse- and fine-scale estimates. These results suggest the need for higher resolution diet ED data when determining growth projections for juvenile Chinook Salmon. With the aid of the AFDW model presented in this thesis, the effort required to obtain these data is greatly reduced. / Graduate / 2020-03-25

The diet an organism keeps is crucial in sustaining its health and fitness. The fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans are excellent models for nutritional studies due to their small size, large progeny numbers, quick development, and modifiable laboratory diets. Here I examine these two organisms in order to better understand the complex interrelationship between an animal and its diet. Previous work has shown that in the wild numerous organisms are capable of selecting specific nutrients in a non-random manner in order to maximize fitness. However, the genetic underpinnings driving these nutrient choices remain elusive. Female fruit flies consume higher levels of protein following mating to prepare for the costs of reproduction. I examined the role of S6 Kinase (S6K), a downstream effector of the nutrient-responsive target of rapamycin pathway, in mediating this decision. I demonstrate that neuronal S6K activity and serotonin are involved in regulating protein consumption when allowed to choose nutrients freely as well as following macronutrient deprivation; suggesting that they may play a role in mediating postmating dietary switch and maintaining nutrient balance. Modulating levels of dietary components can have extensive impacts on processes such as development, fecundity, and metabolism in multiple organisms. However, the influence of dietary genetics on the consumer is virtually unknown. I performed a screen feeding single-gene mutants of E. coli to C. elegans and monitored the effects on the insulin-like signalling pathway (ILS). When mutated, genes involved in multiple processes and functions in E. coli enhanced activity of the ILS downstream transcription factor, DAF-16. One mutant strain of E. coli I pursued had a knockout of the cAMP-producing, adenylate cyclase gene. Addition of exogenous cAMP to the diet containing live, metabolically active E. coli rescued all the effects of the mutant on C. elegans; thereby suggesting that bacterial metabolism of dietary cAMP can influence the C. elegans ILS. Collectively, my work demonstrates how the nutrient-sensing pathways of the consumer can shape and be shaped by interactions with its diet. These studies contribute to a better understanding of the consumer-diet relationship, and could help guide future work to investigate the role of diet in disease, quality of life, and longevity.

非傳染性疾病是目前全球最常見的疾病之一。不健康的食相信是導致非傳染性疾病增加的主要因素之一。因此，我們就食對乳腺癌的形成和膽固醇代謝調控的影響進行了研究。 / 在去除卵巢的祼鼠模型中，我們研究了長期和短期熱量限制對乳腺癌腫瘤增殖的影響。14週齡的小鼠被隨機分為5組：自由攝食組 (AL)；熱量攝入控制在AL80% 的20%CCR組；熱量攝入控制在AL的70% 的30%CCR組；熱量攝入控制在AL的65% 的35%CCR組和短期熱量限制 （SCR）組 (前3.5週熱量攝入控制在AL的65%，之後的13.5週自由攝食)。10週後，熱量限制組的腫瘤體積明顯較AL組小 (P < 0.05)。排除攝食對體重的影響，SCR組的腫瘤重量明顯較AL組小 (P < 0.05)。本實驗結果表明，在此動物模型中，短期熱量限制能有效抑制乳腺癌細胞的增殖。 / 此外，我們還研究了芹菜素在肝細胞中對膽固醇代謝的影響。芹菜素是一種常見的黃酮類化合物。研究發現，在WRL-68細胞中，芹菜素能夠劑量依賴性的抑制3 - 羥基-3 - 甲基 - 戊二酸單酰輔酶還原酶 (HMGCR)和固醇調節元件結合蛋白-2 (SREBP-2) 信使RNA和蛋白的表達及其啟動子的轉錄活性。綜上所述，在肝細胞中，芹菜素能有效抑制HMGCR和SREBP-2的表達，從而達到降低膽固醇的效果。 / 總括而言，本研究表明在去除卵巢的祼鼠模型中，短期熱量限制能有效抑制乳腺癌細胞的生長和芹菜素能有效抑制HMGCR和SREBP-2的表達。 / Non-communicable diseases (NCD) are one of the leading causes of mortality in the developed and under-developing countries. Diet is a major risk factor of NCD. In the present study, effects of diet modification on breast cancer development and cholesterol metabolism were investigated. / In the first part of this study, the effect of chronic and short-term calorie restriction (CR) on breast tumor growth in ovariectomized nude mice was investigated. The calorie-restricted dietary regimen limited the total fat intake only. 14 week-old ovariectomized female nude mice were randomly assigned to ad libitum fed (AL), 20%CCR (17-week 80% of AL), 30%CCR (17-week 70% of AL), 35%CCR (17-week 65% of AL) and short-term CR (3.5-week 65% of AL followed by 13.5-week 100% AL consumption) groups. Starting from 10 weeks after transplant of cells, the tumor volumes in all calorie-restricted groups were significantly smaller (P < 0.05) than that in ad libitum control. At sacrifice, the tumor weight in short-term CR was significantly smaller (P < 0.05) than that in ad-libitum control after normalized with body weight. This indicated that short-term CR could suppress tumor in this model. / In the second part of this study, the effect of apigenin on cholesterol metabolism was investigated. Apigenin is one of the most abundant flavonoids. In the present study, we investigated the effect of apigenin on several cholesterol-related gene expression in hepatic cells. In WRL-68 cells treated with apigenin, promoter transcription activity, mRNA and protein expression of HMGCR and SREBP-2 were significantly decreased in a dose-dependent manner. Taken together, we concluded that apigenin inhibited HMGCR and SREBP-2 gene expressions in hepatic cells, which might elicit the hypocholesterolemic effects. / In conclusion, our study has demonstrated that short-term CR could significantly block the breast tumor growth in a mice model and apigenin could inhibit the expression of HMGCR and SREBP-2 in liver cell lines. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Wong, Tsz Yan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 83-99). / Abstracts also in Chinese. / ACKNOWLEGEMENTS --- p.i / ABSTRACT --- p.ii / 摘要 --- p.iv / list of abbreviations --- p.v / list of figures --- p.vii / list of tables --- p.IX / TABLE of CONTENTS --- p.X / Chapter 1 --- CHAPTER 1 --- p.1 / General Introduction --- p.1 / Chapter 1.1 --- Calorie Restriction and the Prevention of Postmenopausal Breast Cancer --- p.2 / Chapter 1.1.1 --- Breast Cancer --- p.2 / Chapter 1.1.2 --- Epidemiology of Excess Body Weight and Cancer Risk --- p.3 / Chapter 1.1.3 --- Calorie Restriction and Cancer Prevention --- p.7 / Chapter 1.1.4 --- Mechanistic Targets of Calorie Restriction --- p.8 / Chapter 1.1.4.1 --- Effect of Calorie Restriction on Estrogen --- p.8 / Chapter 1.1.4.1 --- Effect of Calorie Restriction on Cell Cycle Regulation --- p.12 / Chapter 1.1.4.1 --- Effect of Calorie Restriction on Apoptosis --- p.14 / Chapter 1.2 --- Effect of Apigenin on Cholesterol Homeostasis --- p.17 / Chapter 1.2.1 --- Cardiovascular Disease and Blood Cholesterol --- p.17 / Chapter 1.2.2 --- Molecular Regulation of Cholesterol Metabolism --- p.21 / Chapter 1.2.2.1 --- HMG-CoA Reductase --- p.21 / Chapter 1.2.2.2 --- CYP7A1 --- p.24 / Chapter 1.2.2.3 --- Apolipoprotein A-1 --- p.26 / Chapter 1.2.2.4 --- Low Density Lipoprotein Receptor --- p.29 / Chapter 1.2.2.5 --- Sterol Regulatory Element Binding Proteins --- p.31 / Chapter 1.2.3 --- Flavonoid and its Association with Cholesterol Metabolism --- p.36 / Chapter 1.2.4 --- Apigenin: A Potential Alternative --- p.39 / Chapter 2 --- CHAPTER 2 --- p.41 / MATERIALS AND METHODS --- p.41 / Chapter 2.1 --- Chemicals and Materials --- p.41 / Chapter 2.1.1 --- Chemicals --- p.41 / Chapter 2.1.2 --- Plasmids --- p.41 / Chapter 2.2 --- Cell Culture --- p.41 / Chapter 2.2.1 --- Maintainance of Cells --- p.41 / Chapter 2.2.2 --- Preparation of Cell Stock --- p.42 / Chapter 2.2.3 --- Cell Recovery from Liquid Nitrogen Stock --- p.42 / Chapter 2.3 --- Measurement of Cell viability --- p.43 / Chapter 2.4 --- Semi-Quantitative and Quantitative RT-PCR Assay --- p.43 / Chapter 2.4.1 --- RNA Isolation and cDNA Synthesis --- p.43 / Chapter 2.4.2 --- Quantitative Real Time PCR Assay --- p.43 / Chapter 2.4.2.1 --- Real Time PCR Using TaqMan Probe --- p.43 / Chapter 2.4.2.2 --- Real Time PCR Using SYBR Green Dye --- p.44 / Chapter 2.4.2.3 --- Statistical Analysis of 2⁻ΔΔ{U+A7F0}{U+1D40} Comparative Gene Expression --- p.44 / Chapter 2.5 --- Western Blot Analysis --- p.46 / Chapter 2.6 --- Measurement of Promoter Activity --- p.46 / Chapter 2.6.1 --- Plasmid Preparation --- p.46 / Chapter 2.6.2 --- Transient Transfection and Dual-Luciferase Assay --- p.47 / Chapter 2.7 --- Animal Experiment Design --- p.47 / Chapter 2.7.1 --- Animal Model and Dietary Regimens --- p.47 / Chapter 2.7.2 --- Tissue Sample Collection --- p.50 / Chapter 2.7.3 --- Plasma Estradiol Determination --- p.50 / Chapter 2.7.4 --- Protein and RNA extraction --- p.50 / Chapter 2.8 --- Statistical Analysis --- p.50 / Chapter 3 --- Chapter 3 --- p.51 / EFFECT OF CHRONIC AND short-term calorie restriction on breast tumor growth in ovariectomized nude mice --- p.51 / Chapter 3.1 --- Introduction --- p.51 / Chapter 3.2 --- Objectives --- p.52 / Chapter 3.3 --- Results --- p.53 / Chapter 3.3.1 --- Food Intakes, Body, Liver and Uterus Wet Weights of the Mice --- p.53 / Chapter 3.3.2 --- Tumor Development --- p.57 / Chapter 3.3.3 --- Plasma Estradiol Level --- p.62 / Chapter 3.3.4 --- Estradiol Responsive Gene expression in Tumors --- p.63 / Chapter 3.3.5 --- Cell Apoptotic and Cell Cycle-Regulated Protein expression in Tumors --- p.65 / Chapter 3.4 --- Discussion --- p.67 / Chapter 4 --- CHAPTER 4 --- p.69 / Apigenin inhibits the expression of hmg-coa reductase and srebp-2 in hepatic cells --- p.69 / Chapter 4.1 --- Introduction --- p.69 / Chapter 4.2 --- Objectives --- p.70 / Chapter 4.3 --- Results --- p.70 / Chapter 4.3.1 --- Effect of Apigenin on Cell Viability --- p.70 / Chapter 4.3.2 --- Effect of Apigenin on HMGCR, CYP7A1, LDLR, ApoA-1, SREBP-1 and SREBP-2 mRNA expressions --- p.72 / Chapter 4.3.3 --- Effect of Apigenin on HMGCR, LDLR, ApoA-1 and SREBP-2 Promoter Transcription Activity --- p.75 / Chapter 4.3.4 --- Effect of Apigenin on HMGCR, SREBP-1 and SREBP-2 Protein Expression --- p.77 / Chapter 4.3.5 --- Role of Estrogen Receptor in Apigenin induced SREBP-2 Inhibition --- p.79 / Chapter 4.4 --- Discussion --- p.80 / Chapter 5 --- CHAPTER 5 --- p.82 / SUMMARY --- p.82 / References --- p.83

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Resumo: O presente estudo avaliou a validade relativa de um Questionário Quantitativo de Freqüência Alimentar (QQFA), previamente validado para população adulta, para crianças de 5 a 10 anos de idade do município de Mirandópolis, estado de São Paulo. A validade foi testada por meio de comparação entre os valores estimados pela média de três dias de Registro Alimentar (método referência) e os valores obtidos pelo QQFA. O estudo foi realizado com 151 crianças de ambos os sexos e seus responsáveis, os quais responderam um QQFA e, posteriormente, 3 dias de Registro Alimentar. Os dados foram calculados utilizando os programas Nutri 2.5 e Dietsys e analisados utilizando-se coeficiente de correlação de Pearson, ajustados para caloria e corrigidos pela variância intrapessoal. Observou-se uma variabilidade alta no consumo da dieta das crianças, com as maiores razões de variância para energia e cálcio. Os coeficientes de correlação de Pearson obtidos após ajuste pela caloria e correção pela variância variam entre 0,15 a 0,81. A média dos coeficientes de correlação foi de 0,40. Esses resultados indicam a capacidade do QQFA em classificar os indivíduos segundo seu consumo habitual para a maioria dos nutrientes, porém é aconselhável que o instrumento seja calibrado, uma vez que os macronutrientes como carboidratos, lipídios e proteína apresentaram baixas correlações. / Abstract: The present study has evaluated the relative validity of a Quantitative Food Frequency Questionnaire (QFFQ), previously validated to the adult population, for children from 5 to 10 years old from Mirandópolis, São Paulo. The validity was obtained by comparing the estimated values of the average of 3 Day Diet Record (reference method) with the values obtained by QFFQ. The study was performed with 151 children of both sexes and their responsible, who answered the QFFQ and, in a sequence, 3 Day Diet Record. The data was calculated by using the Nutry 2.5 and Dietsys programs. Comparison among calculated data were analyzed by correlation coefficient of Pearson, adjusted for calorie and corrected by the intra personal variance. It was observed a large variability in the consumption of the children's diet, with the largest variance ratio for energy and calcium. The correlation coefficients of Pearson obtained, after calorie adjustment and correction for the variance, varied in the range of 0.15 to 0.81. The obtained average correlation coefficient was 0.40. The calculated results indicate the capacity of QFFQ in classifying the individuals according to their habitual consumption for the majority of nutrients. However, it is advisable the instrument calibration, once macronutrients as carbohydrates, lipids and protein showed low correlations with the real consumption. / Orientador: Maria de Lourdes Pires Bianchi / Coorientador: Jacqueline Pontes Monteiro / Banca: João Bosco Faria / Banca: Simon Carmelo Junior / Mestre

All over the world, adolescent obesity is a serious health problem. Many researchers have focused on diet and exercise, because those behaviors are modifiable risk factors for obesity. To reduce or prevent the prevalence of adolescent obesity, contributions of diverse contextual factors to adolescents’ diet and exercise have been studied. However, little is known about peer influences on adolescents’ diet and exercise, compared to the studies of other contextual factors such as parents and school. In addition, in contrast to Western countries with higher prevalence of adolescent obesity, few studies have been conducted in countries with different cultures. Exploring the influence of peers on diet and exercise of adolescents in those countries could help to develop culturally-appropriate interventions to prevent adolescents from becoming obese. Thus, the purpose of this set of three studies was to examine adolescents’ diet and exercise in the context of peer factors and relationships. The purpose of the first study was to systematically review research assessing contribution of peer to adolescents’ diet and exercise. Twenty four articles were identified, using the electronic databases, PubMed, CINAHL, Web of Science, and SCOPUS. According to the findings from this review, the diet and exercise of adolescents was positively associated with that of their peers. Additionally, gender, the type of diet and exercise, and the closeness of friends could influence these associations. The second study identified the parent-, school-, and peer-factors contributing to dietary and exercise behaviors of adolescents in the United States, by using data from the Health Behaviour of School-Aged Children study. Findings from the current analysis indicated that parent- and peer-factors could influence either diet or exercise of adolescents; while school-factor were found to be associated only with adolescents’ diet. The third study explored the diet and exercise of Korean female adolescents within their classroom-based peer networks. Using social network analysis, dietary behaviors of female adolescents in this study were clustered within their classrooms. Several adolescents played a role in bridging two or more peer networks. However, less information about female adolescents’ exercise behaviors within classroom-based peer network was obtained. In summary, peers are an important contextual factor for developing adolescents’ diet and exercise behaviors that could contribute to adolescent obesity. These associations could be influenced by the characteristics of friendships such as gender of friends, the closeness of friends, and network characteristics of friendships. Peers can be potential targets for interventions to reduce or prevent the development of adolescent obesity.

Summary: Although the study of nutrition during the last forty years has received considerable attention, there are still fields of the science about which our knowledge is very incomplete. In this country, in particular, there is little information even about the gross chemical composition of our foodstuffs -- a subject which must surely form the basis of any dietry constituents present in foods is of value to anyone concerned with the planning of accurate diets, or the investigation of the nutritional status of a community. It is well known that the figures, even for carbohydrate, protein and fat, compiled by workers in different parts of the world, vary widely. In accurate work it would therefore be incorrect to use such figures which were compiled in another country. This must necessarily occur in New Zealand because at present no complete and systematic analysis of our foods had been made, and hence there are no comprehensive tables. Further-more, there are many native products for which there are neither comparable overseas figures nor any New Zealand analyses of constituents--Introduction.

Background Polycystic ovary syndrome (PCOS) is a common endocrine condition in women associated with obesity, reproductive and metabolic abnormalities. It improves with weight loss, however currently no specific dietary recommendations exist and there may be abnormalities in appetite regulation in PCOS that contribute to difficulty in weight management. Aims To assess the effect of 1) short and long-term weight loss and weight maintenance strategies on weight loss, reproductive and metabolic parameters in overweight women with PCOS and to 2) assess the relative effect of weight loss on cardiovascular risk factors and 3) postprandial appetite, appetite hormones (ghrelin, CCK, PYY) and food intake in overweight women with and without PCOS. Results Overweight women with PCOS followed an 8-week weight loss (2 meal replacements/day, 4904.4±127 kJ, n=32) followed by a 6 month carbohydrate (<120 g/day) or fat restricted (<50 g/day) weight maintenance regime (n=23). Reductions in weight (5.6±2.4 kg) and improvements in body composition, insulin, reproductive hormones and menstrual cyclicity occurred and were sustained equivalently for both diet groups. We then assessed the effect of weight loss (4.2±0.7 kg over 8 weeks as described above) in overweight women with (n=15) and without (n=17) PCOS on cardiovascular risk factors. All subjects had similar improvements in body composition, triglycerides, reproductive hormones and fasting and post-prandial insulin. C-reactive protein decreased with weight loss for non-PCOS women (-1.2±0.5 mg/L, P=0.025) but not for PCOS women. We finally assessed appetite regulation in PCOS. Women with (n=20) and without (n=12) PCOS followed a standard protein (55% carbohydrate, 15% protein) or high protein diet (40% carbohydrate, 30% protein) for 16 weeks (~6000 kJ/day). Non-PCOS subjects were more satiated (P=0.001) and less hungry (P=0.007) after the test meals and had a 70% higher fasting baseline ghrelin (P=0.011), a greater increase in fasting ghrelin (57.5 versus 34.0%, P=0.033), a greater post-prandial ghrelin decrease at week 16 (113.5±46.3 versus 49.3±12.2 pg/mL, P=0.05) and a greater maximal decrease in post-prandial ghrelin (-144.1±58.4 versus -28.9±14.2 pg/mL, P=0.02) following weight loss than subjects with PCOS. Lastly, women with (n=14) and without (n=14) PCOS undertook an 8-week weight loss regime (4.2±0.7 kg as described above). At week 0 and 8, women with PCOS again displayed lower ghrelin levels (P=0.01 and P=0.097 respectively) and a lesser post-prandial ghrelin decrease (P=0.048 and P=0.069 respectively) but similar post-prandial appetite, buffet consumption and fasting or post-prandial peptide YY and cholecystokinin compared to women without PCOS. Conclusion Meal replacements and moderate macronutrient restriction are effective strategies for the dietary management of PCOS. Equivalent weight losses improved cardiovascular risk factors similarly for overweight women with and without PCOS with the exception of CRP which did not decrease with weight loss for overweight women with PCOS. PCOS status is associated with altered fasting and post-prandial ghrelin levels but is not consistently associated with other impairments in post-prandial gut peptides or food intake. Further investigation is required to assess if appetite regulation is impaired in PCOS and the optimal strategies and amount of weight loss for improvement of reproductive and metabolic parameters in PCOS. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1282329 / Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2007

Thesis (M.S.)--Ohio University, June, 2007. / Title from PDF t.p. Includes bibliographical references.

Current ACOG guidelines recommend exercise during a low-risk pregnancy for 30 minutes on most, if not all days of the week. However, little is known about how the volume of exercise performed during pregnancy affects fetoplacental size. In addition, the confounding effects of maternal nutrient intake and weight gain, and how they interact with exercise volume to influence fetoplacental size have not been appropriately addressed. Therefore, the purpose of this study was to examine the effects of varying maternal exercise volumes on neonatal birthweight and placental volume, while addressing the influence of maternal nutrient intake and weight gain. Subjects evaluated for this study included pregnant women who walked during gestation (n=26), performed non-walking aerobic exercise during gestation (n=30), or remained as sedentary controls (n=32). At 16, 20, 24, 28, 32, 36 weeks gestation, women recorded their nutrient intake for 3 consecutive days. Additionally, they kept monthly exercise logs indicating the type and duration of their exercise. Nutrient variables calculated included average daily Calorie intake, average daily carbohydrate intake, average daily protein intake, average daily fat intake, and average daily fiber intake. Exercise volume was calculated as the average number of minutes per week spent performing exercise. Latent growth modeling was the statistical procedure used to analyze how change in maternal exercise volume and nutrient intake throughout gestation affects neonatal outcomes. Neonatal outcomes measured were birthweight, corrected birthweight for gestational age, sex, race, and socioeconomic status, and placental volume at delivery. Maternal walking volume had no effect on newborn birthweight or corrected birthweight, while it was inversely related to placental size at birth. Maternal non-walking aerobic exercise volume was inversely related with newborn birthweight, while there was a trend toward an inverse relationship with corrected birthweight and placental volume. Controlling for Calorie intake strengthened the relationship between any form of exercise volume and infant birthweight. Calorie intake, carbohydrate intake, and protein intake were all positively related to infant birthweight. Fiber intake was significantly inversely related to placental volume. Finally, maternal exercise volume and nutrient intake were not related to maternal weight gain. This data suggests that neonatal outcome will be affected by variations in exercise protocol. In addition, nutrient intake is a potentially confounding variable that should be examined when undertaking studies addressing the role of maternal exercise on neonatal outcome.