The relationship between body composition and bone mineral density in women Purpose: The purpose of this study was to investigate the relationships between body composition (fat and lean mass), body weight, body mass index (BMI) and bone mineral density (BMD) and bone mineral content (BMC) in women across the age span. Methods: 1046 healthy Caucasian women (49.9 ± 15.9 years old) were recruited and categorized to four age groups, ranging from 18 to 35 years old, 35 years to before the age of menopause, menopause to 65 years and over 65 years old. Each different age group was further categorized according to subjects' body mass index (BMI < 25, BMI =25-30, and BMI > 30). Measurements included anthropometrics, body composition and BMC/BMD by dual-energy x-ray absorptiometry (DXA). Results: Subjects in the younger groups were taller, weight less and had greater total body BMC/BMD and BMD at spine, femoral neck, and total femur (p<0.05) compared with older subjects. Obese women had higher total lean and fat mass, and the highest BMD/BMC in all skeletal sites (p<0.05) among different age groups. Weight, BMI, total lean, and total fat mass were positively correlated with total body BMC/BMD, BMD of all skeletal sites among different age groups. The results from multiple linear regression models revealed that weight was a significant predictor of total body BMC/BMD, BMD of all skeletal sites in women of different age groups, gonadal status, and different BMI, except overweight women. Both lean and fat mass were important determinants of total body BMC/BMD, BMD at femur and forearm in premenopausal women though total lean mass had greater effect than total fat mass. Total fat mass was the only significant predictor of total body BMC/BMD, BMD at other sites in postmenopausal women. Furthermore, total fat mass became more important with the increased body weight. Further analysis of covariance in subjects stratified by body weight and percent body fat revealed that high percent body fat seemed to have negative effect on bone mass in total body BMC/BMD and BMD at spine, femoral neck and forearm when mechanical loading effect of body weight was controlled. Conclusions: These results show that overweight/obese women had higher BMD in all skeletal sites than normal-weight women. Lean mass was an important predictor of BMD in premenopausal women and fat mass became more important in postmenopausal women. Higher fat mass however, may not have beneficial effect on bone mass when mechanical loading of weight is accounted for. / A Dissertation submitted to the Department of Nutrition, Food and Exercise Sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy. / Spring Semester, 2010. / December 4, 2009. / Lean mass, Fat mass, BMD, Caucasian women / Includes bibliographical references. / Jasminka Z. Ilich-Ernst, Professor Directing Dissertation; Ken Brummel-Smith, University Representative; Doris A. Abood, Committee Member; Maria Spicer, Committee Member.

Introduction: Atherosclerosis is a complex disease caused by gradual build-up of plaque inside the arteries leading to hardening of the arteries. Atherosclerosis is not only the major cause of death in the United State, but also a worldwide healthcare burden. Aging is regarded as an independent and the most important risk factor for atherosclerosis after controlling other known factors. The accumulation of senescent cells in vivo during aging contributes to senescent phenotypes leading to organismal aging and age-related diseases. Autophagy is a tightly regulated catabolic process of cellular self-degradation. SQSTM1/p62, an autophagy adaptor, regulates autophagy by recruiting damaged proteins and organelles. Impaired autophagy in vascular aging causes inefficient removal of damaged and dysfunctional mitochondria in vascular cells leading to increased ROS production and inflammation in the vessel wall and eventually atherosclerosis. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases are major source of ROS in the vasculature. Nox4 plays an important role in maintaining vasculature health, however high levels of Nox4 induce oxidative stress leading to CVD progression. Our preliminary data showed that p62 gene deficiency increased senescence and the expression of Nox4, but not Nox1, in vitro. Therefore, we hypothesized that down-regulation of p62 up-regulates Nox4 expression, which increases the levels of ROS, accelerating vascular senescence and atherosclerosis. Methods: We tested the role of p62 in senescence using p62 knock out (p62-/-) and measuring senescence in aortas of males and females in vivo and in VSMCs in vitro. Senescence was measured using SA- -gal. Protein expression was measured using western blot. To test the role of p62 in atherosclerosis, we generated a ApoE-/-p62-/- animal model and measure plaque accumulation in aortas of males and females in response to high fat diet. Results: Both male and female p62-/- mice showed obese phenotypes and started to increase body weight at 4 and 6 months of age, respectively. SA- -gal activity was increased in aortas of male p62-/- mice before and after the increase in body weight, and was also increased in aortas of 5 to 8 month-old female p62-/- mice. The molecular mechanism involved in p62 deficiency-induced senescence was tested in mouse aortic smooth muscle cells (MASMs). p62-/- MASMs showed increased SA- -gal activity and production of ROS, including hydrogen peroxide, superoxide, and mitochondrial ROS, as well as expression of Nox4, signaling proteins, including phosphorylated Akt, p38MAPK and ERK, and phosphorylated PGC1 that associated with mitochondrial dysfunction. Overexpression of Nox4 by adenovirus upregulated SA- -gal activity in wild type MASM cells, while downregulation of Nox4 by short hairpin RNA (shNox4) reduced SA- -gal activity in p62-/- MASMs, suggesting the Nox4 is required for p62 deficiency-induced senescence. Furthermore, the upregulation of Nox4 by p62 deficiency was mediated by a transcription-dependent mechanism, since inhibition of transcription using actinomycin D reduced Nox4 expression in p62-/- MASMs and mRNA levels of p62 were higher in p62-/-, compared with control cells. Antioxidants including N-acetyl cysteine (NAC) and mitoTEMPO, a mitochondrial ROS scavenger, showed not affect in Nox4 expression in p62+/+ and p62-/- cells, but decreased senescence in both cell types, suggesting that ROS is responsible for p62 deficiency-induce senescence, but not for Nox4 upregulation. Moreover, NAC treatment decreased expression of phosphorylated Akt and PGC1 . Confirming the physiological role of Nox4 in vivo, Nox4 was upregulated in aortas of males at all ages, but not female p62-/- mice. We observed that p62 gene deficiency only increased atherosclerotic plaque on the aortic arch in male ApoE-/-p62-/- mice at 4 months of age, but not in young male animals or in females. Surprisingly, atherosclerotic plaque was reduced in aortas isolated from 1 year old ApoE-/-p62-/- mice for both male (total aortas) and female (total, arch and descending aortas). Conclusions: p62 deficiency upregulates Nox4 transcription increasing Nox4 protein expression, causing increased cytosolic ROS and mitochondrial ROS production via Akt-PGC1 pathway, which leads to vascular senescence in vitro. Senescence could be Nox4 dependent in males, but not in female mice. p62 deficiency-induced senescence is not associated with increased atherosclerosis development or with the onset of obesity. p62 deficiency protects mice from atherosclerosis during natural aging. / A Dissertation submitted to the Department of Nutrition, Food and Exercise Sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy. / Spring Semester 2018. / March 23, 2018. / Atherosclerosis, Nox4, Oxidative Stress, Senescence, SQSTM1/p62 / Includes bibliographical references. / Gloria Salazar, Professor Directing Dissertation; Mike Overton, University Representative; Jeong-Su Kim, Committee Member; Maria Spicer, Committee Member.

abstract: The Adequate Intake (AI) level for total fiber for adults is 14 grams per 1,000 kilocalories per day; however, only 12.9% of Americans met their total fiber needs according to the 2015-2016 National Health and Nutrition Examination Survey (NHANES). A lower frequency of home-cooked meals and a higher frequency of restaurant meals have been cited as a possible explanation for the low dietary fiber intake among Americans, and according to the Social-Ecological Model, the retail food environment can influence our food choices such as the choice to eat at home or eat out. The objective of this study is to examine the relationship between a dynamic measurement of exposure to the retail food environment and fiber intake (total fiber, soluble fiber, insoluble fiber, and pectin). This is a secondary analysis of data from the Community of Mine study, a cross-sectional study of 602 adults residing in San Diego County, California. Dynamic exposure to the retail food environment was assessed using Global Positioning Systems (GPS) data collected by the Qstarz GPS device worn by each participant. Fiber intake was assessed using two 24-hour dietary recalls. Multivariate regression analysis was used to assess correlations. Descriptive results showed no significant differences in dynamic exposure to the retail food environment by sex, Hispanic ethnicity, and income. There were significant differences in fiber intake by sex and ethnicity. The results of the multivariate regression analysis suggest that exposure to the retail food environment is not associated with fiber intake among a subset of American adults. / Dissertation/Thesis / Masters Thesis Nutrition 2020

BACKGROUND: Aortic aneurysm (AA) affects 15, 000 individuals in the United States and 221,900 individuals in China die every year due to the dissection and rupture of an AA. Genetic disorders such as Marfan’s syndrome, increase the risk of developing AA. Our work seeks to identify novel molecular mechanisms that could become much needed therapeutic targets to prevent AA. We previously showed that the lysine deacetylase sirtuin-1 (SirT1) is crucial to protect the vascular wall against inflammatory and oxidant insults. We hypothesize that an increased oxidative stress in the vascular wall of patients with Marfan’s syndrome, inhibits SirT1 by oxidative post-translational modifications leading to vascular wall remodeling and AA. METHODS: To test our hypothesis we used fibrillin-1 mutant mice (Fbn1mgR/mgR), a genetic model of Marfan’s syndrome prone to AA, and wild type (WT) controls. Aortic sections or vascular smooth muscle cells (VSMC) homogenates from WT and Fbn1mgR/mgR were prepared and processed for dihydroethidium staining, NAD/NADH measurements and in-gel zymography, respectively. In addition, we generated a mutant sirtuin-1 construct plasmid resistant to oxidative post-translational modifications as a novel tool to determine the role of sirtuin-1 in AA. RESULTS: Our results indicate that there is an increase in oxidative stress and metalloproteinase activity in the thoracic aorta of Fbn1mgR/mgR compared to WT, while NAD/NADH is not significantly increased. In addition, we successfully generated a mutant redox-resistant sirtuin-1 plasmid for future studies. CONCLUSION: Our preliminary data strongly suggest that targeting oxidative stress and/or preventing oxidative post-translational modifications of SirT-1 represent a potential therapeutic avenue to prevent or ameliorate AA in patients as risk, such as those with Marfan’s syndrome.

PURPOSE: The purpose of the present investigation was to examine the effects of Branched-chain amino acid (BCAA) administration on the exercise time to exhaustion in sedentary individuals. The central fatigue hypothesis proposes that, by maintaining a favourable plasma free Tryptophan (TRP) to BCAA ratio, BCAA supplementation may have the ability to reduce the rate of entry of TRP into certain areas of the brain. TRP is the metabolic pre-cursor of serotonin. Serotonin is a chemical neurotransmitter, which appears to have a role to play in the control of lethargy, tiredness and sleep. It has been suggested that reductions in TRP concentrations in the brain will decrease brain serotonin synthesis which may help to delay the onset of this form of fatigue, known as central fatigue. METHODS: Ten, healthy, non-obese and non-active males aged between 18 and 25 participated in the study. Each participant performed two submaximal exercise bouts until volitional fatigue, while receiving either a BCAA supplement (50% leucine,30% valine, 20% isoleucine) or a placebo (PLAC). Cardiorespiratory measures of VO2 (ml.kg.min, VCO2 (l/min), Ve (l/min), RER and heart rate (bpm) were recorded throughout. RPE values were taken during each trial. Post-exercise cognitive assessments of reaction time, memory recall and attention capacity were performed following each treatment. RESULTS: Exercise time to exhaustion was significantly longer during the BCAA (96.02 + 15 mins) trial when compared to the PLAC (86 + 14 mins) trial (P<0.05). No significant differences in any of the cardiorespiratory measures were observed between trials or at exhaustion. No significant differences in RPE were found between treatments. Post-exercise memory recall demonstrated no observable differences between trials. Following the BCAA trial simple reaction time scores were significantly faster than the PLAC trial (210 + 40msec v's 226 + 37msecs) (P<0.05). Participants concentration levels were improved following the BCAA trial as evidenced by a significantly lower recorded error score in a paper and pencil cancellation test (1.3 + 1.3 v's 4.7 + 3.1) (P<0.05). CONCLUSIONS: The present investigation demonstrated that supplementation of BCAA during prolonged submaximal exhaustive exercise resulted in a significantly longer exercise duration in a sedentary population. Although it cannot be firmly concluded that the BCAA administered were not utilised for metabolic purposes by skeletal muscle, improvements in post-exercise cognitive performance tend to suggest that the BCAA administered had a role to play in offsetting feelings of fatigue and tiredness experienced by a sedentary population and that this fatigue may be of central origin. / A Thesis submitted to the Department of Nutrition, Food and Exercise Sciences in partial fulfillment of the requirements for the degree of Master of Science. / Summer Semester, 2003. / June 18, 2003. / Branched-Chain Amino Acid, Central Fatigue, Serotonin, BCAA / Includes bibliographical references. / Emily Haymes, Professor Directing Dissertation; Anahita Mistry, Committee Member; Laurie Grubbs, Committee Member.

Prospective studies and animal research suggest that apple or its bioactive components modulate lipid metabolism, and reduce fat mass and the production of proinflammatory molecules. However, there is a paucity of such research in humans. Hence, we conducted a one-year clinical trial evaluating the cardioprotective effects of apple consumption in postmenopausal women. We hypothesized that regular intake of apple favorably improves lipid profiles, reduces atherogenic risk ratios, C-reactive protein (CRP) levels, and the levels of oxidative stress markers in postmenopausal women. This study was conducted in postmenopausal women because a decline in estrogen levels places them at a higher risk for cardiovascular disease (CVD). Qualified women (160) were randomly assigned to one of the two dietary intervention groups: dried apple (75 g/day) or dried plum (comparative control). Overnight fasting blood samples were collected at baseline, 3-, 6-, and 12-month to measure various parameters. Confounding factors that may influence lipid metabolism such as physical activity and dietary intake were also assessed. The findings indicated that daily incorporation of dried fruits into diet did not affect total energy intake throughout the study period. More importantly, the additional daily caloric intake of approximately 240 from dried apple not only did not increase body weight but lowered it by 1.5 kg compared to baseline body weight. In terms of lipid profiles, apple consumption significantly reduced serum levels of TC and LDL-C by 14% and 23%, respectively. In addition, atherogenic risk ratios such as TC/HDL-C and LDL-C/HDL-C decreased in postmenopausal women that consumed dried apple compared to control. The present study also suggests that regular apple consumption improves other important parameters involved in CVD such as reducing lipid hydroperoxide (33%) and CRP (32%) levels. In conclusion, regular apple consumption is encouraged because of its favorable effects on lipid profiles, oxidative status, and proinflammatory molecules. / A Dissertation submitted to the Department of Nutrition, Food and Exercise Sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy. / Fall Semester, 2010. / October 29, 2010. / Apple, Cardiovascular Health, Postmenopausal Women / Includes bibliographical references. / Kenneth Brummel-Smith, University Representative; Jeong-Su Kim, Committee Member.

No description available.

Nutrient intake and anthropometric measurement data of children enrolled in the Western Massachusetts Growth Study (WMGS) were examined and correlated with maternal attitudinal and knowledge indices, to test the hypothesis that maternal attitudes, nutrition knowledge, and practices affected the child's rate of growth. Data were obtained at 12, 18, and 24 months of age on subjects who had been enrolled in the WMGS since birth. Males were taller and heavier at all age intervals than females. Differences between sexes in weight and length measurements were significant at the .01 level. Differences between the WMGS subjects and children represented by NCHS growth data were small. Analysis of nutrient intakes showed that WMGS subjects consumed higher levels of nutrients at most age intervals than did subjects in the Child Research Council (CRC) study. Iron intakes between the two groups differed markedly; WMGS children's consumption increased over the period from 12 to 24 months of age, while CRC subjects showed a decrease in iron consumption over the same time period. Vitamin C intakes of WMGS subjects were higher than those of CRC subjects at all intervals. Mother's attitudes toward food additives were examined in relation to the types and frequencies of additive-containing foods fed to their children. Chi square analysis revealed few relationships between maternal attitudes and the child's food consumption. In general, maternal attitudes toward food additives were poor predictors of the child's food consumption behavior. Regression analysis was done to identify the strongest set of probable influences upon the child's attitude toward eating. The sex and range of foods accepted by the child were shown to have an effect upon attitude toward eating. Males, in general, had less positive attitudes toward eating than did females. The more acceptant a child was toward a variety of foods, the more positive was his attitude toward eating. Path analysis was performed to determine the ways the attitudes and practices of the mother affected the child. The dependent variables in this analysis were the differences between the child's actual weight and actual height at 24 months and the predicted weight and height at 24 months (as determined by regression analysis). Independent variables were those maternal attitudes and practices most highly correlated with the dependent variable. Results of analyses show that attitudes of the mother have only one direct effect upon a child's weight. Permissiveness had a negative effect upon weight; the more permissive a mother was toward the child's eating behavior, the more the child's weight differed negatively from the predicted weight at 24 months. The mother's food acceptances were shown to have a positive effect upon the child's food acceptances; in turn, the child's food acceptances had a positive effect upon the child's weight. The greater a child's acceptance of food, the greater was the difference between the child's actual weight and predicted weight. No significant results were observed for the effects of maternal attitudes and practices upon the child's height. Within the ranges of intake observed in this study, the level of nutrient intakes of the children could not be shown to have a measurable effect upon growth.

Abstract not available

OBJECTIVE: To investigate the effects of statin exposure on insulin secretion and metabolism in pancreatic beta cells in order to determine possible mechanisms that may contribute to the increased risk of developing Type 2 Diabetes that has been associated with taking statins. METHODS: Simvastatin and Pitavastatin were prepared to resemble the intracellular active form of the compound by converting the lactone, when present to a carboxyl group. These statins were then incubated at varying concentrations (0-200 nM) with clonal pancreatic β-cells (INS-1) for variable amounts of time (24-72 hours). Glucose-stimulated insulin secretion was measured from INS-1 cells cultured at low (4 mM) and high (11 mM) glucose with and without statin incubation. Results were measured using a homogenous time-resolved fluorescence (HTRF) insulin assay kit (Cisbio). The effect of statins on INS-1 cellular metabolism was determined by measuring oxygen consumption rate using a Seahorse XFe96 analyzer (Agilent Technologies). Statin effects on intracellular Ca2+ ([Ca2+]i) was examined in INS-1 cells cultured on glass bottom dishes loaded with the calcium indicator Fura-2 AM (Invitrogen) and mounted on an Olympus fluorescence microscope. RESULTS: Simvastatin significantly inhibited GSIS and depleted insulin content in a dose-dependent manner (25-200 nM) after 72-hour exposure. However, when normalized for insulin content, inhibition was not observed. In contrast, pitavastatin did not affect GSIS, but did decrease insulin content in a dose-dependent manner (25-200 nM). At both high and low glucose, simvastatin (200 nM) increased the frequency and amplitude of intracellular calcium ([Ca2+]) oscillations at 1, 3, and 12 mM glucose. Furthermore, simvastatin increased mitochondrial respiration at low glucose, in cells exposed to the highest dose of simvastatin (200 nM). CONCLUSION: Inhibition of GSIS by simvastatin and not pitavastatin, confirmed previous results from our lab that indicate that statins may have differential mechanistic effects on β-cells. Furthermore, intracellular calcium ([Ca2+])i imaging revealed that cells exposed to simvastatin (200 nM) had increased oscillation frequency and amplitude at basal (1, 3 mM) and high (12 mM) glucose conditions, indicating a potential difference in basal insulin secretion that may contribute to hyperinsulinemia. Lastly, mitochondrial respiration at low glucose increased in cells exposed to the highest dose of simvastatin (200 nM), suggesting that statins may play a role in decreasing energy efficiency.