Department of Nutrition

Very high physical activity predicts higher diet quality in healthy young adults, as measured by the Healthy Eating Index 2005

2013-04-01T22:38:13Z

Very high physical activity predicts higher diet quality in healthy young adults, as measured by the Healthy Eating Index 2005 Johnson, Angela K. Physical inactivity and unhealthful diet are major risk factors for noncommunicable diseases, and strategies worldwide now focus on improving diet and encouraging physical activity (PA). Participation in PA lowers the risk for numerous chronic diseases, while a healthful diet also offers resistance to disease. However, practicing both behaviors offers greater protection than practicing either behavior alone. Research evaluating the relationship of diet and PA has focused primarily on nutrients or food groups. Little research exists on PA and overall diet quality, and no research has used the Healthy Eating Index 2005 (HEI-2005) to assess diet quality in healthy young adults, the objective of the current study. To this end, a convenience sample of 70 healthy, young adults was recruited from a university community in 2005-2006. Dietary intake was measured with 7-d weighed food records and HEI-2005 scores were computed to assess diet quality. PA was obtained from 7-d activity records accounting for all minutes of each day. Linear regression models were used to assess the association of HEI-2005 scores to participation in moderate- and vigorous-intensity PA. In this sample, HEI-2005 scores increased as weekly minutes of PA increased (p=0.006, B=0.007). When PA was examined categorically, only the VeryHighPA (≥841 min/week) group had diet quality scores significantly higher than the LowPA (≤420 min/week) group, independent of age, BMI, and gender (p=0.033, B=7.987). Further studies are warranted to clarify the relationship of these health behaviors, an especially important topic as prevalence of obesity and chronic disease continues to rise. Graduation date: 2013

Changes in body composition and metabolic syndrome risk factors : response to energy-restriction, protein intake, and high intensity interval training

2013-03-28T20:55:19Z

Changes in body composition and metabolic syndrome risk factors : response to energy-restriction, protein intake, and high intensity interval training Pilolla, Kari D. Metabolic syndrome (MetS) and abdominal obesity (AbOb) increase the risk of developing cardiovascular disease and diabetes. Energy restriction (ER), highprotein (PRO) intake and high-intensity interval training (HIT) can independently improve MetS and AbOb. However, ER reduces metabolically active lean body mass (LBM) in addition to body fat (BF). Purpose: To determine the effects of a 16-wk ER diet with 2 levels of PRO (15% or 25% of energy), plus HIT, on MetS risk factors, AbOb, and body composition in women. Methods: Sedentary, premenopausal women (age=35±10y) with AbOb (waist circumference [WC] ≥80cm) were randomized to a 16-wk ER diet (-300kcals/d) with 15% (15PRO; n=17) or 25% (25PRO; n=18) of energy from PRO, plus 45min/d, 3d/wk HIT and 45min/d, 2d/wk continuous moderate-intensity exercise (CME) (-200kcals/d). Diet and physical activity (PA) were assessed using 4-d weighed food and PA records, respectively; diet and exercise compliance were assessed monthly with multiple-pass 24-h recalls and weekly tracking logs. Body weight (BW), WC, DXA-assessed body composition (BF [%], BF [kg], trunk fat [kg], and LBM [kg]), blood lipids (total cholesterol [TC], high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], triglycerides [TG]), glycemic markers (fasting plasma glucose [FPG], insulin, and homeostatic model assessment for insulin resistance [HOMA-IR], beta cell function [HOMA-%β] and insulin sensitivity [HOMA-%S]) and resting blood pressure (BP) (systolic BP [SBP]; diastolic BP [DBP]) were assessed pre/post-intervention. Repeated measures analysis of variance and two sample t-tests were used at analyze the date. Results are reported as means±standard deviations. Results: There were significant time, but not group, differences in BW (-5.1±2.6kg, p=0.0141), WC (- 7.3±3.6cm, p<0.0001), TC (-18.1±17.4mg/dL, p<0.0001), LDL-C (12.2± 16.2mg/dL, p<0.0001), TG (-25.3±56.2mg/dL, p=0.0064), insulin (-2.1±4.2mg/dL, p=0.0048), HOMA-IR (-0.2±0.5, p=0.0062), HOMA-%β (-12.1±35.2%, p=0.0497), HOMA-%S (28.5±78.4%, p=0.0357), and SBP (-3±9mmHg, p=0.214). There were significant group x time differences in DBP (15PRO=-5±8mmHg, 25PRO=- 2±8mmHg; p=0.0024). There were no time or group differences in FPG or HDLC. There were significant time, but not group, effects on changes in BW (-5.1kg± 2.6, p<0.0001), BF (-3.3±1.6%, p<0.0001), and LBM (-0.6kg±1.5, p=0.0283). The 15PRO group lost more absolute whole BF (-5.2kg vs. -3.9kg, p=0.0355) and trunk fat (-3.1kg vs. -2.2kg) vs. the 25PRO group. Conclusion: Both diets significantly improved BW, AbOb, MetS risk factors, glycemic control, and BF (%); LBM (kg) loss was similar in both groups. Compared to the 15PRO diet had significantly greater absolute BF-kg and trunk fat-kg losses. Increased PRO intake did not improve AbOb or MetS risk beyond ER and HIT/CME. The impact of HIT/CME and the greater (-1.3kg) changes in BW in the 15PRO group may have contributed significantly to the changes in absolute BF and trunk fat. More research is needed to separate the impact of HIT/CME and weight loss from the impact of PRO during ER. Graduation date: 2013; Access restricted to the OSU Community at author's request from March 28, 2013 - March 28, 2014

Dietary intake associated with serum versus urinary carboxymethyl-lysine, a major advanced glycation end product, in adults: the Energetics Study

2013-01-24T20:02:02Z

Dietary intake associated with serum versus urinary carboxymethyl-lysine, a major advanced glycation end product, in adults: the Energetics Study Semba, R. D.; Ang, A.; Talegawkar, S.; Crasto, C.; Dalal, M.; Jardack, P.; Traber, M. G.; Ferrucci, L.; Arab, L. Background/Objectives: Advanced glycation end products (AGEs) are implicated in the pathogenesis of atherosclerosis, diabetes and kidney disease. The objective was to describe dietary intake, the dominant source of exposure to AGEs, with carboxymethyl-lysine (CML), a major AGE, in serum and urine, respectively. Subjects/Methods: Serum and urinary CML were measured in 261 adults, aged 21-69 years, and compared with diet as assessed by six separate 24-h dietary recalls. Results: Median (25th, 75th percentile) serum and urinary CML concentrations were 686 (598, 803) mu g/l and 1023 (812, 1238) mu g/gm creatinine. There was no correlation between serum and urinary CML (r = -0.02, P = 0.78). Serum CML was positively correlated with intake of soy, fruit juice, cold breakfast cereal, non-fat milk, whole grains, fruit, non-starchy vegetables and legumes, and negatively correlated with intake of red meat. Intake of fast food was not significantly correlated with serum CML. Urinary CML was positively correlated with intake of starchy vegetables, whole grains, sweets, nuts/seeds and chicken, and negatively correlated with intake of fast foods. Intake of AGE-rich foods such as fried chicken, French fries, bacon/sausage and crispy snacks were not significantly correlated with serum or urinary CML, except for a significant negative correlation between fried chicken and serum CML. Conclusions: These findings suggest that the high consumption of foods considered high in CML is not a major determinant of either serum or urinary CML. Further work is needed to understand the relationship of AGEs in blood and urine with the metabolism of dietary AGEs. To the best of our knowledge, one or more authors of this paper were federal employees when contributing to this work. This is the publisher’s final pdf. The published article is copyrighted by Nature Publishing Group and can be found at: http://www.nature.com/.

Vitamin E and K interactions : investigating mechanisms of reduced vitamin K status in response to excess vitamin E

2013-01-15T17:57:55Z

Vitamin E and K interactions : investigating mechanisms of reduced vitamin K status in response to excess vitamin E Farley, Sherry Mae The primary goal of my studies was to elucidate the mechanisms for the well-recognized interaction between two nutrients, vitamins E and K. The outcomes from my studies assess mechanisms for adverse effects of vitamin E and provide novel information on mechanisms for vitamin K homeostasis. These findings will provide information relevant for assessing optimal intakes of vitamins E and K. This dissertation presents studies aimed at evaluating three different mechanisms by which vitamin K status could be decreased by increases in whole body vitamin E concentrations in rats supplemented with vitamin E by subcutaneous injections (100 mg α-tocopherol (α-T)/ kg body weight per day), the model system developed in the Traber lab. The tested mechanisms by which vitamin E leads to reduced vitamin K status were: 1) increasing vitamin K metabolism, 2) decreasing menaquinone-4 (MK-4) synthesis from dietary phylloquinone (PK) and 3) potentiating vitamin K excretion through xenobiotic pathways. Two approaches were undertaken to evaluate the hypothesis that vitamin E increases vitamin K metabolism. In Aim 1.1, the in vitro omega-hydroxylation of vitamin K by human cytochrome P450 CYP4F2 (expressed in insect microsomes) was tested because CYP4F2 is considered the limiting step in the catabolism of both vitamins. Chapter 2 shows that CYP4F2 more rapidly hydroxylated vitamin K compared with vitamin E. Moreover, vitamin E did not stimulate vitamin K metabolism in vitro. Thus, it is unlikely vitamin E stimulates vitamin K metabolism in vivo by direct interaction with the CYP4F2 enzyme-substrate complex. In Aim 1.2, the in vivo urinary and biliary excretion of vitamin K metabolites was investigated. Chapter 3 shows that α-T-injected rats significantly increased urinary excretion of vitamin E catabolites, but no increases in urinary vitamin K catabolites were found. Chapter 4 shows that α-T-injected rats increased biliary excretion of 5C-aglycone, a major vitamin K catabolite shared by MK-4 and PK. However, the overall in vivo excretion of vitamin K catabolites was not changed when urinary excretion was also taken into account. Aim 2 evaluated the hypothesis that α-T interferes with the conversion of PK to MK-4 because α-T and PK have similar side-chains. In Aim 2.1, conversion of PK or MN to MK-4 was tested in vivo. Rats were fed semi-purified diets containing equimolar concentrations of either PK or MN for 10 days, then α-T injections were undertaken. Chapter 3 shows that extra-hepatic tissues from α-T injected rats contained significantly lower MK-4 concentrations irrespective of whether the rats were fed PK or MN. These findings show that if vitamin E is interfering with the metabolic mechanism of MK-4 synthesis, then it is not specific to the cleavage of PK's side chain. In Aim 2.2, conversion of deuterium-labeled PK (d₄-PK) to d₄-MK-4 was used to evaluate the extra-hepatic tissue uptake of d₄-PK in α-T-injected rats. Rats were fed semi-purified diets containing equimolar concentrations of d₄-PK similar to my previous study for 10 days then α-T injections were undertaken for 7 days. Chapter 5 shows that total (labeled and unlabeled) vitamin K concentrations decreased in extra-hepatic tissues from α-T injected rats fed d₄-PK. Both d₄-MK-4 and d₄-PK concentrations decreased, suggesting that MK-4 concentrations were dependent upon those of d₄-PK. These findings suggest that PK, and not MN, is the primary substrate for MK-4 synthesis in extra-hepatic tissues. Moreover, both d₄-MK-4 and d₄-PK decreased in α-T-injected rats demonstrating that vitamin E's untoward effect on vitamin K status is likely a mechanism that is shared by both vitamin K forms and not specific to MK-4 synthesis. Recycling of vitamin K from the epoxide was not examined in this study and interference with the recycling mechanism for either PK or MK-4 in α-T injected rats has not been examined. Vitamin E metabolism is greatly increased in α-T-injected rats by increasing various xenobiotic pathways. Thus, vitamin K status was hypothesized to decrease in α-T-injected rats as a result of the up-regulation of these pathways. As shown in Aim 1, urinary vitamin K metabolite excretion was not increased in α-T-injected rats. In Aim 3.1, the biliary excretion of vitamins E and K were examined to evaluate whether the increased expression in biliary transporters, such as MDR1, led to increased vitamin K and E excretion via the bile. Chapter 4 shows that α-T increased in bile over the week of vitamin E injections and α-CEHC was the major vitamin E form excreted in bile. Although biliary PK secretion was unchanged and biliary MK-4 was undetectable, increased excretion of a major catabolite of both PK and MK-4, 5C-aglycone, was observed. In Aim, 3.2, the gene expression of enzymes and transporters in liver and extra-hepatic tissues as mechanisms involved in regulating their concentrations in these tissues was assessed. In Chapters 3 and 5, increased expression of biliary transporters were observed, one of which is known to bind the vitamin K intermediate MN as its substrate. It is possible other vitamin K catabolites, in addition to 5C-and 7C-aglycone, may have been excreted that were unaccounted for, e.g. MN or vitamin K epoxide metabolites. In summary, my studies have shown vitamin K status is decreased in α-T-injected rats because PK and MK-4 concentrations are decreased in many extra-hepatic tissues. Although metabolism of vitamin K was not stimulated in response to α-T injections, increased excretion of a vitamin K catabolite was measured in the bile; however it may not account for all of the vitamin K loss observed in tissues. Alternatively, transport of PK and MN to extra-hepatic tissues or MK-4 recycling may have been inhibited in response to vitamin E. Further studies are needed to distinguish between these mechanisms. Graduation date: 2013