Subject(s)
Blood Donors , Blood Transfusion , Donor Selection , Heavy Metal Poisoning/etiology , Iatrogenic Disease , Metals, Heavy/adverse effects , Metals, Heavy/blood , Age Factors , Birth Weight , Child , Child, Preschool , Heavy Metal Poisoning/blood , Heavy Metal Poisoning/diagnosis , Humans , Infant , Infant, Extremely Low Birth Weight , Infant, Newborn , Risk Assessment , Risk FactorsABSTRACT
BACKGROUND: Prenatal toluene exposure can cause neurodevelopmental disabilities similar to fetal alcohol syndrome. Both share neuroanatomic pathologies similar to children with mutations in L1 cell adhesion molecule (L1). L1 mediates neurite outgrowth (NOG) via signaling through ERK1/2, which require trafficking of L1 through lipid rafts. Our objective is to determine if toluene inhibits L1-mediated NOG and toluene inhibits L1 signaling at concentrations achieved during occupational exposure. METHODS: Concentrations of toluene reflective of blood concentrations achieved in solvent abusers and occupational settings are used. Cerebellar granule neurons (CGN) harvested from postnatal day 6 rat pups are plated on coverslips coated with poly-L-lysine (PLL) alone or PLL followed by laminin. L1 is added to the media of CGN plated on PLL alone. Toluene is added 2 h after plating. Cells are fixed at 24 h and neurite length is measured. ERK1/2 activation by L1 in CGN is analyzed by immunoblot. RESULTS: Toluene significantly reduced mean neurite length of CGN exposed to L1 but not laminin. Toluene significantly reduced L1-mediated ERK1/2 phosphorylation. CONCLUSION: Results suggest that toluene inhibits L1-lipid raft interactions at occupationally relevant concentrations and may lead to a fetal solvent spectrum disorder similar to fetal alcohol spectrum disorder.
Subject(s)
Extracellular Signal-Regulated MAP Kinases/metabolism , Neural Cell Adhesion Molecule L1/metabolism , Neurites/drug effects , Toluene/adverse effects , Animals , Female , Laminin/metabolism , Maternal Exposure , Membrane Microdomains , Neurons/drug effects , Occupational Exposure/prevention & control , Phosphorylation , Pregnancy , Prenatal Exposure Delayed Effects , Rats , Rats, Sprague-DawleyABSTRACT
Children interact with the physical environment differently than adults, and are uniquely susceptible to environmental toxicants. Routes of absorption, distribution, metabolism, and target organ toxicities vary as children grow and develop. This article summarizes the sources of exposure and known adverse effects of toxicants that are ubiquitous in our environment, including tobacco smoke, ethanol, solvents, heavy metals, volatile organic compounds, persistent organic pollutants, and pesticides. Preventive strategies that may be used in counseling children and their families are highlighted.
Subject(s)
Disease Susceptibility , Environmental Exposure , Adolescent , Child , Child Development , Child, Preschool , Humans , Infant , Risk FactorsABSTRACT
INTRODUCTION: Resistance training is an effective method to decrease body fat (BF) and increase fat-free mass (FFM) and fat oxidation (FO). Dairy foods containing calcium and vitamin D might enhance these benefits. This study investigated the combined effects of habitual yogurt consumption and resistance training on body composition and metabolism. METHODS: Untrained women (N = 35) participated in an 8-wk resistance-training program. The yogurt group (Y) consumed 3 servings of yogurt containing vitamin D per day, and the control groups maintained their baseline low-dairy-calcium diet. Postexercise, Y consumed 1 of the 3 servings/d fat-free yogurt, the protein group consumed an isocaloric product without calcium or vitamin D, and the carbohydrate group consumed an isocaloric product without protein. Strength, body composition, fasted resting metabolic rate (RMR) and FO, and serum 25-hydroxyvitamin D were measured before and after training. RESULTS: Calories (kcal x kg-1 x d-1) and protein (g x kg-1 x d-1) significantly increased from baseline for Y. FFM increased (main effect p = .002) and %BF decreased (main effect .02) for all groups with training, but Group x Time interactions were not observed. RMR and FO did not change with training for any group. CONCLUSION: Habitual consumption of yogurt during resistance training did not augment changes in body composition compared with a low-dairy diet. Y decreased %BF as a result of training, however, even with increased calorie consumption.
Subject(s)
Adipose Tissue/metabolism , Basal Metabolism/physiology , Body Composition/physiology , Muscle, Skeletal/physiology , Resistance Training/methods , Yogurt , Adolescent , Adult , Body Composition/drug effects , Energy Intake/physiology , Female , Humans , Muscle, Skeletal/metabolism , Nutritional Physiological Phenomena/physiology , Nutritional Status , Young AdultABSTRACT
OBJECTIVE: The purpose of this study was to investigate the impact of dietary calcium or dairy product intake on total energy expenditure (TEE), fat oxidation, and thermic effect of a meal (TEM) during a weight loss trial. METHODS AND PROCEDURES: The intervention included a prescribed 500-kcal deficit diet in a randomized placebo-controlled calcium or dairy product intervention employing twenty-four 18 to 31-year-old (22.2+/-3.1 years, mean +/- s.d.) overweight women (75.5+/-9.6 kg). TEM and fat oxidation were measured using respiratory gas exchange after a meal challenge, and TEE was measured by doubly labeled water. Fat mass (FM) and lean mass (fat-free mass (FFM)) were measured by dual-energy X-ray absorptiometry. Subjects were randomized into one of these three intervention groups: (i) placebo (<800 mg/day calcium intake); (ii) 900 mg/day calcium supplement; (iii) three servings of dairy products/day to achieve an additional 900 mg/day. RESULTS: There were no group effects observed in change in TEE; however, a group effect was observed for fat oxidation after adjusting for FFM (P=0.02). The treatment effect was due to an increase in fat oxidation in the calcium-supplemented group of 1.5+/-0.6 g/h, P=0.02. Baseline 25-hydroxyvitamin D (25OHD) was positively correlated with TEM (R=0.31, P=0.004), and trended toward a correlation with fat oxidation (P=0.06), independent of group assignment. Finally, the change in log parathyroid hormone (PTH) was positively correlated with the change in trunk FM (R=0.27, P=0.03). DISCUSSION: These results support that calcium intake increases fat oxidation, but does not change TEE and that adequate vitamin D status may enhance TEM and fat oxidation.
Subject(s)
Calcium Carbonate/therapeutic use , Calcium, Dietary/therapeutic use , Dairy Products , Dietary Supplements , Energy Metabolism/drug effects , Lipid Metabolism/drug effects , Obesity/diet therapy , Overweight/diet therapy , Weight Loss/drug effects , Absorptiometry, Photon , Adult , Body Composition , Body Temperature Regulation/drug effects , Calcifediol/blood , Calorimetry, Indirect , Female , Humans , Obesity/metabolism , Overweight/metabolism , Oxidation-Reduction , Parathyroid Hormone/blood , Time Factors , Treatment Outcome , United StatesABSTRACT
The purpose of this study was to test the effect of acute dairy calcium intake on exercise energy metabolism and endurance performance. Trained female runners completed two trials. Each trial consisted of a 90-min glycogen depletion run followed by a self-paced 10K time trial, conducted one hour after consumption of a high dairy (500 mg Ca+2) or low dairy (80 mg Ca+2) meal. During the 90-min run, blood samples and respiratory gases were collected. No treatment main effects of acute dairy intake were found for respiratory exchange ratio (RER), calculated fat oxidation, lactate, glycerol, or 10K time. Following this protocol, acute dairy calcium intake did not alter fat utilization or endurance performance in trained female runners.
