bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anthropometric Indices and the Incidence of Hypertension: A Comparative Analysis
Authors: Fuchs Flávio D. , Gus Miguel , Moreira Leila B. , Moraes Renan S. , Wiehe Mário , Pereira Gérson M. , Fuchs Sandra C. 
Published: April 2008

AbstractObjective: To investigate the association between several anthropometric measurements of obesity with the incidence of hypertension.Research Methods and Procedures: Participants were 592 individuals free of hypertension, selected at random from the community. In the baseline evaluation, they were submitted to completed measures of demographics, anthropometrics, blood pressure, and other risk factors for hypertension. Incident hypertension was defined by blood pressure equal or higher than 140/90 mm Hg or use of blood pressure‐lowering drugs.Results: During a mean follow‐up time of 5.6 ± 1.1 years, 127 developed hypertension. The hazard ratios for the development of hypertension, adjusted for age, baseline blood pressure, gender, and alcohol consumption, were 1.042 (p = 0.091) for BMI, 1.023 (p = 0.028) for waist circumference, 1.042 (p = 0.013) for waist‐to‐height ratio, 1.061 (p = 0.014) for waist‐to‐height2 index, 1.079 (p = 0.022) for waist‐to‐height3 index, and 1.033 (p = 0.006) for the waist‐to‐hip ratio.Discussion: The correction of the circumference of waist for stature or hip circumference improves its performance in the prediction of the incidence of hypertension.
Adiponectin Levels during Low‐ and High‐Fat Eucaloric Diets in Lean and Obese Women
Authors: Berk Evan S. , Kovera Albert J. , Boozer Carol N. , Pi‐Sunyer F.X. , Johnson Julia A. , Albu Jeanine B. 
Published: April 2008

AbstractObjective: Adiponectin influences insulin sensitivity (SI) and fat oxidation. Little is known about changes in adiponectin with changes in the fat content of eucaloric diets. We hypothesized that dietary fat content may influence adiponectin according to an individual's SI.Research Methods and Procedures: We measured changes in adiponectin, insulin, glucose, and leptin in response to high‐fat (HF) and low‐fat (LF) eucaloric diets in lean (n = 10) and obese (n = 11) subjects. Obese subjects were further subdivided in relation to a priori SI.Results: We found significantly higher insulin, glucose, and leptin and lower adiponectin in obese vs. lean subjects during both HF and LF. The mean group values of these measurements, including adiponectin (lean, HF 21.9 ± 9.8; LF, 20.8 ± 6.6; obese, HF 10.0 ± 3.3; LF, 9.5 ± 2.3 ng/mL; mean ± SD), did not significantly change between HF and LF diets. However, within the obese group, the insulin‐sensitive subjects had significantly higher adiponectin during HF than did the insulin‐resistant subjects. Additionally, the change in adiponectin from LF to HF diet correlated positively with the obese subjects’ baseline SI.Discussion: Although in lean and obese women, group mean values for adiponectin did not change significantly with a change in fat content of a eucaloric diet, a priori measured SI in obese subjects predicted an increase in adiponectin during the HF diet; this may be a mechanism that preserves SI in an already obese group.
Cariporide Counteracts Atherosclerosis‐related Functions in Monocytes from Obese and Normal Individuals
Authors: Kaloyianni Martha , Zolota Zacharoula , Paletas Konstantinos , Tsapas Apostolos , Koliakos George 
Published: April 2008

AbstractObjective: This study aimed to show the effect of high glucose concentrations in combination with a pharmaceutical analog of the Na+/H+ antiport inhibitor, cariporide, on scavenger receptor CD36 expression, cell adhesion, and cell migration of human monocytes derived from obese and normal individuals.Research Methods and Procedures: Monocytes were isolated from six healthy obese individuals and six healthy age‐ and sex‐matched controls by use of whole blood Percoll sedimentation and plastic surface monocyte binding. The density of CD36 scavenger receptors on the surface of monocytes was assessed by the use of a fluorescent fluorescein isothiocyanate (FITC)‐linked monoclonal antibody. Transmigration of monocytes through laminin‐1–coated filters was performed on 5‐μm pore Transwell culture inserts. Monocyte attachment to laminin was estimated by a solid phase assay.Results: High glucose concentrations caused an increase in monocytes from normal and obese individuals in the expression of CD36 receptors and positively influenced monocyte migration and adhesion to laminin. Cariporide together with glucose counteracted these effects. The effects of migration and adhesion of monocytes to laminin were specific to glucose, because the effect was significantly higher when monocytes were incubated in the presence of 20 mM of glucose than in the presence of 20 mM of fructose. Monocytes from obese subjects showed greater response than in normal to all of the studied effects, with the highest response in laminin attachment.Discussion: The data of this study suggest that cariporide counteracts atherosclerosis‐related functions through Na+/H+ antiport inhibition in monocytes from both normal and obese individuals.
Familial Resemblance in Eating Behaviors in Men and Women from the Quebec Family Study
Authors: Provencher Véronique , Pérusse Louis , Bouchard Luigi , Drapeau Vicky , Bouchard Claude , Rice Treva , Rao D.C. , Tremblay Angelo , Després Jean‐Pierre , Lemieux Simone 
Published: April 2008

AbstractObjective: It is commonly recognized that genetic, environmental, behavioral, and social factors are involved in the development of obesity. The family environment may play a key role in shaping children's eating behaviors. The purpose of this study was to estimate the degree of familial resemblance in eating behavioral traits (cognitive dietary restraint, disinhibition, and susceptibility to hunger).Research Methods and Procedures: Eating behavioral traits were assessed with the Three‐Factor Eating Questionnaire in 282 men and 402 women (202 families) from the Quebec Family Study. Familial resemblance for each trait (adjusted for age, sex, and BMI) was investigated using a familial correlation model.Results: The pattern of familial correlation showed significant spouse correlation for the three eating behavior phenotypes, as well as significant parent‐offspring and sibling correlations for disinhibition and susceptibility to hunger. According to the most parsimonious model, generalized heritability estimates (including genetic and shared familial environmental effects) reached 6%, 18%, and 28% for cognitive dietary restraint, disinhibition, and susceptibility to hunger, respectively.Discussion: These results suggest that there is a significant familial component to eating behavioral traits but that the additive genetic component appears to be small, with generalized heritability estimates ranging from 6% to 28%. Thus, non‐familial environmental factors and gene‐gene and gene‐environmental interactions seem to be the major determinants of the eating/behavioral traits.
Dietary Patterns and the Metabolic Syndrome in Obese and Non‐obese Framingham Women**
Authors: Sonnenberg Lillian , Pencina Michael , Kimokoti Ruth , Quatromoni Paula , Nam Byung‐Ho , D'Agostino Ralph , Meigs James B. , Ordovas Jose , Cobain Mark , Millen Barbara 
Published: April 2008

AbstractObjectives: To examine the relationship between habitual dietary patterns and the metabolic syndrome (MetS) in women and to identify foci for preventive nutrition interventions.Research Methods and Procedures: Dietary patterns, nutrient intake, cardiovascular disease (CVD), and MetS risk factors were characterized in 1615 Framingham Offspring‐Spouse Study (FOS) women. Dietary pattern subgroups were compared for MetS prevalence and CVD risk factor status using logistic regression and analysis of covariance. Analyses were performed overall in women and stratified on obesity status; multivariate models controlled for age, apolipoprotein E (APOE) genotypes, and CVD risk factors.Results: Food and nutrient profiles and overall nutritional risk of five non‐overlapping habitual dietary patterns of women were identified including Heart Healthier, Lighter Eating, Wine and Moderate Eating, Higher Fat, and Empty Calories. Rates of hypertension and low high‐density lipoprotein levels were high in non‐obese women, but individual MetS risk factor levels were substantially increased in obese women. Overall MetS risk varied by dietary pattern and obesity status, independently of APOE and CVD risk factors. Compared with obese or non‐obese women and women overall with other dietary patterns, MetS was highest in those with the Empty Calorie pattern (contrast p value: p < 0.05).Discussion: This research shows the independent relationship between habitual dietary patterns and MetS risk in FOS women and the influence of obesity status. High overall MetS risk and the varying prevalence of individual MetS risk factors in female subgroups emphasize the importance of preventive nutrition interventions and suggest potential benefits of targeted behavior change in both obese and non‐obese women by dietary pattern.
Dietary Fat Intake and Insulin Resistance in Black and White Children
Authors: Weigensberg Marc J. , Ball Geoff D.C. , Shaibi Gabriel Q. , Cruz Martha L. , Gower Barbara A. , Goran Michael I. 
Published: April 2008

AbstractObjective: The purpose of this study was to determine whether dietary fat intake above current Acceptable Macronutrient Distribution Range (AMDR) guidelines was associated with greater insulin resistance in black and white children.Research Methods and Procedures: We studied 142 healthy children (n = 81 whites, n = 61 blacks), 6.5 to 14 years old. Dietary composition was determined by repeated 24‐hour dietary recall, body composition by DXA, visceral fat by computed tomography, and insulin sensitivity (SI) and acute insulin response to glucose (AIRg) by frequently sampled intravenous glucose tolerance test. Subjects were categorized by ethnicity (white/black) and dietary fat intake (above‐AMDR/within‐AMDR guidelines), and differences were analyzed by 2 × 2 analysis of covariance, adjusting for covariates.Results: After adjusting for total body fat, gender, and Tanner stage, subjects consuming dietary fat above AMDR intake guidelines had lower SI and higher AIRg. This effect was specific to black children (32% lower SI and 62% higher AIRg in above‐AMDR compared with within‐AMDR blacks) and was not seen in whites.Discussion: In black, but not white, children, those with dietary fat intake above current AMDR guidelines had lower SI and higher AIRg than those who met AMDR guidelines. These findings support current AMDR guidelines for dietary fat in black children and adolescents. The mechanism(s) underlying the ethnic differences in the relationship between dietary fat intake and SI in children require further investigation.
Urinary F2‐Isoprostanes Are Not Associated with Increased Risk of Type 2 Diabetes
Authors: Il'yasova Dora , Morrow Jason D. , Wagenknecht Lynne E. 
Published: April 2008

AbstractObjective: Free radicals have been implicated in the etiology of type 2 diabetes. Cross‐sectional studies have demonstrated associations between oxidative damage and type 2 diabetes. However, no prospective data on this association are available.Research Methods and Procedures: A case control study was conducted within the prospective cohort of the Insulin Resistance Atherosclerosis Study: 26 cases who developed type 2 diabetes in the follow‐up period and 26 controls who remained free of type 2 diabetes were randomly selected. Oxidative status was assessed by measuring 2, 3‐dinor‐5, 6‐dihydro‐15‐F2t‐isoprostane (F2‐IsoPM) in baseline urine samples using gas chromatography/mass spectroscopy. Type 2 diabetes was defined by serial oral glucose tolerance tests and World Health Organization criteria.Results: Urinary F2‐IsoPM varied between 0.18 and 2.60 ng/mg creatinine; 25th/50th/75th percentiles were 0.42, 0.60, and 0.89, respectively. A trend toward higher levels were observed in women and in persons with impaired glucose tolerance at baseline (p= 0.1). F2‐IsoPM increased with BMI (r= 0.36,p= 0.01). After adjustment for age, gender, baseline impaired glucose tolerance status, and BMI, F2‐IsoPM levels were inversely associated with development of type 2 diabetes: odds ratio = 0.32 (95% confidence interval, 0.12 to 0.81) for the difference between the 75th and 25th percentiles.Discussion: These results suggest that oxidative damage is not a cause of type 2 diabetes. Positive cross‐sectional associations of F2‐IsoPM with the risk factors for diabetes, BMI, and impaired glucose tolerance and inverse associations with development of type 2 diabetes indicate that F2‐IsoPM might reflect a compensatory mechanism.
Low‐ and High‐Carbohydrate Diets: Body Composition Differences in Rats
Authors: McNeel Ronald L. , Mersmann Harry J. 
Published: April 2008

AbstractObjective: To determine differences in adipose tissue mass, cell size, and lipid metabolism transcripts and differences in composition of body weight loss and energy expenditure (EE) after isoenergetic, energy‐restricted intake of low‐carbohydrate/high‐fat/high‐protein (LC) and high‐carbohydrate/low‐fat/moderate‐protein (HC) diets.Research Methods and Procedures: Ten‐week old female Sprague‐Dawley rats were fed a high‐fat diet ad libitum for 8 weeks to induce weight gain and fat deposition. Weight‐matched rats were then assigned to isoenergetic LC (Atkins) and HC (American Dietary Association Exchange) diets for 10 weeks at 65% of ad libitum energy intake.Results: There was no significant difference in the serum lipid profiles or amount of body weight lost between the HC and LC groups, whereas a higher insulin sensitivity index (p < 0.01) resulted from the HC compared with the LC diet. Compared with the post‐restriction LC group, the HC group demonstrated (p < 0.05) higher EE during active hours, lower mRNA levels for the lipogenic genes peroxisome proliferator‐activated receptor γ2, lipoprotein lipase, and, adipocyte fatty acid binding protein, decreased adipocyte cell volume, and decreased fat mass.Discussion: Results indicated down‐regulation of lipogenic genes, decreased fat mass, and, therefore, improved body composition in the post‐restriction HC compared with the LC group. The small mean differences between the two diet groups (p = 0.11) in 24‐hour EE over the 10 weeks of diet intervention would account for the majority of the lower mean body weights in the post‐restriction HC group. These data suggest that macronutrient composition of the diet influences body composition and indicate a distinction between HC and LC diets.
Hyperphagia and Obesity in Na,K‐ATPase α2 Subunit‐Defective Mice
Authors: Kawakami Kiyoshi , Onaka Tatsushi , Iwase Michiko , Homma Ikuo , Ikeda Keiko 
Published: April 2008

AbstractObjective: The Na,K‐ATPase α2 subunit gene (Atp1a2) is expressed in the brain, skeletal muscles, heart, and adipocytes. Specific function of the α2 subunit, such as involvement in differentiation and function of adipocytes, has not been addressed. The aim of this study was to examine whether Atp1a2‐defective heterozygous mice show obesity and reveal the mechanisms underlying the obesity.Research Methods and Procedures: We measured the differentiation and glucose uptake function of in vitro‐differentiated adipocytes derived from embryonic fibroblasts of Atp1a2‐defective mice. Food intake, body temperature, metabolic rate, and spontaneous activity and mRNA levels of neuropeptide genes were compared between the heterozygous and wild‐type adult mice.Results: Atp1a2 heterozygous female mice developed obesity after middle age. The time course of in vitro adipocyte differentiation of embryonic fibroblasts isolated from wild type, heterozygous, and homozygous mice was not different, glucose and Rb uptake activities of the in vitro‐differentiated adipocytes were not altered, and the effects of insulin on glucose uptake and those of monensin and ouabain on Rb uptake were similar among the genotypes. However, food intake in the light phase was significantly greater in the heterozygous mice than the wild type in the 24‐hour dark‐light cycle, whereas it was similar under constant‐light condition. Body temperature, metabolic rate at rest, and spontaneous motor activity of the heterozygous mice were similar to those of the wild type. Orexin mRNA level was lower in heterozygous than wild‐type mice.Discussion: The Na,K‐ATPase α2 subunit is not involved in the differentiation or in glucose and Rb uptake function of in vitro‐differentiated adipocytes. Hyperphagia is the likely primary cause of obesity in Atp1a2 heterozygous mice.
Altered Hypothalamic Signaling and Responses to Food Deprivation in Rats Fed a Low‐Carbohydrate Diet
Authors: Kinzig Kimberly P. , Scott Karen A. , Hyun Jayson , Bi Sheng , Moran Timothy H. 
Published: April 2008

AbstractObjective: To model how consuming a low‐carbohydrate (LC) diet influences food intake and body weight.Research Methods and Procedures: Food intake and body weight were monitored in rats with access to chow (CH), LC‐high‐fat (HF), or HF diets. After 8 weeks, rats received intracerebroventricular injections of a melanocortin agonist (melanotan‐II) and antagonist (SHU9119), and feeding responses were measured. At sacrifice, plasma hormones and hypothalamic expression of mRNA for proopiomelanocortin (POMC), melanocortin‐4 receptor, neuropeptide Y (NPY), and agouti related protein (AgRP) were assessed. A second set of rats had access to diet (chow or LC‐HF) for 4 weeks followed by 24 h food deprivation on two occasions, after which food intake and hypothalamic POMC, NPY, and AgRP mRNA expression were measured.Results: HF rats consumed more food and gained more weight than rats on CH or LC‐HF diets. Despite similar intakes and weight gains, LC‐HF rats had increased adiposity relative to CH rats. LC‐HF rats were more sensitive to melanotan‐II and less sensitive to SHU9119. LC‐HF rats had increased plasma leptin and ghrelin levels and decreased insulin levels, and patterns of NPY and POMC mRNA expression were consistent with those of food‐deprived rats. LC‐HF rats did not show rebound hyperphagia after food deprivation, and levels NPY, POMC, and AgRP mRNA expression were not affected by deprivation.Discussion: Our results demonstrate that an LC diet influences multiple systems involved in the controls of food intake and body weight. These data also suggest that maintenance on an LC‐HF diet affects food intake by reducing compensatory responses to food deprivation.
The Association between Plasma Adiponectin and Insulin Sensitivity in Humans Depends on Obesity
Authors: Kantartzis Konstantinos , Fritsche Andreas , Tschritter Otto , Thamer Claus , Haap Michael , Schäfer Silke , Stumvoll Michael , Häring Hans‐Ulrich , Stefan Norbert 
Published: April 2008

AbstractObjective: In humans, low plasma adiponectin concentrations precede a decrease in insulin sensitivity and predict type 2 diabetes independently of obesity. However, it is possible that the contribution of adiponectin to insulin sensitivity is not equally strong over the whole range of obesity.Research Methods and Procedures: We investigated the cross‐sectional association between plasma adiponectin levels and insulin sensitivity in different ranges of body fat content [expressed as percentage of body fat (PFAT)] in a large cohort of normal glucose‐tolerant subjects (n = 900). All individuals underwent an oral glucose tolerance test (OGTT), and 299 subjects additionally a euglycemic hyperinsulinemic clamp. In longitudinal analyses, the association of adiponectin at baseline with change in insulin sensitivity was investigated in a subgroup of 108 subjects.Results: In cross‐sectional analyses, the association between plasma adiponectin and insulin sensitivity, adjusted for age, gender, and PFAT, depended on whether subjects were lean or obese [p for interaction adiponectin × PFAT = <0.001 (OGTT) and 0.002 (clamp)]. Stratified by quartiles of PFAT, adiponectin did not correlate significantly with insulin sensitivity in subjects in the lowest PFAT quartile (R2 = 0.10, p = 0.13, OGTT; and R2 = 0.10, p = 0.57, clamp), whereas the association in the upper PFAT quartile was rather strong (R2 = 0.36, p < 0.0001, OGTT; and R2 = 0.48, p = 0.003, clamp). In longitudinal analyses, plasma adiponectin at baseline preceded change in insulin sensitivity in obese (n = 54, p = 0.03) but not in lean (n = 54, p = 0.68) individuals.Discussion: These data suggest that adiponectin is especially critical in sustaining insulin sensitivity in obese subjects. Thus, interventions to reduce insulin resistance by increasing adiponectin concentrations may be effective particularly in obese, insulin‐resistant individuals.
Low 25‐Hydroxyvitamin D Does Not Affect Insulin Sensitivity in Obesity after Bariatric Surgery
Authors: Manco Melania , Calvani Menotti , Nanni Giuseppe , Greco Aldo V. , Iaconelli Amerigo , Gasbarrini Giovanni , Castagneto Marco , Mingrone Geltrude 
Published: April 2008

AbstractObjective: A positive correlation between levels of 25‐hydroxyvitamin D [25(OH)D] and insulin sensitivity has been shown in healthy subjects. We aimed to test the hypothesis that concentration of 25(OH)D influences insulin sensitivity in obesity before and after weight loss.Research Methods and Procedures: We investigated the relation between serum 25(OH)D and insulin sensitivity (estimated by euglycemic‐hyperinsulinemic clamp) in 116 obese women (BMI ≥ 40 kg/m2) evaluated before and 5 and 10 years after biliopancreatic diversion (BPD). Body composition was estimated by the isotope dilution method.Results: Prevalence of hypovitaminosis D was 76% in the obese status and 91% and 89% at 5 and 10 years after BPD, respectively, despite ergocalciferol supplementation. 25(OH)D concentration decreased from 39.2 ± 22.3 in obesity (p = 0.0001) to 27.4 ± 16.4 and 25.1 ± 13.9 nM 5 and 10 years after BPD, respectively. Whole‐body glucose uptake increased from 24.27 ± 4.44 at the baseline to 57.29 ± 11.56 and 57.71 ± 8.41 μmol/kgfat free mass per minute 5 and 10 years after BPD, respectively (p = 0.0001). Predictor of 25(OH)D was fat mass (R2 = 0.26, p = 0.0001 in obesity; R2 = 0.20, p = 0.02 after BPD). Parathormone correlated with fat mass (R2 = 0.19; p = 0.0001) and BMI (R2 = 0.053; p = 0.01) and inversely with M value (R2 = 0.16; p = 0.0001), but only in obese subjects.Discussion: A high prevalence of hypovitaminosis D was observed in morbid obesity both before and after BPD. Low 25(OH)D did not necessarily imply increased insulin resistance after BPD, a condition where, probably, more powerful determinants of insulin sensitivity overcome the low circulating 25(OH)D levels. However, the present data cannot exclude some kind of influence of vitamin D status on glucose and insulin metabolism.