bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stunting at 2 Years in Relation to Body Composition at 9 Years in African Urban Children**
Authors: Cameron Noël , Wright Melanie M. , Griffiths Paula L. , Norris Shane A. , Pettifor John M. 
Published: April 2008

AbstractObjective: To determine whether African urban children who were stunted at 2 years of age demonstrated an altered body composition by the end of childhood, before entering puberty, at 9 years of age.Research Methods and Procedures: This was a mixed‐longitudinal study of 330 prepubertal African children (182 boys) from Soweto‐Johannesburg, South Africa. Anthropometric data at 2 years of age were compared with anthropometric, DXA‐determined body composition and fat patterning in late childhood (7 to 9 years).Results: Children who had been stunted at 2 years were significantly shorter and lighter than non‐stunted children at 7 to 9 years, but there were no differences in their BMI or centralization of body fat. Previously stunted status significantly predicted reduced weight and height at 7 to 9 years but did not predict BMI, body composition, or fat patterning after controlling for potential confounding factors. The odds ratio for stunting at 2 years as a predictor of overweight at 7 to 9 years was not significant at 1.09 (95% confidence limits: 0.30, 3.98).Discussion: Greater BMI in stunted infants does not demonstrate a tendency toward overweight or obesity but is a reflection of the greater reduction in height rather than weight in stunted children. Stunted children may be programmed to accumulate greater body fat at central sites during adolescence, but we have been unable to show that these changes are evident before the initiation of pubertal development.
Identifying the Energy Gap: Magnitude and Determinants of 5‐Year Weight Gain in Midage Women
Authors: Brown Wendy J. , Williams Lauren , Ford Jessica H. , Ball Kylie , Dobson Annette J. 
Published: April 2008

AbstractObjective: The aims of this study were to estimate average yearly weight gain in midage women and to identify the determinants of weight gain and gaining weight at double the average rate.Research Methods and Procedures: The study sample comprised 8071 participants (45 to 55 years old) in the Australian Longitudinal Study on Women's Health who completed mailed surveys in 1996, 1998, and 2001.Results: On average, the women gained almost 0.5 kg per year [average 2.42 kg (95% confidence interval, 2.29 to 2.54) over 5 years]. In multivariate analyses, variables associated with energy balance (physical activity, sitting time, and energy intake), as well as quitting smoking, menopause/hysterectomy, and baseline BMI category were significantly associated with weight gain, but other behavioral and demographic characteristics were not. After adjustment for all of the other biological and behavioral variables, the odds of gaining weight at about twice the average rate (>5 kg over 5 years) were highest for women who quit smoking (odds ratio = 2.94; 95% confidence interval, 2.17, 3.96). There were also independent relationships between the odds of gaining >5 kg and lower levels of habitual physical activity, more time spent sitting, energy intake (but only in women with BMI > 25 at baseline), menopause transition, and hysterectomy.Discussion: The average weight gain equates with an energy imbalance of only about 10 kcal or 40 kJ per day, which suggests that small sustained changes in the modifiable behavioral variables could prevent further weight gain.
Corticosteroid Binding Globulin Gene Polymorphism Influences Cortisol Driven Fat Distribution in Obese Women
Authors: Barat Pascal , Duclos Martine , Gatta Blandine , Roger Patrick , Mormede Pierre , Moisan Marie‐Pierre 
Published: April 2008

AbstractHypothalamo‐pituitary‐adrenal axis has been reported to influence fat mass distribution in obesity. We investigated the hypothesis that corticosteroid‐binding globulin (CBG) polymorphism could influence obesity, metabolic, or hypothalamo‐pituitary adrenal (HPA) axis activity parameters. In 44 obese pre‐menopausal women, a microsatellite located within the CBG gene was analyzed, providing three genotypes: 86/86 (n = 29), 86/90 (n = 14), and 90/90 (n = 1). No significant difference was found for obesity, metabolic, and HPA axis activity parameters between the genotypes 86/86 and 86/90. Looking for differences in correlations between HPA axis activity parameters and obesity or metabolic parameters between the two genotypes, genotype 86/90 showed a strong correlation between salivary cortisol after dexamethasone (0.25 mg) suppression test and waist‐to‐hip ratio (r = −0.84, p = 0.0007), whereas this correlation was weaker for genotype 86/86 (r = −0.34, p = 0.09). These data were completed with an analysis of the BclI polymorphism of the glucocorticoid receptor (GR) gene. There was an association between this GR polymorphism and both awakening salivary cortisol and postdexamethasone salivary cortisol but no association for obesity or metabolic parameters. We concluded that CBG gene polymorphisms might modulate the influence of the HPA axis on the fat mass distribution in this population.
Effects of Interaction between Angiotensin I‐Converting Enzyme Polymorphisms and Lifestyle on Adiposity in Adolescent Greeks
Authors: Moran Colin N. , Vassilopoulos Christos , Tsiokanos Athanasios , Jamurtas Athanasios Z. , Bailey Mark E.S. , Wilson Richard H. , Pitsiladis Yannis P. 
Published: April 2008

AbstractGenetic variation in the human angiotensin I‐converting enzyme (ACE) gene has been associated with many heritable traits, including obesity. Herein, we report the results of a study of obesity‐related phenotypes and lifestyle in 1016 teen‐aged Greeks. We show that there is a strong association (p = 0.001) between subcutaneous fat and the ACE insertion/deletion (I/D) polymorphism in females, possession of genotypes containing the D allele being associated with increased fat thickness. This association is strongest in females who participate in no extra exercise and accounts for 6.5% of the phenotypic variance in fat thickness by ANOVA. The association is additive, with the mean phenotypic values in heterozygotes intermediate between the means of the two homozygotes, and the association acts at both extremes of the fat thickness distribution in a classical polygenic manner. Other ACE polymorphisms (rs4424958, rs4311) that define major haplotypes in European populations fail to provide stronger associations with the subcutaneous fat phenotype. Because ACE I/D is the polymorphism most strongly associated with circulating ACE levels in European populations, we propose that the functional allelic differences that influence circulating ACE levels also mediate the associations with the obesity‐related phenotypes studied here.
Treatment of Morbid Obesity in Low‐income Adolescents: Effects of Parental Self‐monitoring
Authors: Kirschenbaum Daniel S. , Germann Julie N. , Rich Barry H. 
Published: April 2008

AbstractObjective: This study examined the extent to which consistency of self‐monitoring by participants and their parents was related to weight control over an initial period of 3 months within the context of a treatment program for morbidly obese low‐income minority adolescents.Research Methods and Procedures: Eighty‐three obese adolescents (mean age, 13.0 years; 51% boys; 92% African American; mean BMI, 43.0 kg/m2; mean BMI z‐score, 6.0) and at least one parent participated in a long‐term treatment program that included a very‐low‐fat dietary focus, weekly group cognitive‐behavior therapy, monthly nutrition education classes, a 12‐week physical therapy class, and medical monitoring.Results: Participants who self‐monitored on the majority of days compared with those who did not self‐monitor at all or who self‐monitored infrequently attended more sessions and generally lost more weight over the first 3 months. Although parents signed behavioral contracts committing to self‐monitor their own eating and exercising over the first month, only 12% did so. Nonetheless, participants whose parents self‐monitored were much more likely to self‐monitor consistently and lose weight during the first 3 months.Discussion: These results indicate that self‐monitoring is a cornerstone of successful weight control even for morbidly obese low‐income minority adolescents; targeting consistency of self‐monitoring among these high‐risk weight controllers and their parents should be just as important as it is for more affluent and less overweight adolescents.
Sensitivity of ob/ob Mice to Leptin‐Induced Adipose Tissue Apoptosis
Authors: Della‐Fera Mary Anne , Choi Yang‐Ho , Hartzell Diane L. , Duan Juihua , Hamrick Mark , Baile Clifton A. 
Published: April 2008

AbstractObjective: ob/ob mice have increased sensitivity to many of leptin's effects. The primary objective of this experiment was to determine whether ob/ob mice demonstrated increased sensitivity to leptin‐induced adipose tissue apoptosis.Research Methods and Procedures: Fifteen‐week‐old female ob/ob and Ob/? mice received 0 (saline), 2.5, or 10 μg/d leptin for 14 days through subcutaneous (sc) osmotic minipumps. Food intake (FI), body temperature, physical activity, and body weight were measured daily. Body composition and weights and adipose tissue apoptosis (percentage DNA fragmentation) of inguinal, parametrial, and retroperitoneal fat pads were determined at the end of the study.Results: FI decreases were more pronounced in ob/ob. Leptin (10 μg/d) decreased total FI 71% in ob/ob and 34% in Ob/? (p < 0.05). Body weight was decreased by both doses of leptin in ob/ob (p < 0.01) but was unchanged in Ob/?. Leptin increased body temperature in ob/ob but not in Ob/?. Physical activity was increased 400% by 10 μg/d leptin in ob/ob (p < 0.01) but decreased 13% in Ob/? (p < 0.01). Body fat content of ob/ob was reduced by both leptin doses, whereas only 10 μg/d leptin decreased body fat in Ob/?. Fat pad weights were decreased similarly by leptin in both genotypes. However, apoptosis was increased by leptin in all three fat pads in ob/ob, whereas Ob/? showed significant increases only in retroperitoneal.Discussion: ob/ob mice had greater overall sensitivity to leptin. Although ob/ob mice appeared to be more sensitive than Ob/? mice to leptin‐induced adipose tissue apoptosis, there were differences among adipose depots in responsiveness to leptin‐induced apoptosis.
Low Recognition of Childhood Overweight and Disease Risk among Native‐American Caregivers**
Authors: Adams Alexandra K. , Quinn Rachel A. , Prince Ronald J. 
Published: April 2008

AbstractObjectives: Pediatric obesity is a significant and increasing problem in Native‐American communities. The aim of this study was to determine whether parents and other caregivers from three Wisconsin tribes recognized overweight children. We also assessed caregiver attributes associated with levels of concern for risk of future overweight and chronic disease.Research Methods and Procedures: Data were obtained from child health screenings and caregiver surveys. Participants included 366 kindergarten‐through‐second grade child–caregiver dyads. Children's BMI percentiles were calculated and compared with caregiver responses. We assessed the relationships between predictors of caregiver concern for health risk factors and recognition of overweight.Results: Twenty‐six percent of children were overweight (≥95th percentile), and 19% were at risk for being overweight (≥85th to <95th percentile) using Centers for Disease Control standards. Caregivers recognized only 15.1% of overweight children. Factors predictive of child overweight recognition included a child BMI >99th percentile and grandmother as caregiver. Overall, caregivers were more concerned about diabetes and cardiovascular disease than obesity. Parents with diabetes and heart disease were more concerned than others about risk for these diseases; however, only diabetic parents made a connection between child weight status and future risk of obesity‐related disease. Child sex, child age, and parental education level were not significant predictors for caregiver recognition of an overweight child.Discussion: Most caregivers did not recognize overweight children or associate excess weight with increased risk of disease. When designing community interventions, it is crucial to incorporate caregivers’ attitudes and beliefs regarding childhood overweight and risk of future disease.
Contribution of Different Mechanisms to Compensation for Energy Restriction in the Mouse
Authors: Hambly Catherine , Speakman John R. 
Published: April 2008

AbstractObjective: Restriction of energy intake produces weight loss, but the rate of loss is seldom sustained. This is presumed to be a consequence of compensatory reductions in energy expenditure, although the exact contributions of different components to the energy budget remain uncertain. We examined the compensatory responses of mice to a 20% dietary restriction.Research Methods and Procedures: We measured body mass, body fatness, body temperature, and the components of daily energy expenditure for 50 MF1 mice. Forty mice were then placed on a restricted diet at 80% of their ad libitum intake for 50 days. The remaining 10 mice continued to feed ad libitum. Ten days before the end of the restriction period, the same measurements were taken.Results: There were no significant differences between the control and restricted groups in any parameters before restriction. During the restriction period, body mass increased in both the control and restricted groups, but at a slower rate in the restricted mice. The control group increased in both fat and fat free mass; however, although the restricted group increased fat to the same extent as the controls, fat free mass increased to a lesser extent. The contributions of the different components of the expended energy to compensate for the reduced energy intake were energy deposition, 2.2%; resting metabolic rate, 22.3%; and activity, 75.5%.Discussion: Mice were able to compensate almost completely for the restricted energy intake that was achieved by altering the amount of energy required for each component of the energy budget except digestive efficiency.
Retrograde Gastric Electrical Stimulation Reduces Food Intake and Weight in Obese Rats
Authors: Yin Jieyun , Chen Jiande D.Z. 
Published: April 2008

AbstractObjective: To investigate the therapeutic potential of retrograde gastric electrical stimulation (RGES) for obesity in a rodent model of obesity.Research Methods and Procedures: The study was performed in 12 obese Zucker rats implanted with two pairs of gastric serosal electrodes, one pair for stimulation and the other for recording intrinsic gastric myoelectrical activity. It was composed of an acute study in three sessions to study the effect of RGES on intrinsic gastric myoelectrical activity and acute food intake and a chronic phase to study the short‐term effect of RGES on weight. RGES was performed through the distal stomach using long pulses at a frequency of tachygastria (known to induce gastric hypomotility).Results: RGES completely entrained intrinsic gastric myoelectrical activity and turned it into tachygastria at a certain strength. RGES reduced acute food intake compared with the control (p < 0.01). A 2‐week treatment of RGES resulted in a significant reduction in food intake (p = 0.002) and a significantly greater weight loss than sham stimulation (p = 0.004).Discussion: RGES at a tachygastrial frequency reduces food intake and results in weight loss in obese Zucker rats, and its effect is probably attributed to the introduction of tachygastria in the stomach.
Mapping Quantitative Trait Loci Affecting Variation in Drosophila Triacylglycerol Storage
Authors: De Luca Maria , Yi Nengjun , Allison David B. , Leips Jeff , Ruden Douglas M. 
Published: April 2008

AbstractObjective: Recent genetic studies indicate that Drosophila melanogaster could be a powerful model to identify genes involved in mammalian adipocyte differentiation and fat storage. The objective of our study was to identify quantitative trait loci (QTLs) that contribute to variation in triacylglycerol (TAG) storage in two D. melanogaster laboratory strains.Research Methods and Procedures: We used two genetic mapping procedures to identify loci with main and epistatic effects on TAG storage. First, using 68 recombinant inbred lines derived from the unrelated Oregon R and Russian 2b strains, we mapped the location of QTLs affecting TAG storage using both composite interval mapping and Bayesian epistatic methods. Second, we used the quantitative deficiency mapping procedure to identify candidate genes affecting this trait within one of the QTLs identified on the second chromosome. For both mapping experiments, flies were cultured in standard conditions. TAG content of 4‐ to 5‐day‐old flies, adjusted for live body mass and total proteins, was used as the phenotypic measure.Results: Multiple QTLs associated with variation in TAG storage were identified by the genome‐wide recombination mapping method, and some of them were sex‐specific. The QTLs had main effects, but a male‐specific epistatic interaction between two QTLs was also found. Finally, two closely linked QTLs were detected by deficiency mapping at 57E1‐57E3 and 57E4‐57F1 on chromosome 2, the first of which causes female‐specific variation in TAG between the Oregon R and 2b strains.Discussion: Our results suggest that variation in TAG storage in D. melanogaster is controlled by different genetic mechanisms and different sets of QTLs in male and female flies.
A Common β2‐Adrenoceptor Gene Haplotype Protects against Obesity in Swedish Women
Authors: Jiao Hong , Dahlman Ingrid , Eriksson Per , Kere Juha , Arner Peter 
Published: April 2008

AbstractThe β2‐adrenoceptor gene may be of particular importance for human obesity because catecholamines have a central role in energy expenditure both as neurotransmitters and hormones. The gene is highly polymorphic, and individual polymorphisms have previously been examined for their relationship to obesity, but results are conflicting. We performed a haplotype analysis of the β2‐adrenoceptor gene in 1354 women and 421 men, all healthy and at least second generation Scandinavian and with a large interindividual variation in body fat mass. We found three common haplotypes. One of these haplotypes, identified as T, A, C, C at nucleotide positions −47, 46, 79, and 491, was in its homozygote form more common among lean (18%) than obese (13%) women (p = 0.0028), but there was no association with obesity in men (p = 0.47). Women who were homozygous for this haplotype had lower BMI (p = 0.009) and percentage body fat (p = 0.005) in comparison with those having other haplotypes or being heterozygous for TACC. The data suggest an important role of the β2‐adrenoceptor gene in obesity because a common haplotype has recessive protective effects against excess body fat, at least in women.
Mediating Effects of Inflammatory Biomarkers on Insulin Resistance Associated with Obesity
Authors: Wexler Deborah J. , Hu Frank B. , Manson JoAnn E. , Rifai Nader , Meigs James B. 
Published: April 2008

AbstractObjective: Obesity is associated with elevated levels of biomarkers of inflammation and endothelial dysfunction [including C‐reactive protein (CRP), E‐selectin, and intercellular adhesion molecule‐1], as well as insulin resistance (IR) and type 2 diabetes. We tested the hypothesis that these biomarkers mediate associations among obesity, IR, and risk of diabetes.Research Methods and Procedures: We stratified 510 initially non‐diabetic women in the Nurses’ Health Study cohort into four phenotypes above/below median BMI (27 kg/m2) and waist circumference (81 cm): low BMI‐low waist (LBLW; N = 190), low BMI‐high waist (LBHW; N = 74), high BMI‐low waist (HBLW; N = 27), and high BMI‐high waist (HBHW; N = 219).Results: In models assessing associations of weight phenotype with IR [fasting insulin (FI)], adjusted for age and diabetes risk factors, mean FI was higher comparing HBHW women (13.6 μU/mL, p < 0.0001) and LBHW (11.5 μU/mL, p = 0.02) with LBLW women (8.6 μU/mL); HBLW and LBLW women were not significantly different. Differences in FI levels were most strongly attenuated after adjustment for E‐selectin comparing LBHW with LBLW women (11.7 vs. 9.7 μU/mL, p = 0.2).Discussion: In logistic regression models, LBHW predicted diabetes (risk factor‐adjusted relative risk 2.06, 1.05 to 6.40), compared with LBLW, but was no longer significant after adjustment for E‐selectin or CRP. After adjusting for CRP and E‐selectin, only HBHW and E‐selectin were significantly associated with risk of diabetes. In women with central adiposity and low BMI, endothelial dysfunction and inflammation may mediate the relationship among central fat, IR, and incident diabetes.
Opposite Contributions of Trunk and Leg Fat Mass with Plasma Lipase Activities: The Hoorn Study
Authors: Bos Griët , Snijder Marieke B. , Nijpels Giel , Dekker Jacqueline M. , Stehouwer Coen D.A. , Bouter Lex M. , Heine Robert J. , Jansen Hans 
Published: April 2008

AbstractObjective: Lipoprotein lipase (LPL) and hepatic lipase (HL) are essential in hydrolysis of triglyceride‐rich lipoproteins. LPL activity is negatively, whereas HL activity is positively, associated with total body fat. We determined the associations of trunk and leg fat mass with plasma LPL and HL activities in a cross‐sectional study.Research Methods and Procedures: LPL and HL activities were determined in post‐heparin plasma in a sample of 197 men and 209 women, 60 to 87 years of age. A total body DXA scan was performed to determine trunk and leg fat mass.Results: In women, but not in men, trunk fat mass was negatively associated with LPL activity, whereas leg fat mass was positively associated, after mutual adjustment and adjustment for age. Standardized βs (95% confidence interval) for trunk and leg fat mass were −0.24 (−0.41; −0.08) and 0.14 (−0.02; 0.31), respectively (interaction by sex, p = 0.03). Larger trunk fat mass was associated with higher HL activity in men [0.48 (0.28; 0.68)] and women [0.40 (0.24; 0.56)]. A negative association of leg fat mass and HL activity was observed in men, although not statistically significant [−0.13 (−0.33; 0.06)], and in women [−0.28 (−0.38; −0.18)].Discussion: Abdominal fat is associated with unfavorable and femoral fat with favorable LPL and HL activities in plasma.
Evaluation of Prader‐Willi Syndrome Gene MAGEL2 in Severe Childhood‐Onset Obesity
Authors: O'Neill Megan A. , Farooqi I. Sadaf , Wevrick Rachel 
Published: April 2008

AbstractMAGEL2 is one of the five genes inactivated in Prader‐Willi Syndrome, a neurodevelopmental chromosome microdeletion disorder modified by genomic imprinting. By early childhood, individuals with Prader‐Willi Syndrome exhibit hypothalamic dysfunction, including hyperphagia, and become obese in the absence of behavioral intervention. Murine Magel2 is highly expressed in the hypothalamus during development. We screened the MAGEL2 open reading frame for mutations in genomic DNA samples from hyperphagic but non‐dysmorphic individuals with severe childhood‐onset obesity. Although no mutations likely to affect gene function were identified, we identified three variant alleles. We conclude that severe childhood‐onset obesity is not commonly caused by MAGEL2 mutations.