bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasma Levels of Adiponectin, a Novel Adipocyte‐Derived Hormone, in Sleep Apnea**
Authors: Wolk Robert , Svatikova Anna , Nelson Christy A. , Gami Apoor S. , Govender Kogilan , Winnicki Mikolaj , Somers Virend K. 
Published: April 2008

AbstractObjective: Obstructive sleep apnea (OSA) is associated with obesity, sympathetic activation, systemic inflammation, and cardiovascular morbidity. Obesity, β‐adrenergic agonists, and inflammation are linked to decreased expression and/or secretion of an adipose tissue‐derived antiatherogenic hormone, adiponectin. The purpose of the study was to investigate whether OSA affected plasma levels of adiponectin, which might help explain OSA‐associated cardiovascular morbidity.Research Methods and Procedures: We randomly selected 68 otherwise healthy male subjects, either with moderate/severe OSA [apnea‐hypopnea index (AHI) ≥ 20; n = 35] or without OSA (AHI ≤ 5; n = 33). The diagnosis of OSA was made based on prospective full polysomnography. Adiponectin was measured before polysomnography between 8 and 10 PM.Results: AHI was higher in the OSA group (49.5 ± 4.4 vs. 2.9 ± 0.4 events/h; p < 0.001). OSA subjects were also more obese, with greater BMI (33 ± 1 vs. 30 ± 1; p = 0.016) and percentage body fat (29 ± 1% vs. 26 ± 1%; p = 0.030). Adiponectin levels were 7.67 ± 0.73 and 6.33 ± 0.51 μg/mL in the OSA and non‐OSA groups, respectively, and this difference was significant in covariate analysis (taking into account age, hemodynamic characteristics, measures of body fat, and OSA severity) (p = 0.009). After excluding from both groups the subjects with extreme BMI, such that the OSA and non‐OSA study cohorts had similar BMI and percentage body fat, subjects with OSA had significantly higher plasma adiponectin (8.49 ± 0.92 vs. 6.32 ± 0.55 μg/mL; p = 0.042), differences also evident in covariate analysis (p = 0.017).Discussion: Plasma adiponectin levels are elevated in otherwise healthy subjects with OSA. Therefore, low adiponectin is unlikely to explain the association between OSA and cardiovascular disease.
Is Maternal Psychopathology Related to Obesigenic Feeding Practices at 1 Year?
Authors: Farrow Claire V. , Blissett Jacqueline M. 
Published: April 2008

AbstractObjective: To investigate the relationship between maternal psychopathological symptomatology during pregnancy and at 6 and 12 months postnatally and maternal use of controlling and restrictive feeding practices at 1 year.Research Methods and Procedures: Eighty‐seven women completed a measure of psychological distress during pregnancy and at 6 and 12 months postpartum, and at 12 months postnatally these women reported their usage of controlling and restrictive feeding practices and were observed feeding their infants.Results: General psychological distress, particularly anxious psychopathology, during pregnancy and at 6 and 12 months postnatally was significantly associated with maternal use of restrictive feeding practices at 1 year, even when controlling for length of breast‐feeding and the infants’ weights at 1 year. Contrary to expectations, depression and eating psychopathology as measured by the SCOFF eating disorder measure during pregnancy or at 6 or 12 months postnatally were not associated with the use of controlling or restrictive feeding practices at 1 year.Discussion: These findings indicate that anxious maternal psychopathology may partially explain the development of maternal use of restriction when feeding.
Correlates of Persistent Thinness in Black and White Young Women
Authors: Franko Debra L. , Thompson Douglas , Russell Rachel , Schreiber George B. , Crawford Patricia B. , Daniels Stephen R. , Striegel‐Moore Ruth H. 
Published: April 2008

AbstractObjective: To examine health and psychosocial correlates of persistent thinness in black and white young adult women.Research Methods and Procedures: 1830 females (n = 988 black, n = 842 white) who participated in the National Heart, Lung, and Blood Institute Growth and Health Study were asked to indicate their current body size from a series of nine pictograms (1, emaciated to 9, obese). Persistent thinness was defined as having at least seven non‐missing measurement points between ages 9 to 18 with a body size rating of <4 at all points. Generalized linear models were used to examine whether persistently thin women differed from comparison women on cardiovascular disease risk factors measured at age 18.5 and psychosocial variables measured at age 21.5. Prospective associations between psychological measures in childhood and persistent thinness through the course of adolescence were also examined.Results: In the sample, 145 women (7.9%) met criteria for persistent thinness and 1685 women (92.1%) were classified as not persistently thin. Persistently thin women had a later age of menarche, fewer weight concerns, and healthier eating attitudes, were less likely to have had a child, came from higher socioeconomic backgrounds, and had significantly lower blood pressure and higher high‐density lipoprotein‐cholesterol than comparison women. Differences were not found on measures of depression or health services use. Girls with higher self‐esteem in childhood were more likely to remain persistently thin throughout adolescence.Discussion: Persistently thin women seem to be healthier on several indicators relative to comparison women, and race did not moderate these differences.
Achieving Healthy Weight in African‐American Communities: Research Perspectives and Priorities
Authors: Kumanyika Shiriki K. , Gary Tiffany L. , Lancaster Kristie J. , Samuel‐Hodge Carmen D. , Banks‐Wallace Joanne , Beech Bettina M. , Hughes‐Halbert Chanita , Karanja Njeri , Odoms‐Young Angela M. , Prewitt T. Elaine , Whitt‐Glover Melicia C. 
Published: April 2008

AbstractThe longstanding high burden of obesity in AfricanAmerican women and the more recent, steeper than average rise in obesity prevalence among African‐American children constitute a mandate for an increased focus on obesity prevention and treatment research in African‐American communities. The African‐American Collaborative Obesity Research Network (AACORN) was formed to stimulate and support greater participation in framing and implementing the obesity research agenda by investigators who have both social and cultural grounding in AfricanAmerican life experiences and obesity‐related scientific expertise. AACORN's examination of obesity research agenda issues began in 2003 in conjunction with the Think Tank on Enhancing Obesity Research at the National Heart, Lung, and Blood Institute (NHLBI). The assessment was subsequently expanded to take into account the overall NIH strategic plan for obesity research, literature reviews, and descriptions of ongoing studies. In identifying priorities, AACORN members considered the quality, quantity, focus, and contextual relevance of published research relevant to obesity prevention and treatment in African‐American adults or children. Fifteen recommended research priorities are presented in five categories adapted from the NHLBI Think Tank proceedings: health effects, social and environmental context, prevention and treatment, research methods, and research training and funding. These recommendations from an African‐American perspective build on and reinforce certain aspects of the NHLBI and overall NIH research agendas by providing more specific rationale and directions on areas for enhancement in the type of research being done or in the conceptualization and implementation of that research.
Glucose‐dependent Insulin Modulation of Oscillatory Lipolysis in Perifused Rat Adipocytes
Authors: Getty‐Kaushik Lisa , Richard Ann‐Marie T. , Corkey Barbara E. 
Published: April 2008

AbstractObjective: We showed glucose‐dependent lipolytic oscillations in adipocytes that are modulated by free fatty acids (FFAs). We hypothesized that the oscillations are driven by oscillatory glucose metabolism that leads to oscillatory formation of α‐glycerophosphate (α‐GP), oscillatory removal of long‐chain coenzyme A (LC‐CoA) by α‐GP to form triglycerides, and oscillatory relief of LC‐CoA inhibition of triglyceride lipases. This study examined the effect of insulin on this hypothesis.Research Methods and Procedures: Samples were collected every minute from perifused rat adipocytes during the basal state followed by insulin (±glucose) or isoproterenol (±insulin; n = 4 each).Results: Insulin caused a significant increase in glycerol release (18%), with a concomitant significant decrease in FFA release (38%). Without glucose, insulin had no effect on glycerol release while still decreasing FFA release (35%). Insulin (5 μU/mL) attenuated the response of lipolysis to isoproterenol (∼3‐fold increase with isoproterenol vs. 2‐fold increase with insulin + isoproterenol). However, 1 mU/mL insulin amplified the lipolytic response (∼5‐fold increase in glycerol release with insulin + isoproterenol), with a concomitant increase in FFA reesterification (no increase in FFA release compared with isoproterenol alone).Discussion: We interpret these results to be due to insulin's ability to increase glucose uptake and conversion to α‐GP, thus removing LC‐CoA inhibition of triglyceride lipases. While the physiological importance of lipolytic oscillations remains to be determined, we hypothesize that such an oscillation may play an important role in the delivery of FFAs to the liver, β cells, and other tissues.
Thyroid‐Stimulating Hormone Stimulates Interleukin‐6 Release from 3T3‐L1 Adipocytes through a cAMP‐Protein Kinase A Pathway
Authors: Antunes Tayze T. , Gagnon AnneMarie , Bell Andrea , Sorisky Alexander 
Published: April 2008

AbstractObjective: Thyroid‐stimulating hormone (TSH) is a novel modulator of adipokine release from human and mouse adipocytes. The aim of our study was to identify the signal transduction pathways activated by TSH that stimulate interleukin (IL)‐6 production.Research Methods and Procedures: Mouse 3T3‐L1 preadipocyte and differentiated adipocyte cell cultures were studied. The effect of 0 to 1 μM TSH on IL‐6 protein release into the medium over 0 to 24 hours was assessed. TSH signaling pathways responsible for regulating IL‐6 were studied through the use of 1 μM forskolin, 100 μM 8‐pCPT‐2′‐O‐Me‐cAMP, 10 μM H89, 50 μM PD98059, and 2 μg/mL actinomycin D.Results: TSH stimulated IL‐6 release by 2.6‐fold from 3T3‐L1 adipocytes at concentrations as low as 0.01 μM but did not alter IL‐6 production of corresponding preadipocytes. Forskolin (elevates intracellular cAMP) stimulated IL‐6 release from 3T3‐L1 adipocytes (n = 3, p < 0.005), and H89, an inhibitor of cAMP‐dependent protein kinase A (PKA), reduced TSH‐stimulated IL‐6 release by 66% (n = 3, p < 0.01), indicating a requirement for cAMP‐dependent PKA. Inhibition of the mitogen‐activated protein kinase pathway with PD98059 did not affect TSH‐stimulated IL‐6 release. Activation of an alternate cAMP target, the exchange protein of cAMP, with 8‐pCPT‐2′‐O‐Me‐cAMP, had no effect on IL‐6 release. TSH raised the level of IL‐6 mRNA, and blockade of transcription with actinomycin D abrogated IL‐6 protein release by TSH (n = 3, p < 0.05).Discussion: TSH stimulates IL‐6 release from differentiated 3T3‐L1 adipocytes, but not preadipocytes, by signaling through cAMP‐PKA to activate IL‐6 gene transcription.
Evidence in Female Rhesus Monkeys (Macaca mulatta) that Nighttime Caloric Intake is not Associated with Weight Gain
Authors: Sullivan Elinor L. , Daniels Alejandro J. , Koegler Frank H. , Cameron Judy L. 
Published: April 2008

AbstractObjective: To evaluate the hypothesis that nighttime consumption of calories leads to an increased propensity to gain weight.Research Methods and Procedures: Sixteen female rhesus monkeys (Macaca mulatta) were ovariectomized and placed on a high‐fat diet to promote weight gain, and we examined whether monkeys that ate a high percentage of calories at night were more likely to gain weight than monkeys that ate the majority of calories during the day.Results: Within 6 weeks post‐ovariectomy, calorie intake and body weight increased significantly (129 ± 14%, p = 0.04; 103 ± 0.91%, p = 0.02, respectively). Subsequent placement on high‐fat diet led to further significant increases in calorie intake and body weight (368 ± 56%, p = 0.001; 113 ± 4.0%, p = 0.03, respectively). However, there was no correlation between the increase in calorie intake and weight gain (p = 0.34). Considerable individual variation existed in the percentage of calories consumed at night (6% to 64% total daily caloric intake). However, the percentage of calorie intake occurring at night was not correlated with body weight (r = 0.04; p = 0.87) or weight gain (r = 0.07; p = 0.79) over the course of the study. Additionally, monkeys that showed the greatest nighttime calorie intake did not gain more weight (p = 0.94) than monkeys that showed the least nighttime calorie intake.Discussion: These results show that eating at night is not associated with an increased propensity to gain weight, suggesting that individuals trying to lose weight should not rely on decreasing evening calorie intake as a primary strategy for promoting weight loss.
Intramyocellular Lipid Content and Molecular Adaptations in Response to a 1‐Week High‐Fat Diet
Authors: Schrauwen‐Hinderling Vera B. , Kooi Marianne Eline , Hesselink Matthijs K.C. , Moonen‐Kornips Esther , Schaart Gert , Mustard Kirsty J. , Hardie D. Grahame , Saris Wim H.M. , Nicolay Klaas , Schrauwen Patrick 
Published: April 2008

AbstractObjective: To investigate molecular adaptations that accompany the elevation of intramyocellular lipid (IMCL) content on a high‐fat (HF) diet for 1 week.Research Methods and Procedures: Ten subjects consumed a normal‐fat (NF) diet for 1 week, followed by an HF diet for another week. After both dietary periods, we determined the IMCL content by proton magnetic resonance spectroscopy in the vastus lateralis muscle and quantified changes in gene expression, protein content, and activity in biopsy samples. We investigated genes involved in carbohydrate and fatty acid handling [lipoprotein lipase, acetyl‐coenzyme A carboxylase (ACC) 2, hormone‐sensitive lipase, hexokinase II, and glucose transporter 4] and measured protein levels of CD36 and phosphorylated and unphosphorylated ACC2 and the activity of adenosine monophosphate‐activated kinase.Results: IMCL content was increased by 54% after the HF period. Lipoprotein lipase mRNA concentration was increased by 33%, whereas ACC2 mRNA concentration tended to be increased after the HF diet. Hexokinase II, glucose transporter 4, and hormone‐sensitive lipase mRNA were unchanged after the HF diet. ACC2 and CD36 protein levels, phosphorylation status of ACC2, and adenosine monophosphate‐activated kinase activity did not change in response to the HF diet.Discussion: We found that IMCL content in skeletal muscle increased after 1 week of HF feeding, accompanied by molecular adaptations that favor fat storage in muscle rather than oxidation.
Effect of Low‐ and High‐Calcium Dairy‐Based Diets on Macronutrient Oxidation in Humans
Authors: Melanson Edward L. , Donahoo William T. , Dong Fran , Ida Therese , Zemel Michael B. 
Published: April 2008

AbstractObjective: Higher calcium and dairy intakes may be associated with lower body weights, but a mechanism in humans has yet to be elucidated. We compared the effects of a dairy‐based high‐calcium diet and a low‐calcium diet on macronutrient oxidation.Research Methods and Procedures: Subjects (10 men and nine women) consumed a low‐dairy (LD, ∼one serving per day, ∼500 mg Ca2+/d) or high‐dairy (HD, ∼three to four servings per day, ∼1400 mg Ca2+/d) energy balance diet for 1 week. Each diet condition was performed twice. On the 7th day, subjects were studied in a room calorimeter under one of four study conditions, applied in a randomized crossover design. Within each diet condition, subjects were studied under conditions of energy balance and acute energy deficit. The deficit (−600 kcal/d) was induced only for the 24 hours that subjects resided in the room and was achieved by a combination of caloric restriction and exercise.Results: Under energy balance conditions, there was no effect of diet treatment on respiratory quotient or 24‐hour macronutrient oxidation. Under energy deficit conditions, 24‐hour fat oxidation was significantly increased on the HD diet (HD with deficit = 136 ± 13 g/d, LD with deficit = 106 ± 7 g/d, p = 0.02).Discussion: Consumption of a dairy‐based high‐calcium diet increased 24‐hour fat oxidation under conditions of acute energy deficit. We hypothesize that these effects are due to an increased fat oxidation during exercise.
ACDC/Adiponectin and PPAR‐γ Gene Polymorphisms: Implications for Features of Obesity
Authors: Tankó László B. , Siddiq Afshan , Lecoeur Cécile , Larsen Philip J. , Christiansen Claus , Walley Andrew , Froguel Philippe 
Published: April 2008

AbstractObjective: The main purpose of this study was to investigate associations of single‐nucleotide polymorphisms (SNPs) in the adipocyte C1q and collagen domain‐containing (ACDC) gene and its regulator, the nuclear peroxisome proliferator‐activated receptor (PPAR)‐γ gene, with body fat mass and its topographical distribution in postmenopausal women.Research Methods and Procedures: Participants were 1501 healthy women, 60 to 85 years old, who were genotyped for four SNPs in the ACDC gene (−11391G/A, −11377C/G, +45T/G, +276G/T) and the Pro12Ala SNP in the PPAR‐γ gene. Total body fat mass and the central to peripheral fat mass ratio (CFM/PFM ratio) were measured using DXA. Adiponectin and homeostasis model assessment of insulin resistance were measured in 287 subjects.Results: The −11377C/G SNP was associated with adiponectin (p < 0.001) and the CFM/PFM ratio (p = 0.005); the G allele being associated with low adiponectin and high CFM/PFM ratio. Similar associations of adiponectin (p = 0.0001) and the CFM/PFM ratio (p = 0.002) characterized the 1_2 (G_G) promoter haplotype (11391G/A_−11377C/G). Genotype variation of SNP Pro12Ala was associated with total body fat mass (p = 0.04); women with GG being the most obese (p = 0.01). The Ala/Ala (GG) genotype of Pro12Ala SNP interacted with the CC genotype of SNP‐11377C/G in the determination of BMI (p = 0.001), when analyzed using a codominant model.Discussion: Polymorphisms in the ACDC gene are associated with body fat distribution, whereas the Pro12Ala polymorphism in PPAR‐γ is associated with overall adiposity, apparently in interaction with an ACDC promoter SNP.
Meta‐analysis on the G‐308A Tumor Necrosis Factor α Gene Variant and Phenotypes Associated with the Metabolic Syndrome
Authors: Sookoian Silvia C. , González Claudio , Pirola Carlos J. 
Published: April 2008

AbstractObjective: The G‐308A tumor necrosis factor (TNF) α gene variant has been associated with obesity, insulin resistance, and hypertension. We performed a systematical review of the literature by means of a meta‐analysis to assess the association of the G‐308A TNFα polymorphism with the components of the metabolic syndrome.Research Methods and Procedures: Studies were identified by searches of the literature for reports using the terms: diabetes, insulin resistance, hypertension, obesity or metabolic syndrome and TNF, variants or polymorphism or alleles, and Nco or −308. From 824 reports, we included 31 observational studies, case control and cohort at baseline, which analyzed the association between the TNFα polymorphism and one or more components of the metabolic syndrome. A fixed effect model was used to pool data from individual studies.Results: Obesity [odds ratio, 1.23; 95% confidence interval (CI), 1.045 to 1.45; p = 0.013] in a total of 3562 individuals from eight homogeneous studies, systolic arterial blood pressure (standardized difference, 0.132; 95% CI, 0.016 to 0.25; p < 0.03) in a total of 1624 individuals from four homogeneous studies and plasma insulin levels (standardized difference, 0.095; 95% CI, 0.020 to 0.17; p = 0.013) in a total of 3720 subjects from 16 homogeneous studies were positively associated with the −308A variant.Discussion: These results indicate that individuals who carried the −308A TNFα gene variant are at 23% risk of developing obesity compared with controls and showed significantly higher systolic arterial blood pressure and plasma insulin levels, supporting the hypothesis that the TNFα gene is involved in the pathogenesis of the metabolic syndrome.
Total and Regional Fat Distribution is Strongly Influenced by Genetic Factors in Young and Elderly Twins
Authors: Malis Charlotte , Rasmussen Eva L. , Poulsen Pernille , Petersen Inge , Christensen Kaare , Beck‐Nielsen Henning , Astrup Arne , Vaag Allan A. 
Published: April 2008

AbstractObjective: Indirect estimates of obesity such as BMI seem to be strongly influenced by genetic factors in twins. Precise measurements of total and regional fat as determined by direct techniques such as DXA scan have only been applied in a few twin studies. The aim of the present study was to estimate the heritability (h2) of total and regional fat distribution in young and elderly Danish twins.Research Methods and Procedures: Monozygotic (108) and dizygotic (88) twins in two age groups (25 to 32 and 58 to 66 years) underwent anthropometric measurements and DXA scans. Intraclass correlations and etiologic components of variance were estimated for total and regional fat percentages using biometric modeling.Results: The intraclass correlations demonstrated higher correlations for all fat percentages among monozygotic twins as compared with dizygotic twins. The biometric modeling revealed a major genetic component (h2) of total (h2young = 0.83, h2elderly = 0.86) and regional fat percentages (trunk, h2young = 0.82, h2elderly = 0.85; lower body, h2young = 0.83, h2elderly = 0.81; and trunk/lower body, h2young = 0.83, h2elderly = 0.71) in both the young and elderly twins.Discussion: The h2 estimates emphasize that body fat and distribution as determined by DXA scan are under extensive genetic control.
Stability of the Association between Birth Weight and Childhood Overweight during the Development of the Obesity Epidemic
Authors: Rugholm Susi , Baker Jennifer L. , Olsen Lina W. , Schack‐Nielsen Lene , Bua Jenny , Sørensen Thorkild I. A. 
Published: April 2008

AbstractObjective: To assess whether changes in the birth weight distribution or changes in the association of birth weight with the later risk of childhood overweight have contributed to the development of the obesity epidemic.Research Methods and Procedures: A Danish population‐based cohort study of 124,615 girls and 128,346 boys (ages 6 to 13 years), born between 1936 and 1983, were studied. Birth weight and annual measurements of height and weight were obtained from school health records. Overweight was defined by BMI in relation to internationally accepted criteria. The relative risk of being overweight by birth weight was calculated separately for each age, sex, and time period.Results: The birth weight distribution remained relatively stable over time. Compared with children with a birth weight of 3.0 to 3.5 kg, the risk of overweight increased consistently with each increase in birth weight category among girls and boys and at all ages between 6 and 13 years. Furthermore, the association between birth weight and increased risk of overweight in childhood remained stable across a 48‐year period.Discussion: The increase in the prevalence of overweight could not be explained by time trends in the distribution of birth weight or by changes in the association between birth weight and the later risk of overweight over time. This implies that, unless the prenatal environment influences the later risk of overweight without increasing birth weight, the environmental influences contributing to the obesity epidemic in children of school age operate in the early postnatal period.