bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparison of Methods for Achieving 24‐Hour Energy Balance in a Whole‐Room Indirect Calorimeter
Authors: Grunwald Gary K. , Melanson Edward L. , Forster Jeri E. , Seagle Helen M. , Sharp Teresa A. , Hill James O. 
Published: April 2008

AbstractObjective: To evaluate and compare methods for achieving 24‐hour energy balance in a whole‐room indirect calorimeter.Research Methods and Procedures: Twenty‐four‐hour energy expenditure (EE) for 34 healthy adults (16 women, 18 men) was measured in a calorimeter during a prestudy day and on a subsequent nonconsecutive assessment day (AD). Several methods for estimating EE on the AD using activity factors or regression equations with data available before the AD [anthropometrics, body composition, resting metabolic rate (RMR), sleeping metabolic rate (SMR) on prestudy day, 24‐hour EE on prestudy day] were compared for predictive accuracy.Results: Use of a 24‐hour calorimeter stay gave the smallest mean absolute error (119 ± 16 kcal/d) and smallest single maximum error (361 kcal/d). However, several other methods were only slightly, and not significantly, less accurate (e.g., mean absolute error = 131 ± 17, 140 ± 20, and 141 ± 22 kcal/d and greatest error = 384, 370, and 593 kcal/d for anthropometric, RMR, and SMR regression equations, respectively). Fat‐free mass alone and SMR with a simple activity factor were seen to be less accurate.Discussion: Our results indicate that there may be some improvement in achieving 24‐hour energy balance in a metabolic chamber by using a preceding 24‐hour calorimeter stay; that only slightly less accurate predictions can be obtained using a combination of anthropometric, body composition, and/or RMR measurements; and that there is little or no advantage in using SMR from a previous overnight calorimeter stay.
Soluble Leptin Receptor and Soluble Receptor‐Bound Fraction of Leptin in the Metabolic Syndrome
Authors: Sandhofer Anton , Laimer Markus , Ebenbichler Christoph F. , Kaser Susanne , Paulweber Bernhard , Patsch Josef R. 
Published: April 2008

AbstractObjective: In obesity, plasma leptin is high and soluble leptin receptor (sOb‐R) levels are low, resulting in a low fraction of bound leptin. The aim of this study was to investigate the influence of insulin resistance (IR) and the metabolic syndrome (MS) on sOb‐R concentration and the bound‐free ratio of leptin.Research Methods and Procedures: sOb‐R, leptin levels, and homeostasis model assessment (HOMA) index for IR were determined in 76 middle‐aged obese or overweight men.Results: Concentration of sOb‐R and soluble receptor‐bound fraction of leptin were lowest in the highest tertile of HOMA‐IR. sOb‐R and the bound‐free ratio of leptin correlated with HOMA‐IR, leptin concentration, and waist‐to‐hip ratio independently of age, BMI, and fat mass. Leptin and waist‐to‐hip ratio were the sole independent determinants of sOb‐R concentration, and BMI, HOMA‐IR, and visceral adipose tissue were independent determinants of the bound fractin of leptin. sOb‐R concentration and the bound fraction of leptin decreased with increasing numbers of components of the MS, resulting in lower sOb‐R concentration and a lower fraction of bound leptin in men with the MS.Discussion: IR and abdominal obesity are associated with low sOb‐R concentration and low bound‐free ratio of leptin independent of fat mass. Low sOb‐R concentration and low bound‐free ratio of leptin segregate with components of the MS. We suggest that low sOb‐R levels and a low fraction of specifically bound leptin are markers of leptin resistance, which is independently associated with IR and abdominal obesity and may constitute an additional component of the MS.
Human Mesenchymal Stem Cells as an in Vitro Model for Human Adipogenesis
Authors: Janderová Lenka , McNeil Michele , Murrell Angela N. , Mynatt Randall L. , Smith Steven R. 
Published: April 2008

AbstractObjective: To validate the human mesenchymal stem cells (hMSCs) as a new in vitro model for the study of human adipogenesis, to develop the optimal protocol for the differentiation of hMSCs into adipocytes, and to describe effect of mitogen‐activated protein kinase on hMSC differentiation into adipocytes.Research Methods and Procedures: hMSCs, obtained commercially, were differentiated by exposure to insulin, dexamethasone, indomethacin, and 3‐isobutyl‐1‐methylxanthine three times for 3 days each. Various differentiation conditions were examined to optimize differentiation as measured by Oil Red O staining. The gene expression during adipogenic conversion was assessed by reverse‐transcription polymerase chain reaction, real‐time reverse‐transcription polymerase chain reaction, and Western blotting.Results: hMSCs differentiated into adipocytes to a different extent depending on the experimental conditions. We have found that differentiation medium based on medium 199 and containing 170 nM insulin, 0.5 mM 3‐isobutyl‐1‐methylxanthine, 0.2 mM indomethacin, 1 μM dexamethasone, and 5% fetal bovine serum was optimal. However, the replacement of fetal bovine serum with rabbit serum (15%) led to further enhancement of differentiation. Inhibition of mitogen‐activated protein kinase activation also facilitated adipogenic conversion of hMSCs. The pattern of genes expressed during hMSC differentiation into adipocytes (adipsin, peroxisome proliferator‐activated receptor‐γ, CCAAT/enhancer‐binding protein‐β, GLUT4, and leptin) was similar to that observed in other in vitro adipocyte models.Discussion: hMSCs are renewable sources of noncommitted precursors that are able to differentiate into mature adipocytes under the proper hormonal and pharmacological stimuli. Thus, hMSCs represent a new model for the study of human adipogenesis.
Association of Obesity, but not Diabetes or Hypertension, with Glucocorticoid Receptor N363S Variant
Authors: Lin Ruby C.Y. , Wang Xing Li , Dalziel Bronwen , Caterson Ian D. , Morris Brian J. 
Published: April 2008

AbstractObjective: To determine whether the N363S variant in the glucocorticoid receptor (encoded by nuclear receptor subfamily 3, group C, member 1: NR3C1) is associated with obesity, type 2 diabetes, or hypertension.Research Methods and Procedures: This was a cross‐sectional case‐control study involving 951 Anglo‐Celtic/Northern European subjects from Sydney. This study consisted of the following: 1) an obesity clinic group, most of whom had “morbid obesity” (mean BMI for group = 43 ± 8 kg/m2; n = 152); 2) a type 2 diabetes clinic group (n = 356); 3) patients with essential hypertension who had a strong family history (n = 141); and 4) normal healthy controls (n = 302). N363S genotype, BMI, and a range of other parameters relevant to each group were measured.Results: Compared with the frequency of 0.04 in nonobese healthy subjects, the S363 allele was significantly higher in obesity clinic patients (0.17; p = 5.6 × 10−8), subjects with diabetes who were also obese (0.09; p = 0.0045), subjects with hypertension who were also overweight (0.08; p = 0.0016), and overweight healthy subjects (0.12; p = 0.0004).Discussion: The NR3C1 N363S variant is associated with obesity and overweight in a range of patient settings but is not associated with hypertension or type 2 diabetes.
The Peroxisome Proliferator‐Activated Receptor α L162V Mutation Is Associated with Reduced Adiposity
Authors: Bossé Yohan , Després Jean‐Pierre , Bouchard Claude , Pérusse Louis , Vohl Marie‐Claude 
Published: April 2008

AbstractObjective: To determine the contribution of the peroxisome proliferator‐activated receptor α (PPARα) L162V mutation to the variation of several indexes of body fatness obtained from healthy adults who participated in the Quebec Family Study.Research Methods and Procedures: The PPARα L162V mutation was determined by a mismatch polymerase chain reaction method. Adiposity phenotypes were obtained by standardized anthropometric measurements, underwater weighing technique, and computed tomography.Results: For all adiposity phenotypes, subjects carrying the V162 allele had lower values compared with L162 homozygotes (HMZs) [BMI (kg/m2): 27.8 ± 7.6 vs. 26.0 ± 5.6, p < 0.05; percentage body fat: 28.5 ± 10.7 vs. 25.7 ± 10.1, p < 0.05; waist circumference (cm): 89.0 ± 18.1 vs. 85.7 ± 15.8, p = 0.07; total computed tomography abdominal fat areas (cm2): 406 ± 221 vs. 359 ± 192, p = 0.15; means ± SD for L162 HMZs vs. V162 carriers, respectively]. Differences in cross‐sectional abdominal adipose tissue areas and waist circumference were abolished after adjustment for total body fat mass. Similar trends were observed when results were analyzed by gender, although associations seemed stronger in women. The odds ratio of having a BMI above 30 kg/m2 reached 1.77 (1.02; 3.07, 95% confidence intervals) for L162 HMZs. This risk could be considered marginal on an individual basis, but because 85% of the subjects are affected by this small risk, the impact on the population is important.Discussion: The PPARα V162 allele is associated with reduced adiposity and has a substantial population‐attributable risk.
Dietary Fat Dose Dependently Increases Spontaneous Caloric Intake in Rat
Authors: Warwick Zoe S. 
Published: April 2008

AbstractObjective: To characterize the dose‐response relationship between dietary fat to carbohydrate ratio and spontaneous caloric intake.Research Methods and Procedures: Male Long‐Evans rats consumed milk‐based liquid diets that differed in fat content (17% to 60% of kilocalories) but had equivalent protein content and energy density. In Experiment 1, rats consumed one of the diets (n = 9/diet group) as the sole source of nutrition for 16 days. In Experiment 2, diets were offered as an option to nutritionally complete chow for 4 days followed by a 3‐day chow‐only washout in a randomized within‐subjects design (n = 30). In Experiment 3, nine rats received isocaloric intragastric infusions of diet overnight, with chow available ad libitum. At least two no‐infusion days separated the different diet infusions, which were given in random order. Food intake was measured dailyResults: Dietary fat dose dependently increased total daily kilocalories in each of the three paradigms.Discussion: These data imply that the postingestive effects of carbohydrate and fat differentially engage the physiological substrates that regulate daily caloric intake. These findings reiterate the importance of investigating macronutrient‐specific controls of feeding, rather than prematurely concluding that dietary attributes that covary with fat content (e.g., caloric density and palatability) drive the overeating associated with a high‐fat diet.
The Baboon as a Nonhuman Primate Model for the Study of the Genetics of Obesity
Authors: Comuzzie Anthony G. , Cole Shelley A. , Martin Lisa , Carey K. Dee , Mahaney Michael C. , Blangero John , VandeBerg John L. 
Published: April 2008

AbstractObjective: At present, rodents represent the most common animal model for research in obesity and its comorbidities (e.g., type 2 diabetes and coronary heart disease), however, there are several physiological and developmental differences between rodents and humans reflective of their relatively ancient evolutionary divergence (approximately 65 to 75 million years ago). Therefore, we are currently developing the baboon as a nonhuman primate model for the study of the genetics of obesity.Research Methods and Procedures: At present, we are collecting extensive phenotypic data in a large pedigreed colony (N > 2000) of baboons housed at the Southwest Foundation for Biomedical Research in San Antonio, Texas. The long‐term goal of this project is to identify genes influencing adiposity‐related phenotypes and to test hypotheses regarding their pleiotropic effects on other phenotypes related to increased risk for a variety of common diseases (e.g., coronary heart disease and type 2 diabetes).Results: To date we have obtained various adipose‐specific endocrine measures, adipose tissue biopsies, and estimates of body composition on a substantial portion of our pedigreed colony. The pattern of adipose tissue accumulation follows closely that seen in humans, and we have detected significant additive genetic heritabilities for these obesity‐related phenotypes.Discussion: Given the physiological and developmental similarities between humans and baboons, along with the ability to collect data under well‐controlled situations and the extensive pedigree data available in our colony, the baboon offers an extremely valuable nonhuman primate model for the study of obesity and its comorbidities.
Energy Intake Patterns in Obese Women with Binge Eating Disorder
Authors: Raymond Nancy C. , Neumeyer Brooke , Warren Cortney S. , Lee Susanne S. , Peterson Carol B. 
Published: April 2008

AbstractObjective: For binge eating disorder (BED) to be accepted as a distinct diagnostic category in the Diagnostic and Statistical Manual for Mental Disorders, Fifth Edition, it must be demonstrated that the criteria identify a diagnostic entity that is distinct from bulimia nervosa and obesity. This study examined the difference in total energy intake per day, patterns of energy intake throughout the day, and nutrient content of foods consumed in obese individuals who met the criteria for BED (on binge and non‐binge days) and those who did not.Research Methods and Procedures: Twenty women, 12 who met Diagnostic and Statistical Manual for Mental Disorders, Fourth Edition, criteria for BED and 8 matched obese controls, participated in the study. All participants underwent six random 24‐hour dietary recall telephone interviews conducted by experienced interviewers using the Nutrition Data Software System.Results: The BED group ingested significantly more kilocalories on days when they had binge eating episodes than the obese control group on average. The BED group ate significantly more in the evening on binge days than their control group counterparts. There is some indication in the data that those with BED may be restricting caloric intake. Finally, data indicated that the BED group ate significantly more protein, carbohydrate, and fat on binge days than on non‐binge days. However, the proportion of kilocalories from each nutrient shifted on BED binge days compared with non‐binge days to favor consumption of fat over carbohydrates.Discussion: More research needs to be done to determine if these findings are reproducible. Then, the neurobiological underpinnings of these differences in nutrient intake patterns and nutrient selection can be studied to help to determine the biological basis of the disorder.
Weight‐Loss Practices and Asthma: Findings from the Behavioral Risk Factor Surveillance System
Authors: Ford Earl S. , Mannino David M. , Redd Stephen C. , Mokdad Ali H. , Galuska Deborah A. , Serdula Mary K. 
Published: April 2008

AbstractObjective: To describe weight‐control practices and receipt of weight‐loss advice among obese people with asthma.Research Methods and Procedures: We analyzed data from the 2000 Behavioral Risk Factor Surveillance System.Results: Among 13,953 participants with current asthma, 27.3% had a body mass index of ≥30 kg/m2. Overall, 48.1% of participants with asthma reported trying to lose weight (64.1% among overweight or obese participants and 72.9% among obese participants). Among participants with asthma who were trying to lose or maintain weight, 74.7% reported trying to reduce their energy and/or fat intake, and 57.8% reported using physical activity. Approximately 29.7% were using the recommended combination of energy and/or fat intake reduction and physical activity of ≥150 min/wk. During the 12 months before the interview, 16.2% of overweight and 44.9% of obese participants with asthma reported receiving advice to lose weight. Among obese participants receiving weight‐loss advice, 82.9% reported trying to lose weight compared to 63.8% of participants who did not receive such advice.Discussion: Health professionals can play an important role in educating their patients with asthma about the importance of weight control and assisting their overweight and obese patients in setting appropriate weight goals and helping them achieve those goals.
A Deletion in the α2B‐Adrenergic Receptor Gene and Autonomic Nervous Function in Central Obesity
Authors: Sivenius Katariina , Niskanen Leo , Laakso Markku , Uusitupa Matti 
Published: April 2008

AbstractObjective: We investigated the impact of a three‐amino acid deletion (12Glu9) polymorphism in the α2B‐adrenergic receptor gene on autonomic nervous function. The short form (Glu9/Glu9) of the polymorphism has previously been associated with a reduced basal metabolic rate in obese subjects. Because autonomic nervous function participates in the regulation of energy metabolism, there could be a link between this polymorphism and autonomic nervous function.Research Methods and Procedures: Data of a 10‐year follow‐up study with 126 nondiabetic control subjects and 84 type 2 diabetic patients were used to determine the effects of the 12Glu9 polymorphism on autonomic nervous function. A deep breathing test and an orthostatic test were used to investigate parasympathetic and sympathetic autonomic nervous function. In addition, cardiovascular autonomic function was studied using power spectral analysis of heart rate variability.Results: No significant differences were found in the frequency of the 12Glu9 deletion polymorphism between nondiabetic and diabetic subjects. The nondiabetic men with the Glu9/Glu9genotype, especially those with abdominal obesity, had significantly lower total and low‐frequency power values in the power spectral analysis when compared with other men. Furthermore, in a longitudinal analysis of 10 years, the decrease in parasympathetic function was greater in nondiabetic men with the Glu9/Glu9genotype than in the men with the Glu9/Glu12or Glu12/Glu12genotypes.Discussion: The results of the present study suggest that the 12Glu9 polymorphism of the α2B‐adrenergic receptor gene modulates autonomic nervous function in Finnish nondiabetic men. In the nondiabetic men with the Glu9/Glu9genotype, the general autonomic tone is depressed, and vagal activity especially becomes impaired with time. Furthermore, this association is accentuated by central obesity.
Correlation between Serum Resistin Level and Adiposity in Obese Individuals
Authors: Azuma Koichiro , Katsukawa Fuminori , Oguchi Shuji , Murata Mitsuru , Yamazaki Hajime , Shimada Akira , Saruta Takao 
Published: April 2008

AbstractObjective: Resistin is associated with insulin resistance in mice and may play a similar role in humans. The aim of our study was to examine the relationship of serum resistin level to body composition, insulin resistance, and related obesity phenotypes in humans.Research Methods and Procedures: Sixty‐four young (age 32 ± 10 years), obese (BMI 32.9 ± 5.6), nondiabetic subjects taking no medication, and 15 lean (BMI 21.1 ± 1.3) volunteers were studied cross‐sectionally. Thirty‐five of the subjects were also reevaluated after 1.5 years on a weight reduction program entailing dieting and exercise; changes of serum resistin were compared with changes of BMI, body composition, fat distribution, and several indices of insulin sensitivity derived from plasma glucose and serum insulin levels measured during 75‐g oral glucose tolerance test.Results: In a cross‐sectional analysis, serum resistin was significantly higher in obese subjects than in lean volunteers (24.58 ± 12.93 ng/mL; n = 64 vs. 12.83 ± 8.30 ng/mL; n = 15; p < 0.01), and there was a correlation between resistin level and BMI, when the two groups were combined (ρ = 0.35, p < 0.01). Although cross‐sectional analysis in obese subjects revealed no correlation between serum resistin and parameters related to adiposity or insulin resistance, longitudinal analysis revealed change in serum resistin to be positively correlated with changes in BMI, body fat, fat mass, visceral fat area, and mean glucose and insulin (ρ = 0.39, 0.40, 0.44, 0.50, 0.40, and 0.50; p = 0.02, 0.03, 0.02, <0.01, 0.02, and <0.01, respectively).Discussion: Resistin appears to be related to human adiposity and to be a possible candidate factor in human insulin resistance.
Binge Eating and Eating‐Related Cognitions and Behavior in Ethnically Diverse Obese Women
Authors: Sánchez‐Johnsen Lisa A.P. , Dymek Maureen , Alverdy John , Le Grange Daniel 
Published: April 2008

AbstractObjective: To examine binge eating and eating‐related cognitions and behavior in a sample of ethnically diverse women who are severely obese and seeking bariatric surgery.Research Methods and Procedures: Female bariatric surgery candidates (62 African Americans, 18 Latinas, 130 whites) completed questionnaires on binge eating and eating‐related cognitions and behavior and completed a structured clinical interview to confirm binge‐eating disorder diagnosis.Results: Ethnic minorities and whites did not differ in rates of binge‐eating disorder (26.3%), binges per week (M = 0.95), or dietary restraint. Ethnic minorities reported less disinhibition, and there was a trend to report less hunger awareness than whites. After controlling for BMI and education, ethnicity accounted for significant variance in disinhibition (4%; p < 0.01). Ethnic minorities were younger, became overweight at a later age, and were overweight for fewer years than whites.Discussion: Results suggest that ethnicity exerts an important influence on disinhibition and that ethnic differences are not caused by BMI or education. Findings point to the need to continue to investigate the role of ethnicity, binge eating, and disinhibition in severely obese women, so that culturally appropriate services can be provided.
Turnover of Acinar and Islet Cells in the Pancreas of Monosodium Glutamate‐Treated Obese Mice
Authors: Nakayama Daiju , Magami Yasushi , Azuma Takeshi , Inokuchi Hideto , Furukawa Masaya , Ohyashiki Junko , Yoshimoto Takayuki , Mizuguchi Junichiro , Moriyasu Fuminori , Kawai Keiichi , Hattori Takanori 
Published: April 2008

AbstractObjective: Subcutaneous administrations of monosodium glutamate (MSG) to neonatal animals result in obesity and induce the toxicity on the central nervous system, and furthermore, have an effect on entero‐pancreatic hormone. The effect of MSG on the cell turnover of organs, especially the pancreas, has received little attention until now. This study was designed to examine the effect of MSG on pancreatic cell turnover by immunohistochemistry and [3H]thymidine autoradiography.Research Methods and Procedures: Male JcI‐ICR strain mice were SC injected with MSG (2 mg/g body weight daily) for 5 days after birth, received 112 repeated injections of [3H]thymidine at 6‐hour intervals for 28 days after birth, and then were killed immediately thereafter, or 30, 60, or 120 days after the last injection. Autoradiography was performed on sections immunostained for glucagon, insulin, and somatostatin.Results: After continuous labeling, most pancreatic cells were labeled, and thereafter, labeling of cells decreased in control and MSG‐treated mice. The mean grain counts of acinar cells in MSG‐treated mice decreased more slowly than those in control mice. On the other hand, those of islet cells, including glucagon, insulin, and somatostatin cells, decreased more rapidly in MSG‐treated mice than those in control mice.Discussion: Cell turnover of acinar cells was decelerated and that of islet cells including glucagon, insulin, and somatostatin cells was accelerated in MSG‐treated mice pancreas. MSG‐induced hypothalamic lesions exert the contrary influences on the cell turnover of acinar and islet cells.