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Comparison of thermogenic sympathetic response to food intake between obese and non-obese young women.

OBJECTIVE: Sympathetic nervous system abnormality in humans is still a matter of debate. The present study was designed to examine diet-induced autonomic nervous system activity and metabolic change in obese and non-obese young women. RESEARCH METHODS AND PROCEDURES: Sixteen age- and height-matched obese and non-obese young women participated in this study. Sympathovagal activities were assessed by means of our newly developed spectral analysis procedure of heart-rate variability during the resting condition and after mixed-food ingestion (480 kcal). Energy expenditure was also measured under these two conditions. RESULTS: There was no significant difference in any of the parameters of the heart-rate variability between the obese group and control group during the resting condition. In the control group, both absolute values (221.5 +/- 54.5 vs. 363.8 +/- 43.7 ms2, p < 0.05) and relative values (0.23 +/- 0.03 to 0.36 +/- 0.02, p < 0.05) of a very-low-frequency component and global sympathetic nervous system index (1.46 +/- 0.19 vs. 3.26 +/- 0.61, p < 0.05) were significantly increased after mixed-food ingestion compared with the values obtained after resting condition. However, no such sympathetic response was found in the obese group. Energy expenditure increased in the two groups after the meal, but the magnitude of the increase above the preprandial resting condition was significantly greater in the control group than in the obese group (11.2 +/- 2.3 vs. 6.7 +/- 0.8%, p < 0.05). DISCUSSION: Our data suggest that despite identical sympathovagal activities at the resting condition, obese young women may possess a reduced sympathetic response to physiological perturbation such as mixed food intake, which might be related to lowered capacity of thermogenesis and the state of obesity.

Adult↗

Effort-related calf pain in the obese and long-term changes after surgical obesity treatment.

OBJECTIVE: To compare the prevalence of effort-related calf pain in an obese and a general population and to analyze the incidence of and recovery from such pain after surgical and conventional obesity treatment. RESEARCH METHODS AND PROCEDURES: A random sample of 1135 subjects from a general population was compared with 6328 obese subjects in the Swedish Obese Subjects study. Obese subjects were followed longitudinally, and information about calf pain was obtained from surgically and conventionally treated patients for up to 6 years. RESULTS: In both sexes, self-reported calf pain was more common in the obese than in the general population [odds ratios (ORs) 5.0 and 4.0 in men and women, respectively, p<0.001]. Obese patients undergoing surgery had a lower 6-year incidence of calf pain compared with the conventionally treated control group (ORs 0.39 and 0.61, p<0.05). Among subjects reporting symptoms at baseline, the 6-year recovery rate was higher in the surgical group compared with the control group (ORs 15.3 and 5.9, p<0.001). DISCUSSION: Obese subjects have markedly more problems with effort-related calf pain than the general population. Surgical obesity treatment reduces the long-term risk of developing claudication symptoms and increases the likelihood of recovering from such symptoms.

Adult↗

Dietary patterns and the metabolic syndrome in obese and non-obese Framingham women.

OBJECTIVES: 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.

Abdomen↗

Comparison of body fat composition and serum adiponectin levels in diabetic obesity and non-diabetic obesity.

OBJECTIVE: Clinical aspects of diabetes and obesity are somewhat different, even at similar levels of insulin resistance. The purpose of this study was to determine differences in body fat distribution and serum adiponectin concentrations in diabetic and non-diabetic obese participants. We were also interested in identifying the characteristics of insulin resistance in these two groups, particularly from the standpoint of adiponectin. RESEARCH METHODS AND PROCEDURES: Adiponectin concentrations of 112 type 2 diabetic obese participants and 124 non-diabetic obese participants were determined. Abdominal adipose tissue areas and midthigh skeletal muscle areas were measured by computed tomography. A homeostasis model assessment of the insulin resistance score was calculated to assess insulin sensitivity. The relationships among serum adiponectin, body fat distribution, and clinical characteristics were also analyzed. RESULTS: Both abdominal subcutaneous and visceral fat areas were higher in the non-diabetic obese group, whereas midthigh low-density muscle area was higher in the diabetic obese group. The homeostasis model assessment of the insulin resistance score was similar between groups, whereas serum adiponectin was lower in the diabetic obese group. Abdominal visceral fat (beta = -0.381, p = 0.012) was a more important predictor of adiponectin concentration than low-density muscle (beta = -0.218, p = 0.026) in cases of non-diabetic obesity, whereas low-density muscle (beta = -0.413, p = 0.013) was a better predictor of adiponectin level than abdominal visceral fat (beta = - 0.228, p = 0.044) in diabetic obese patients. DISCUSSION: Therefore, factors involved in pathophysiology, including different serum adiponectin levels and body fat distributions, are believed to be responsible for differences in clinical characteristics, even at similar levels of insulin resistance in both diseases.

Adiponectin↗

Testing of human homologues of murine obesity genes as candidate regions in Finnish obese sib pairs.

The human homologues of recently discovered murine obesity genes provide relevant candidates to study the genetic component of obesity in humans. We analysed the human counterparts to murine obesity genes ob, db, agouti, tub, melanocortin 4-receptor (MC4-R) and mitochondrial uncoupling proteins 2 and 3 (UCP2 and UCP3), as well as two other chromosomal regions reported to be linked to obesity-related phenotypes in restricted populations. We found no significant evidence for linkage to any analysed loci in our total study material of 105 affected sib pairs collected from the genetically homogenous population of Finland. However, several markers on 14 cM chromosomal region flanking the MC4-R gene showed sharing of alleles identical-by-descent (IBD) more frequently than expected. A selected subset of non-diabetic obese sib pairs strengthened the P values down to 0.003 in this particular region. The smallest P value (P = 0.001) was obtained with a marker D18S487 in a subgroup containing only sib pairs with one lean and one obese parent. We therefore screened seven obese subjects included in our sib pair material for sequence changes in their MC4-R gene, but no mutations of apparent causal relationship were found. In conclusion, we could not find evidence for significant contribution of the chromosomal loci corresponding to the murine single gene obesity genes for human morbid obesity, but additional studies are still needed to clarify whether DNA alterations within or adjacent to the MC4-R gene play some role.

Adaptor Proteins, Signal Transducing↗

Autonomic responsiveness to acute cold exposure in obese and non-obese young women.

OBJECTIVE: Conflicting results have emerged over the nature of autonomic nervous system abnormalities in human obesity. This present study was designed to investigate the sympatho-vagal activities and their responsiveness to acute cold exposure in age- and height-matched obese and non-obese young women. SUBJECTS: Twenty-four age- and height-matched obese (Weight: 68.1 +/- 2.64 kg, BMI: 26.3 +/- 0.74 kg/m2, %Fat: 39.9 +/- 1.23%) and non-obese young women (Weight: 46.9 +/- 0.77 kg, BMI: 18.5 +/- 0.18 kg/m2, %Fat: 22.9 +/- 0.8%). MEASUREMENTS: Plasma leptin, insulin, glucose and lipid concentrations were measured at rest. The sympathetic (SNS) and parasympathetic (PNS) nervous system activities were assessed by means of power spectral analysis of heart rate variability (HRV) for 15 min under control (25 degrees C) or acute cold exposure (10 degrees C) conditions. The very low (VLO) frequency component, and SNS (low/high power), and PNS (high/total power) indexes were used to evaluate thermoregulatory sympathetic function, and cardiac sympathetic and parasympathetic nervous activities, respectively. RESULTS: Plasma leptin concentration was significantly greater in the obese than in the control group (47.3 +/- 7.00 vs 12.1 +/- 1.22 ng.ml-1, P < 0.001). There was a highly positive correlation between plasma leptin concentration and percent of body fat (r = 0.863, P < 0.001). During the resting condition, there was no significant difference in any of the parameters of the HRV between the obese and control groups. Upon acute cold exposure, the VLO frequency component associated with thermoregulation (309 +/- 49.9 vs 578 +/- 142.2 ms2, P < 0.05) as well as its responsiveness (25-10 degrees C delta changes: 17 +/- 82.9 vs 326 +/- 138.2 ms2, P < 0.05) were significantly lower in the obese than in the control group. CONCLUSION: Our data indicate that a reduced autonomic, especially sympathetic responsiveness associated with thermoregulation and possibly leptin resistance might be aetiological factors of obesity in young women.

Adult↗

Prevention of obesity--more than an intention. Concept and first results of the Kiel Obesity Prevention Study (KOPS).

OBJECTIVE: Obesity prevention is necessary to address the steady rise in the prevalence of obesity. Although all experts agree that obesity prevention has high priority there is almost no research in this area. The effectiveness of different intervention strategies is not well documented. There is also no structured framework for obesity prevention. DESIGN: Based on (i) our current and limited knowledge and (ii) the idea that prevention of childhood obesity is an effective treatment of adult obesity, the Kiel Obesity Prevention Study (KOPS) was started in 1996. Concept, intervention strategies and first results of KOPS are reported in this paper. KOPS is an ongoing 8 y follow-up study. We first enrolled a large scale cohort of 5 to 7-y-old children, providing sufficient baseline data. KOPS allows further analyses of the role of individual risk factors as well as of long-term effectiveness of different intervention strategies. RESULTS: From 1996 to 1999 a representative group of 2440 5 to 7-y-old children was recruited (ie 30.2% of the total population of 5 to 7-y-old children examined by the school physicians) and a full data set was obtained from 1640 children. Of the children, 340 (20.7%) were considered as overweight and obese, 1108 children (67.6%) were normal weight, and underweight was found in 192 children (11.7%). Of the normal-weight children, 31% or 346 (21.1% of the total population) were considered to have a risk of becoming obese. Cross-sectional data provided evidence that (i) there is an inverse social gradient in childhood overweight as well as health-related behaviours and (ii) parental fatness had a strong influence on childhood overweight. We observed considerable changes in health-related behaviours within 1 y after combined "school-" and "family-based" interventions. Interventions aimed to improve health-related behaviours had significant effects on the age-dependent increases in median triceps skinfolds of the whole group (from 10.9 to 11.3 mm in "intervention schools" vs from 10.7 to 13.0 mm in "control schools", P<0.01) as well as in percentage fat mass of overweight children (increase by 3.6 vs 0.4% per year without and with intervention, respectively; P<0.05). CONCLUSION: First results of KOPS are promising. Besides health promotion, a better school education and social support seem to be promising strategies for future interventions.

Anthropometry↗

Synergistic effects of depressed mood and obesity on long-term cardiovascular risks in 1510 obese men and women: results from the MONICA-KORA Augsburg Cohort Study 1984-1998.

OBJECTIVE: To examine the contribution of depressed mood in obese subjects on the prediction of a future coronary heart disease event (CHD). DESIGN: A prospective population-based cohort study of three independent cross-sectional surveys with 6239 subjects, 45-74 years of age and free of diagnosed CHD, stroke and cancer. During a mean follow-up of 7 years, 179 CHD events occurred among men and 50 events among women. SUBJECTS: A total of 737 (23%) male and 773 (26%) female subjects suffering from obesity (BMI >or=30 kg/m2). MEASUREMENTS: Body weight determined by trained medical staff following a standardized protocol; standardized questionnaires to assess subsyndromal depressive mood and other psychosocial features. RESULTS: The main effect of obesity to predict a future CHD (hazard ratio, HR=1.38, 95% CI 1.03-1.84; P=0.031) and the interaction term of obesity by depression (HR=1.73, 95% CI 0.98-3.05; P=0.060) were borderline significant, both covariate adjusted for multiple risk factors. Relative to the male subgroup with normal body weight and no depression, the male obese group with no depression was not at significantly increased risk for CHD events (HR=1.17, 95% CI 0.76-1.80; P=0.473) whereas CHD risk in males with both obesity and depressed mood was substantially increased (HR=2.32, 95% CI 1.45-3.72, P>0.0001). The findings for women were similar, however, not significant probably owing to lack of power associated with low event rates. Combining obesity and depressed mood resulted in a relative risk to suffer from a future CHD event of HR 1.84 (95% CI 0.79-4.26; P=0.158). CONCLUSIONS: Depressed mood substantially amplifies the CHD risk of middle-aged obese, but otherwise apparently healthy men. The impact of depression on the obesity risk in women is less pronounced.

Adult↗

Immune function, mitogenicity, and angiogenic growth factor concentrations in lean and obese rodent sera: implications in obesity-related prostate tumor biology.

Some studies suggest that several tumors have a greater incidence in those patients with a high fat diet, such as colon, breast, and prostate. However, we wanted to determine the effects of obesity alone, independent of diet, on the progression of prostate tumor growth. Using a genetic model of obese and lean Zucker rats, we wanted to demonstrate any sera differences in the concentration of basic fibroblast growth factor (FGF-2) and vascular endothelial cell growth factor (VEGF), two important factors involved in the growth and progression of prostate cancer. We also wanted to investigate if there were any differences in immune function between the two sera, which could also account for uninhibited tumor growth, as well as differences in mitogenic stimulation. Female Zucker rat obese and lean sera were analyzed using ELISA assays for FGF-2, VEGF, and macrophage inflammatory protein-1 alpha (MIP-1a), as a measure of macrophage function. In addition, the sera of lean and obese sera were plated on wells growing LNCaP prostate cancer cells to determine differences in mitogenicity. We found a greater concentration of FGF-2 in the sera from obese Zucker rats compared to lean Zucker rats: 6.32+/-0.56 vs 3.48+/-0.34 pg/ml, respectively, P<0.05). We also demonstrated a greater concentration of VEGF in obese rat sera compared to lean sera: 54.4+/-4.1 vs 38.0+/-2.9 pg/mL, respectively, P<0.05). We detected a trend in mitogenic stimulation among LNCaP cells along the higher concentrations of the dose-response curve (0.72+/-0.06 vs 0.51+/-0.5). However, this was not statistically significant. In addition, we did not find a significant difference in MIP-1a macrophage activity levels between sera. To conclude, we speculate that the greater concentrations of VEGF and FGF-2 in the sera of obese rodents vs lean rodents may account for some of the differences seen in obesity-related tumor growth seen in the human condition. However, the lack of any sera differences of immune function, as measured by macrophage activity, as well as no significant differences on mitogenic proliferation on LNCaP prostate cancer cells, suggests that other mechanisms may exist to explain differences seen in obesity-related prostate tumor biology.

Angiogenesis Inducing Agents↗

Reduced plasma noradrenaline concentrations in simple-obese and diabetic obese patients.

1. Obesity may be associated with a decreased activity of the sympathetic nervous system and also with a deficiency of the response to stimuli activating the sympathetic nervous system. As insulin activates the sympathetic nervous system, the present study was undertaken to measure the plasma noradrenaline concentration in the fasting state and after 75 g of oral glucose in simple-obese patients (n = 13), in non-insulin-dependent (type 2) diabetic patients (n = 37) and in normal control subjects (n = 12). 2. The fasting plasma noradrenaline concentration was similarly reduced in the simple-obese group and in the diabetic obese group compared with the control group (P = 0.005). The glucose-induced increase in plasma noradrenaline concentration was normal in the simple-obese group, but was abolished in the obese diabetic patients (P = 0.008). 3. Step-wise regression analysis indicated that independent effects on the fasting plasma noradrenaline concentration were exerted by age (r = +0.32, P = 0.002), glucose concentration (r = -0.32, P = 0.02) and the degree of obesity (r = -0.37, P = 0.007), but not by plasma insulin concentration. 4. These results show that obese patients have a reduced fasting plasma noradrenaline concentration independently of accompanying diabetes, but that the response of noradrenaline to oral glucose is only abolished in the obese diabetic patients.

Adult↗

Leptin and metabolic syndrome in obese and non-obese children.

Metabolic syndrome is characterized by a clustering of metabolic abnormalities: insulin resistance - hyperinsulinemia, dyslipidemia (high triglycerides and low HDL - cholesterol serum concentrations), impaired glucose tolerance and/or type 2 diabetes, and hypertension. The aim of this study was to analyse the role of different variables of metabolic syndrome, including leptin, in 74 non-obese children and 68 children with non-syndromal obesity. As metabolic syndrome variables, we have included body mass index, waist circumference, trunk-to-total skinfolds (%), systolic blood pressure, diastolic blood pressure, glucose, uric acid, fasting insulin, triglycerides and high-density lipoprotein-cholesterol (HDL-C). Factor analysis showed 4 factors in each group. In non-obese children, waist circumference, BMI, fasting insulin, triglycerides, trunk-to-total skinfolds (%), leptin and uric acid loaded positively on factor 1, and HDL-C loaded negatively on this factor; systolic and diastolic blood pressure had high positive loadings in factor 2; HDL-C and leptin showed positive loadings and triglycerides and uric acid, negative loadings in factor 3; and, finally, glucose and insulin showed positive loadings in factor 4. These four factors explained 72.16 % of the total variance in the non-obese group. In obese children, BMI, waist circumference, leptin, diastolic blood pressure and systolic blood pressure loaded positively on factor 1; diastolic blood pressure, trunk-to-total skinfolds (%), uric acid and systolic blood pressure showed high positive loadings in factor 2; fasting insulin, glucose and triglycerides showed positive loadings in factor 3; and, finally, triglycerides showed positive loadings and HDL-C negative loadings in factor 4. These four factors explained 74.18 % of the total variance in the obese group. Our results point to a different homeostatic control of metabolic syndrome characteristics in obese and non-obese children. Leptin seems to play a key underlying role in metabolic syndrome, especially in the obese group.

Blood Glucose↗

Comparison of fibrinolytic and metabolic system parameters in obese patients with polycystic ovary syndrome and women with simple obesity.

The present study aimed to assess the fibrinolytic and metabolic system parameters in obese patients with polycystic ovary syndrome (PCOS) and to compare them in obese PCOS patients and women with simple obesity. We studied 19 obese women with PCOS (age: 25.1 +/- 4.6 years, body mass index (BMI): 34.7 +/- 3.9 kg/m2; mean +/- standard deviation) and 20 age- and BMI-matched ovulatory controls. We measured blood levels of 17beta-estradiol, testosterone, prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), dehydroepiandrosterone sulfate (DHEAS), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), glucose and insulin. The following fibrinolytic tests were also performed: euglobulin clot lysis time, plasminogen level, alpha2-antiplasmin activity, plasminogen activator inhibitor-1 activity, fibrinogen concentration and estimated fibrinolytic activity. Testosterone and LH levels were significantly higher in obese women with PCOS (p < 0.01 and p < 0.001, respectively). The groups did not differ with regard to 17beta-estradiol, prolactin, FSH, DHEAS, TC, TG, HDL-C, LDL-C, glucose and insulin. All of the fibrinolysis parameters with the exception of plasminogen were comparable between the two groups. Serum plasminogen level was lower in obese PCOS patients than in women with simple obesity (p < 0.05). Euglobulin clot lysis time was positively correlated with insulin (r = 0.88, p < 0.05) in both groups. Our results show that fibrinolysis is not suppressed in women with PCOS and that there is no difference in fibrinolytic activity between obese patients with PCOS and women with simple obesity.

Adult↗

TBC1D1 is a candidate for a severe obesity gene and evidence for a gene/gene interaction in obesity predisposition.

The molecular etiology of obesity predisposition is largely unknown. Here, we present evidence that genetic variation in TBC1D1 confers risk for severe obesity in females. We identified a coding variant (R125W) in TBC1D1 that segregated with the disease in 4p15-14-linked obesity pedigrees. In cases derived from pedigrees with the strongest linkage evidence, the variant was significantly associated with obesity (P=0.000007) and chromosomes carrying R125W accounted for the majority of the evidence that originally linked 4p15-14 with the disease. In addition, by selecting families that segregated R125W with obesity, we were able to generate highly significant linkage evidence for an obesity predisposition locus at 4q34-35. This result provides additional and confirming evidence that R125W affects obesity susceptibility, delimits the location of an obesity gene at 4q34-35 and identifies a gene/gene interaction that influences the risk for obesity predisposition. Finally, although the function of TBC1D1 is unknown, the protein is structurally similar to a known regulator of insulin-mediated Glut4 translocation.

Chromosomes, Human, Pair 4↗

Follistatin and activin A serum concentrations in obese and non-obese patients with polycystic ovary syndrome.

BACKGROUND: Activin promotes ovarian follicular development, inhibits androgen production and increases FSH and insulin secretion. Follistatin, an activin-binding protein, neutralizes activin bioactivity. Therefore, a decrease in the ratio of activin/follistatin might encourage characteristic features of polycystic ovary syndrome (PCOS). We investigated whether women with PCOS showed disordered follistatin and/or activin serum concentrations. METHODS: The study group included 24 obese and 20 non-obese (body mass index vertical line and <27 kg/m2 respectively) clomiphene-failure PCOS patients. The control group included 16 obese and 46 non-obese patients with normal ovulatory cycles. Blood samples were obtained from the patients on day 3-5 of a progesterone-induced or spontaneous cycle and were assayed for LH, FSH, testosterone, 17-hydroxy-progesterone, androstenedione, follistatin, activin A, fasting glucose and insulin. RESULTS: Follistatin concentrations were comparable between obese and non-obese PCOS patients (mean +/- SE; 1171 +/- 103 and 1045 +/- 159 pg/ml respectively) and significantly higher than their respective controls (628 +/- 61 and 592 +/- 49 pg/ml, P < 0.0001 and P < 0.02 respectively). Activin A concentrations were comparable between the four groups (590 +/- 35, 513 +/- 74, 661 +/- 87 and 595 +/- 43 pg/ml in obese and non-obese PCOS and controls respectively). Stepwise regression analyses for relationships between follistatin or activin A levels and all other variables indicated that follistatin was significantly and independently positively affected by PCOS (P < 0.0001), age (P < 0.02), androstenedione (P < 0.03) and weight (P < 0.05). Activin A was significantly and independently negatively affected by PCOS (P < 0.003) and FSH (P < 0.03), and positively affected by weight (P < 0.009) and androstenedione (P < 0.02). CONCLUSIONS: Serum follistatin is increased in PCOS patients, regardless of obesity. PCOS is the most significant variable that relates to high follistatin and low activin A serum concentration. A high follistatin/activin ratio could well contribute to the pathophysiology of PCOS.

17-alpha-Hydroxyprogesterone↗

Comparative amino acid and protein metabolism in obese and non-obese Zucker rats.

A mixture of [U-14C]amino acids was injected intraperitoneally into fed obese and non-obese Zucker rats that were either growing (8 weeks of age) or at maintenance (17 weeks of age). The metabolic fate of the dietary amino acid pool was determined from the distribution of 14C into carcass lean tissue, carcass lipid, CO2 and urine. In a second experiment, urinary and skeletal muscle 3-methylhistidine content was used to compare the rate of muscle protein breakdown between phenotypes at 8 weeks of age. The obese rat deposited a smaller proportion of its dietary amino acid pool in lean tissue compared with its non-obese control during growth and at maintenance. Obese rats incorporated a greater proportion of dietary amino acids into body lipid at both ages and metabolized a greater proportion of dietary amino acid carbon to CO2 during growth. At 8 weeks of age, the obese rat had a higher fractional rate of muscle protein breakdown and was less efficient at retaining amino acids that had been incorporated into muscle. These latter differences were major factors in producing the variation in dietary amino acid utilization and protein accretion between growing obese and non-obese rats. At maintenance, the variation in dietary amino acid utilization between phenotypes was due principally to the smaller body protein mass of the obese animals.

Aging↗

Children's attitudes and behavioral intentions toward a peer presented as obese: does a medical explanation for the obesity make a difference?

OBJECTIVE: To examine the effect of information on children's attitudes and behavioral intentions toward a peer presented as obese. METHODS: Children (N = 184) were randomly assigned to observe a video of a boy or girl in one of three conditions: average-weight, obese, obese with medical information explaining the obesity. They rated stereotypical attitudes on the Adjective Checklist and behavioral intentions on the Shared Activities Questionnaire (SAQ-B). RESULTS: Ratings were generally more favorable for the average-weight than for the obese condition. However, provision of medical information had a positive effect on attitudes toward the obese peer only for younger children and a negative effect on willingness of older children to share academic activities with the peer. Boys and girls showed more positive behavioral intentions toward the same-sex target child regardless of obesity condition. CONCLUSIONS: Information explaining obesity has a minimal positive effect on children's attitudes and behavioral intentions toward a peer presented as obese.

Analysis of Variance↗

Impaired synthesis and action of antiaggregating cyclic nucleotides in platelets from obese subjects: possible role in platelet hyperactivation in obesity.

BACKGROUND: Subjects with central obesity exhibit platelet hyperactivity, which is involved in the atherosclerotic process and therefore can account for the increased risk of cardiovascular morbidity and mortality. The aim of the study was to evaluate whether alterations of platelet function in obesity involve synthesis and/or action of the two antiaggregating cyclic nucleotides adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP). MATERIALS AND METHODS: In platelets from 16 obese and 15 control subjects we investigated the influence on platelet responses to the Adenosine-5-diphosphate sodium salt (ADP) exerted by (i) prostacyclin analogue Iloprost (0.31-5 nmol L(-1)) and the cAMP analogue 8-bromo-cAMP (10-500 micro mol L(-1)); and by (ii) nitric oxide (NO) donor sodium nitroprusside (SNP) (5-100 micro mol L(-1)) and the cGMP analogue 8-bromo-cGMP (10-500 micro mol L(-1)). IC(50) (minimal concentration of each inhibitor necessary to reduce platelet response to ADP by half) was determined. Iloprost and SNP ability to increase cyclic nucleotides was also measured. RESULTS: Significantly greater IC(50) were observed in obese subjects than in healthy controls (1.59 +/- 0.16 vs. 0.80 +/- 0.08 nmol L(-1), P = 0.0001 for Iloprost, and 27.6 +/- 6.5 vs. 7.0 +/- 1.7 micro mol L(-1), P = 0.006, for SNP); when data from control and obese subjects were pooled together, IC(50) of Iloprost and SNP correlated with the homeostasis model assessment (HOMA IR), which is a parameter used to measure the insulin resistance (r = 0.588, P = 0.029 and r = 0.640, P = 0.006, respectively). Also the antiaggregating effect of 8-Br-cAMP and 8-Br-cGMP was smaller in the obese subjects. Finally, the ability of Iloprost to increase platelet cAMP and the ability of SNP to increase both cGMP and cAMP were reduced in obese subjects. CONCLUSIONS: Platelet resistance to the antiaggregating effects of prostacyclin and NO in obesity is attributable to impairment of cyclic nucleotide synthesis and action. As cyclic nucleotides are the main effectors of platelet antiaggregation, the resistance to them can account for platelet hyperactivity in obesity.

Adult↗

Hypothalamic neuropeptide Y messenger ribonucleic acid levels in pre-obese and genetically obese (fa/fa) rats; potential regulation thereof by corticotropin-releasing factor.

Neuropeptide Y (NPY) is a 36 amino-acid peptide. It is localized within the brain but is also present peripherally. It is a well substantiated orexigenic peptide with several other endocrine and behavioural effects. In this study NPY mRNA levels were measured, using the polymerase chain reaction amplification technique, in the hypothalamus of pre-obese (unweaned 13-day-old), young (weaned 28-day-old) and adult (11-week-old) obese fa/fa rats and compared to those of lean age-matched controls. Before weaning, pre-obese pups had the same NPY mRNA levels as controls. After weaning NPY mRNA levels were increased 2-fold in young 28-day-old and 4-fold in adult obese rats, relative to corresponding controls. When adult obese rats were intracerebroventricularly-treated with ovine corticotropin-releasing hormone (oCRF) for 7 days, they stopped gaining body weight relative to vehicle-infused obese controls. Upon measuring NPY mRNA levels in the hypothalamus of these two groups of animals, it was shown that the high NPY mRNA levels of vehicle-treated (control) obese rats were decreased by 3-fold following the intracerebroventricular oCRF administration. It is proposed that: 1) hypothalamic NPY may play a role in the establishment and maintenance of the genetic obesity syndrome of the fa/fa rat, and 2) maintenance of the genetic obesity syndrome of the fa/fa rat, and 2) hypothalamic NPY could be partly regulated by central CRF.

Adipose Tissue↗