Cardiac Parasympathetic Activity Is Increased by Weight Loss in Healthy Obese Women

Objective: We studied the effect of weight reduction on cardiac parasympathetic activity (PSA) in obese women. We also studied the relationship between the changes of PSA, resting energy expenditure (REE), and major cardiovascular risk factors. Research Methods and Procedures: Changes of cardiac vagal tone, an index of PSA, REE, and major cardiovascular risk factors, were measured in 52 healthy obese women after a 6‐month weight reduction. Ten of the women were remeasured at 12 and 24 months. Cardiac vagal tone was assessed by a vagal tone monitor and REE by indirect calorimeter. Results: Cardiac vagal tone increased significantly (p = 0.046), averaging a 9.5% weight loss in 6 months. The vagal tone increased further with weight loss during the following 6 months, and thereafter, it declined with weight regain. The increase of cardiac vagal tone correlated significantly with decreases of body weight, fat mass, waist circumference, serum insulin, and heart rate. REE adjusted for fat‐free mass and age did not change with weight loss and was not related to cardiac vagal tone at any time‐point. Discussion: Cardiac PSA activity increases with weight loss in obese women. This increase may not be maintained long‐term if body weight is regained. The rise of cardiac PSA is correlated with decreases of body fat mass, abdominal fat, serum insulin, and heart rate. Cardiac PSA is not related to REE.     

25‐Hydroxyvitamin D Concentration Correlates With Insulin‐Sensitivity and BMI in Obesity

The prevalence of hypovitaminosis D is high among obese subjects. Further, low 25‐hydroxyvitamin D (25(OH)D) concentration has been postulated to be a risk factor for type 2 diabetes, although its relation with insulin‐sensitivity is not well investigated. Thus, we aimed to investigate the relationship between 25(OH)D concentration and insulin‐sensitivity, using the glucose clamp technique. In total, 39 subjects with no known history of diabetes mellitus were recruited. The association of 25(OH)D concentration with insulin‐sensitivity was evaluated by hyperinsulinemic euglycemic clamp. Subjects with low 25(OH)D (<50 nmol/l) had higher BMI (P = 0.048), parathyroid hormone (PTH) (P = 0.040), total cholesterol (P = 0.012), low‐density lipoprotein (LDL) cholesterol (P = 0.044), triglycerides (P = 0.048), and lower insulin‐sensitivity as evaluated by clamp study (P = 0.047). There was significant correlation between 25(OH)D and BMI (r = ?0.58; P = 0.01), PTH (r = ?0.44; P < 0.01), insulin‐sensitivity (r = 0.43; P < 0.01), total (r = ?0.34; P = 0.030) and LDL (r = ?0.40; P = 0.023) (but not high‐density lipoprotein (HDL)) cholesterol, and triglycerides (r = 0.45; P = 0.01). Multivariate analysis using 25(OH)D concentration, BMI, insulin‐sensitivity, HDL cholesterol, LDL cholesterol, total cholesterol, and triglycerides, as the cofactors was performed. BMI was found to be the most powerful predictor of 25(OH)D concentration (r = ?0.52; P < 0.01), whereas insulin‐sensitivity was not significant. Our study suggested that there is no cause–effect relationship between vitamin D and insulin‐sensitivity. In obesity, both low 25(OH)D concentration and insulin‐resistance appear to be dependent on the increased body size.     

Serum 25‐Hydroxyvitamin D Concentration,Life Factors and Obesity in Mexican Children

Although current evidence emphasizes a high prevalence of vitamin D deficiency and an inverse association between serum 25‐hydroxyvitamin D (25‐OHD) concentration and obesity, no studies have been conducted in Mexican children. The objective was to determine the prevalence of vitamin D deficiency and its association with obesity and lifestyle factors in a sample of school‐aged Mexican children. A cross‐sectional study of 99 obese and 99 nonobese 6–12 year‐old children, skin phototypes III–V, from six public schools was conducted during summer at latitude 25°40′, in northeastern Mexico. Anthropometric measurements were determined. Serum 25‐OHD was measured by immunoluminometric direct assay. Consumption of foods rich in vitamin D, sunscreen use and vitamin consumption were assessed through applied questionnaires. 62.1% of the subjects had insufficiency of 25‐OHD (21–29 ng/ml) and 20.2% had deficiency (<20 ng/ml). Obese subjects (BMI ≥95th percentile for age and gender) had significantly lower concentration of 25‐OHD than nonobese. Predictors of 25‐OHD concentration were, in order of significance: percentage of body fat, BMI, triceps skin fold, and waist circumference (WC). A significantly higher rate of 25‐OHD deficiency was observed in children with inadequate milk/yoghurt consumption, but no difference was found for other foods, physical activity (PA) or screen‐time. In a multivariate model, being obese was significantly associated with the risk of 25‐OHD deficiency, after adjustment for PA, screen‐time, skin phototype, ingestion of milk/yoghurt, fish, cheese, and carbonated beverages. A high prevalence of vitamin D deficiency and an inverse association between serum 25‐OHD concentration and obesity was found.     

Sitting Time Is Associated With Weight,but Not With Weight Gain in Mid‐Aged Australian Women

The aim of this study was to examine the associations between sitting time, weight, and weight gain in Australian women born in 1946–1951. Data were from 8,233 women who completed surveys for the Australian Longitudinal Study on Women's Health (ALSWH) in 2001, 2004, and 2007. Associations between sitting time and weight, and between sitting time and weight change in each 3‐year period were examined using repeated measures modeling. The associations between weight and change in sitting time were also examined. Analyses were stratified for BMI categories: normal weight (18.5 ≤ BMI < 25), overweight (25 ≤ BMI < 30), and obese (BMI ≥ 30). In cross‐sectional models, each additional hour of sitting time was associated with 110 g (95% confidence interval (CI): 40–180) and 260 g (95% CI: 140–380) additional weight in overweight and obese women, respectively (fully adjusted model). In prospective analyses, sitting time was not consistently associated with weight change, after adjustment for other variables, and weight was not associated with change in sitting time over successive 3‐year periods. In conclusion, although the cross‐sectional associations between sitting time and weight were evident in overweight and obese women, there was no consistent association between sitting time and weight gain. A potential explanation is that prospective associations may only be apparent over longer periods of time. These results do not support a role for reducing sitting time as a short‐term means of weight control in mid‐aged women.     

Vertebral Bone Marrow Fat Is Positively Associated With Visceral Fat and Inversely Associated With IGF‐1 in Obese Women

Recent studies have demonstrated an important physiologic link between bone and fat. Bone and fat cells arise from the same mesenchymal precursor cell within bone marrow, capable of differentiation into adipocytes or osteoblasts. Increased BMI appears to protect against osteoporosis. However, recent studies have suggested detrimental effects of visceral fat on bone health. Increased visceral fat may also be associated with decreased growth hormone (GH) and insulin‐like growth factor 1 (IGF‐1) levels which are important for maintenance of bone homeostasis. The purpose of our study was to assess the relationship between vertebral bone marrow fat and trabecular bone mineral density (BMD), abdominal fat depots, GH and IGF‐1 in premenopausal women with obesity. We studied 47 premenopausal women of various BMI (range: 18–41 kg/m², mean 30 ± 7 kg/m²) who underwent vertebral bone marrow fat measurement with proton magnetic resonance spectroscopy (1H‐MRS), body composition, and trabecular BMD measurement with computed tomography (CT), and GH and IGF‐1 levels. Women with high visceral fat had higher bone marrow fat than women with low visceral fat. There was a positive correlation between bone marrow fat and visceral fat, independent of BMD. There was an inverse association between vertebral bone marrow fat and trabecular BMD. Vertebral bone marrow fat was also inversely associated with IGF‐1, independent of visceral fat. Our study showed that vertebral bone marrow fat is positively associated with visceral fat and inversely associated with IGF‐1 and BMD. This suggests that the detrimental effect of visceral fat on bone health may be mediated in part by IGF‐1 as an important regulator of the fat and bone lineage.     

High-Density Lipoprotein-Associated miR-223 Is Altered after Diet-Induced Weight Loss in Overweight and Obese Males

Background and Aims

microRNAs (miRNAs) are small, endogenous non-coding RNAs that regulate metabolic processes, including obesity. The levels of circulating miRNAs are affected by metabolic changes in obesity, as well as in diet-induced weight loss. Circulating miRNAs are transported by high-density lipoproteins (HDL) but the regulation of HDL-associated miRNAs after diet-induced weight loss has not been studied. We aim to determine if HDL-associated miR-16, miR-17, miR-126, miR-222 and miR-223 levels are altered by diet-induced weight loss in overweight and obese males.

Methods

HDL were isolated from 47 subjects following 12 weeks weight loss comparing a high protein diet (HP, 30% of energy) with a normal protein diet (NP, 20% of energy). HDL-associated miRNAs (miR-16, miR-17, miR-126, miR-222 and miR-223) at baseline and after 12 weeks of weight loss were quantified by TaqMan miRNA assays. HDL particle sizes were determined by non-denaturing polyacrylamide gradient gel electrophoresis. Serum concentrations of human HDL constituents were measured immunoturbidometrically or enzymatically.

Results

miR-16, miR-17, miR-126, miR-222 and miR-223 were present on HDL from overweight and obese subjects at baseline and after 12 weeks of the HP and NP weight loss diets. The HP diet induced a significant decrease in HDL-associated miR-223 levels (p = 0.015), which positively correlated with changes in body weight (r = 0.488, p = 0.032). Changes in miR-223 levels were not associated to changes in HDL composition or size.

Conclusion

HDL-associated miR-223 levels are significantly decreased after HP diet-induced weight loss in overweight and obese males. This is the first study reporting changes in HDL-associated miRNA levels with diet-induced weight loss.     

Decreased Glucagon‐like Peptide 1 Release after Weight Loss in Overweight/Obese Subjects

Objective: Postprandial glucagon‐like peptide 1 (GLP‐1) release seems to be attenuated in obese subjects. Results on whether weight loss improves GLP‐1 release are contradictory. The aim of this study was to further investigate the effect of weight loss on basal and postprandial GLP‐1 release in overweight/obese subjects. Research Methods and Procedures: Thirty‐two overweight/obese subjects participated in a repeated measurement design before (BMI, 30.3 ± 2.8 kg/m²; waist circumference, 92.6 ± 7.8 cm; hip circumference, 111.1 ± 7.4 cm) and after a weight loss period of 6 weeks (BMI, 28.2 ± 2.7 kg/m²; waist circumference, 85.5 ± 8.5 cm; hip circumference, 102.1 ± 9.2 cm). During weight loss, subjects received a very‐low‐calorie diet (Optifast) to replace three meals per day. Subjects came to the laboratory fasted, and after a baseline blood sample, received a standard breakfast (1.9 MJ). Postprandially, blood samples were taken every one‐half hour relative to intake for 120 minutes to determine GLP‐1, insulin, glucose, and free fatty acids from plasma. Appetite ratings were obtained with visual analog scales. Results: After weight loss, postprandial GLP‐1 concentrations at 30 and 60 minutes were significantly lower than before weight loss (p < 0.05). Glucose concentrations were also lower, and free fatty acids were higher compared with before weight loss. Ratings of satiety were increased, and hunger scores were decreased after weight loss (p < 0.05). Discussion: In overweight/obese subjects, GLP‐1 concentrations after weight loss were decreased compared with before weight loss, and nutrient‐related stimulation was abolished. This might be a response to a proceeding negative energy balance. Satiety and GLP‐1 seem to be unrelated in the long term.     

Bupropion for Weight Loss: An Investigation of Efficacy and Tolerability in Overweight and Obese Women

Objective: On the basis of the clinical observations that bupropion facilitated weight loss, we investigated the efficacy and tolerability of this drug in overweight and obese adult women. Research Methods and Procedures: A total of 50 overweight and obese (body mass index: 28.0 to 52.6 kg/m²) women were included. The core component of the study was a randomized, double‐blind, placebo‐controlled comparison for 8 weeks. Bupropion or placebo was started at 100 mg/d with gradual dose increase to a maximum of 200 mg twice daily. All subjects were prescribed a 1600 kcal/d balanced diet and compliance was monitored with food diaries. Responders continued the same treatment in a double‐blind manner for an additional 16 weeks to a total of 24 weeks. There was additional single‐blind follow‐up treatment for a total of 2 years. Results: Subjects receiving bupropion achieved greater mean weight loss (last‐observation‐carried‐forward analysis) over the first 8 weeks of the study (p = 0.0001): 4.9% ± 3.4% (n = 25) for bupropion treatment compared with 1.3% ± 2.4% (n = 25) for placebo treatment. For those who completed the 8 weeks, the comparison was 6.2% ± 3.1% (n = 18) vs. 1.6% ± 2.9% (n = 13), respectively(p = 0.0002), with 12 of 18 of the bupropion subjects (67%) losing over 5% of baseline body weight compared with 2 of 13 in the placebo group (15%; p = 0.0094). In the continuation phase, 14 bupropion responders who completed 24 weeks achieved weight loss of 12.9% ± 5.6% with fat accounting for 73.5% ± 3.7% of the weight lost and no change in bone mineral density as assessed by DXA. Bupropion was generally well‐tolerated in this sample. Discussion: Bupropion was more effective than placebo in achieving weight loss at 8 weeks in overweight and obese adult women in this preliminary study. Initial responders to bupropion benefited further in the continuation phase.     

Association of Pericardial Fat With Liver Fat and Insulin Sensitivity After Diet‐Induced Weight Loss in Overweight Women

Pericardial adipose tissue (PAT) is positively associated with fatty liver and obesity‐related insulin resistance. Because PAT is a well‐known marker of visceral adiposity, we investigated the impact of weight loss on PAT and its relationship with liver fat and insulin sensitivity independently of body fat distribution. Thirty overweight nondiabetic women (BMI 28.2–46.8 kg/m², 22–41 years) followed a 14.2 ± 4‐weeks low‐calorie diet. PAT, abdominal subcutaneous (SAT), and visceral fat volumes (VAT) were measured by magnetic resonance imaging (MRI), total fat mass, trunk, and leg fat by dual‐energy X‐ray absorptiometry and intrahepatocellular lipids (IHCL) by (¹)H‐magnetic resonance spectroscopy. Euglycemic hyperinsulinemic clamp (M) and homeostasis model assessment of insulin resistance (HOMA_IR) were used to assess insulin sensitivity or insulin resistance. At baseline, PAT correlated with VAT (r = 0.82; P < 0.001), IHCL (r = 0.46), HOMA_IR (r = 0.46), and M value (r = ?0.40; all P < 0.05). During intervention, body weight decreased by ?8.5%, accompanied by decreases of ?12% PAT, ?13% VAT, ?44% IHCL, ?10% HOMA2‐%B, and +24% as well as +15% increases in HOMA2‐%S and M, respectively. Decreases in PAT were only correlated with baseline PAT and the loss in VAT (r = ?0.56; P < 0.01; r = 0.42; P < 0.05) but no associations with liver fat or indexes of insulin sensitivity were observed. Improvements in HOMA_IR and HOMA2‐%B were only related to the decrease in IHCL (r = 0.62, P < 0.01; r = 0.65, P = 0.002) and decreases in IHCL only correlated with the decrease in VAT (r = 0.61, P = 0.004). In conclusion, cross‐sectionally PAT is correlated with VAT, liver fat, and insulin resistance. Longitudinally, the association between PAT and insulin resistance was lost suggesting no causal relationship between the two.     

Phenylethanolamine N‐Methyltransferase G‐148A Genetic Variant and Weight Loss in Obese Women

Objective: To understand the impact of the phenylethanolamine N‐methyltransferase (PNMT) G‐148A gene and nutritional variables on weight loss in obese women. Research Methods and Procedures: One hundred forty‐nine women, ages 45 to 65 with a body mass index of >30 kg/m², participated in a 6‐month, open‐label intervention that included sibutramine (15 mg/d) and a monthly health‐education class. Anthropometric measurements, vital signs, food frequency, exercise log, medication compliance, and psychological and sociological questionnaires were completed each month. Genetic polymorphisms of PNMT were determined. Results: Univariate analysis of G/G, G/A, and A/A genotypes against tertiles of percentage of weight loss were significant at 3 but not at 6 months (Pearson χ²: p < 0.006; homozygous/heterozygosity: p < 0.002, p < 0.253, and p < 0.122, respectively). A regression model that included the PNMT genetic variation and certain nutrition and exercise variables demonstrated that only the PNMT gene (β = 0.360, SE 0.585, and p = 0.003) was statistically significant at 6 months, and the total calories (β = ?0.925, SE = 0.004, and p = 0.009), fiber intake (β = 0.621, SE = 0.124, and p = 0.000), and PNMT (β = 0.262, SE = 1.415, and p = 0.024) were significant. Discussion: The homozygosity/heterozygosity of the PNMT gene was highly predictive of significant weight loss with sibutramine during the first 3 months, which highlights the need for specific pharmacotherapy. The early weight‐loss success of those subjects who were homozygous for PNMT may have motivated and selected those that would make further dietary changes, which then augmented their final weight loss.     

Quality of Life after Diet or Exercise-Induced Weight Loss in Overweight to Obese Postmenopausal Women: The SHAPE-2 Randomised Controlled Trial

Introduction

This study investigates the effect of a modest weight loss either by a calorie restricted diet or mainly by increased physical exercise on health related quality of life (HRQoL) in overweight-to-obese and inactive postmenopausal women. We hypothesize that HRQoL improves with weight loss, and that exercise-induced weight loss is more effective for this than diet-induced weight loss.

Methods

The SHAPE-2 trial was primarily designed to evaluate any additional effect of weight loss by exercise compared with a comparable amount of weight loss by diet on biomarkers relevant for breast cancer risk. In the present analysis we focus on HRQoL. We randomly assigned 243 eligible women to a diet (n = 97), exercise (n = 98), or control group (n = 48). Both interventions aimed for 5–6 kg weight loss. HRQoL was measured at baseline and after 16 weeks by the SF-36 questionnaire.

Results

Data of 214 women were available for analysis. Weight loss was 4.9 kg (6.1%) and 5.5 kg (6.9%) with diet and exercise, respectively. Scores of the SF-36 domain ‘health change’ increased significantly by 8.8 points (95% CI 1.6;16.1) with diet, and by 20.5 points (95% CI 13.2;27.7) with exercise when compared with control. Direct comparison of diet and exercise showed a statistically significantly stronger improvement with exercise. Both intervention groups showed a tendency towards improvements in most other domains, which were more pronounced in the exercise group, but not statistically different from control or each other.

Conclusion

In a randomized trial in overweight-to-obese and inactive postmenopausal women a comparable 6%-7% weight loss was achieved by diet-only or mainly by exercise and showed improvements in physical and mental HRQoL domains, but results were not statistically significant in either the diet or exercise group. However, a modest weight loss does lead to a positive change in self-perceived health status. This effect was significantly larger with exercise-induced weight loss than with comparable diet-induced weight loss.

Trial Registration

ClinicalTrials.gov NCT01511276     

Vitamin D in Overweight/Obese Women and Its Relationship With Dietetic and Anthropometric Variables

Overweight/obese persons usually have an inadequate vitamin D status, a situation commonly made worse by an inadequate intake of this vitamin. For this reason, the aim of this study was to analyze dietetic and anthropometric differences in a group of young, overweight/obese Spanish women with respect to their vitamin D status. The study subjects were 66 white Spanish women (aged 20–35 years) with a BMI of 24–35 kg/m². Dietetic, anthropometric, and biochemical data were collected. Women were divided into two groups depending on their serum vitamin D concentrations: LD (women with <90 nmol/l 25(OH)D) and HD (women with ≥90 nmol/l 25(OH)D). The intakes of vitamin D, calcium, and supplements were similar in both groups. The body weight, BMI, and waist circumference of the HD subjects were smaller than those recorded for the LD subjects (68.6 ± 4.2 kg, 26.0 ± 1.3 kg/m², and 79.4 ± 3.4 cm compared to 76.2 ± 9.8, 28.6 ± 3.2 kg/m², and 86.2 ± 9.3 cm, respectively; P < 0.05). The hip circumference and the waist/hip ratio were similar in both groups. A BMI of <27.7 kg/m² (P50) was associated with serum vitamin D concentrations of ≥90 nmol/l (odds ratio = 0.1313; confidence interval: 0.0149–1.1599; P < 0.05). Overweight/obese women are at higher risk of vitamin D deficiency, largely due to excess adiposity rather than inadequate intake.     

Regular Aerobic Exercise,Without Weight Loss,Improves Endothelium‐dependent Vasodilation in Overweight and Obese Adults

Lifestyle modification in the form of weight reduction by caloric restriction alone or in combination with regular aerobic exercise significantly improves endothelium‐dependent vasodilation in overweight and obese adults. We determined whether regular aerobic exercise, independent of weight loss, improves endothelium‐dependent vasodilation in overweight and obese adults. Twenty overweight and obese adults (age 53 ± 1 years; BMI: 30.2 ± 0.8 kg/m²) were studied before and after a 3‐month aerobic exercise training intervention. Forearm blood flow (FBF) responses were determined (via plethysmography) in response to intra‐arterial infusion of acetylcholine and sodium nitroprusside. There were no changes in body mass or composition with the intervention. FBF responses to acetylcholine were ～35% higher (P < 0.01) after (4.1 ± 0.9 to 14.7 ± 4.3 ml/100 ml tissue/min) compared with before (4.2 ± 0.8 to 11.0 ± 3 ml/100 ml tissue/min) exercise training. FBF responses to sodium nitroprusside were unchanged. These results indicate that regular aerobic exercise improves endothelium‐dependent vasodilation in overweight and obese adults, independent of changes in body mass or composition.     

Mediators of Weight Loss and Weight Loss Maintenance in Middle‐aged Women

Long‐term behavioral self‐regulation is the hallmark of successful weight control. We tested mediators of weight loss and weight loss maintenance in middle‐aged women who participated in a randomized controlled 12‐month weight management intervention. Overweight and obese women (N = 225, BMI = 31.3 ± 4.1 kg/m²) were randomly assigned to a control or a 1‐year group intervention designed to promote autonomous self‐regulation of body weight. Key exercise, eating behavior, and body image variables were assessed before and after the program, and tested as mediators of weight loss (12 months, 86% retention) and weight loss maintenance (24 months, 81% retention). Multiple mediation was employed and an intention‐to‐treat analysis conducted. Treatment effects were observed for all putative mediators (Effect size: 0.32–0.79, P < 0.01 vs. controls). Weight change was ?7.3 ± 5.9% (12‐month) and ?5.5 ± 5.0% (24‐month) in the intervention group and ?1.7 ± 5.0% and ?2.2 ± 7.5% in controls. Change in most psychosocial variables was associated with 12‐month weight change, but only flexible cognitive restraint (P < 0.01), disinhibition (P < 0.05), exercise self‐efficacy (P < 0.001), exercise intrinsic motivation (P < 0.01), and body dissatisfaction (P < 0.05) predicted 24‐month weight change. Lower emotional eating, increased flexible cognitive restraint, and fewer exercise barriers mediated 12‐month weight loss (R² = 0.31, P < 0.001; effect ratio: 0.37), but only flexible restraint and exercise self‐efficacy mediated 24‐month weight loss (R² = 0.17, P < 0.001; effect ratio: 0.89). This is the first study to evaluate self‐regulation mediators of weight loss and 2‐year weight loss maintenance, in a large sample of overweight women. Results show that lowering emotional eating and adopting a flexible dietary restraint pattern are critical for sustained weight loss. For long‐term success, interventions must also be effective in promoting exercise intrinsic motivation and self‐efficacy.     

Low 25‐Hydroxyvitamin D Does Not Affect Insulin Sensitivity in Obesity after Bariatric Surgery

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

Effect of Weight Loss on High‐Molecular Weight Adiponectin in Obese Children

Our aim was to determine the influence of weight reduction on total (T‐) and high‐molecular weight (HMW‐) adiponectin in obese (OB) prepubertal children. Seventy OB prepubertal white patients were followed for 18 months and studied after reducing their BMI by 1 (n = 51) and 2 standard deviation scores (SDS) (n = 21) under conservative treatment, and 6 months after achieving weight loss (n = 44). Body composition dual‐energy X‐ray absorptiometry (DXA) and serum levels of T‐ and HMW‐adiponectin, resistin, leptin, leptin soluble receptor (sOB‐R), tumoral necrosis factor‐α and interleukin‐6 were determined. The control group consisted of 61 healthy prepubertal children. At diagnosis T‐adiponectin was higher (P < 0.01; confidence interval (+0.04) — (+0.15)) and HMW‐adiponectin lower (P < 0.001; confidence interval (?0.45) ? (?0.21)) in OB children than in controls. A reduction in body fat increased T‐ and HMW‐adiponectin and sOB‐R (all P < 0.001) and decreased leptin (P < 0.001) and interleukin‐6 levels (P < 0.05). After 6 months of sustained weight reduction a decrease in tumoral necrosis factor‐α (P < 0.01) occurred, whereas weight recovery increased leptin (P < 0.001) and decreased T‐adiponectin (P < 0.05). HMW‐adiponectin levels negatively correlated with homeostasis model assessment (HOMA) index and BMI in the whole cohort (both P < 0.001), as did T‐adiponectin levels and HOMA index in OB patients (P < 0.01), but neither T‐ nor HMW‐adiponectin correlated with body fat content (BFC) in OB children. We conclude that the impairment of T‐ and HMW‐adiponectin levels in childhood obesity is different to that in elder OB patients, showing closer relationship with carbohydrate metabolism parameters than with BFC, but increasing their levels after weight loss and in association with metabolic improvement.     

ADRB2 Haplotype Is Associated With Glucose Tolerance and Insulin Sensitivity in Obese Postmenopausal Women

The β₂‐adrenergic receptor (ADRB2) mediates obesity, cardiorespiratory fitness, and insulin resistance. We examined the hypothesis that ADRB2 Arg16Gly‐Gln27Glu haplotype is associated with body composition, glucose tolerance, and insulin sensitivity in obese, postmenopausal women. Obese (>35% body fat), postmenopausal (age 45–75 years) women (n = 123) underwent genotyping, dual‐energy X‐ray absorptiometry, and computed tomography scans, exercise testing (VO_2max), 2‐h oral glucose tolerance tests (OGTTs), and hyperinsulinemic‐euglycemic clamps (80 mU/m²/min). Analysis of covariance (ANCOVA) tested for differences among haplotypes, with race, % body fat, and VO_2max as covariates. We found that ADRB2 haplotype was independently associated with % body fat, abdominal fat distribution, VO_2max, insulin sensitivity (M/ΔInsulin), and glucose tolerance (ANOVA, P < 0.05 for all). Women homozygous for Gly16–Gln27 haplotype had the highest % body fat (52.7 ± 1.9%), high abdominal fat, low M/ΔInsulin (0.49 ± 0.08 mg/kg/min/pmol/l/10²), and impaired glucose tolerance (IGT) during an OGTT (G₁₂₀ = 10.2 ± 0.9 mmol/l). Women homozygous for Gly16–Glu27 haplotype also had low M/ΔInsulin (0.51 ± 0.05 mg/kg/min/pmol/l/10²) and IGT (G₁₂₀ = 8.2 ± 0.7 mmol/l). Subjects with Arg16–Gln27/Gly16–Gln27 haplotype combination had the highest VO_2max (1.84 ± 0.07 l/min) and M/ΔInsulin (0.7 ± 0.04 mg/kg/min/pmol/l/10²), and normal glucose tolerance (G₁₂₀ = 6.4 ± 0.4 mmol/l), despite being obese. These data show associations of the ADRB2 Arg16Gly‐Gln27Glu haplotype with VO_2max and body composition, and an independent association with glucose metabolism, which persists after controlling for body composition and fitness. This suggests that ADRB2 haplotypes may mediate insulin action, glucose tolerance, and potentially risk for type 2 diabetes mellitus (T2DM) in obese, postmenopausal women.     

The Macrophage‐Specific Serum Marker,Soluble CD163, Is Increased in Obesity and Reduced After Dietary‐Induced Weight Loss

Objective: Soluble CD163 (sCD163) is a new macrophage‐specific serum marker elevated in inflammatory conditions. sCD163 is elevated in obesity and found to be a strong predictor of the development of type 2 diabetes. We investigated whether dietary intervention and moderate exercise was related to changes in sCD163 and how sCD163 is associated to insulin resistance in obesity. Design and Methods: Ninety‐six obese subjects were enrolled: 62 followed a very low energy diet (VLED) program for 8 weeks followed by 3‐4 weeks of weight stabilization, 20 followed a moderate exercise program for 12 weeks, and 14 were included without any intervention. Fasting blood samples and anthropometric measures were taken at baseline and after intervention. Thirty‐six lean subjects were included in a control group. Results: sCD163 was significantly higher in obese subjects (2.3 ± 1.0 mg/l) compared with lean (1.6 ± 0.4 mg/l, P < 0.001). Weight loss (11%) induced by VLED resulted in a reduction and partial normalization of sCD163 to 2.0 ± 0.9 mg/l (P < 0.001). Exercise for 12 weeks had no effect on sCD163. At baseline, sCD163 was significantly correlated with BMI (r = 0.46), waist circumference (r = 0.40), insulin resistance measured by the homeostasis model assessment (HOMA‐IR; r = 0.41; all P < 0.001), and the leptin‐to‐adiponectin ratio (r = 0.28, P < 0.05). In a multivariate linear regression analysis with various inflammatory markers, sCD163 (β = 0.25), adiponectin (β = ?0.24), and high sensitivity C‐reactive protein (hs‐CRP; β = 0.20) remained independently and significantly associated to HOMA‐IR (all P < 0.05). After further adjustment for waist circumference, only sCD163 was associated with HOMA‐IR (P < 0.05). Conclusion: The macrophage‐specific serum marker sCD163 is increased in obesity and partially normalized by dietary‐induced weight loss but not by moderate exercise. Furthermore, we confirm that sCD163 is a good marker for obesity‐related insulin resistance.     

Dietary Weight Loss Decreases Serum Angiotensin-Converting Enzyme Activity in Obese Adults

Objective: To study the effect of dietary weight loss, postural change, and an oral glucose load on serum angiotensin-converting enzyme (ACE) activity in obese adults. Research Methods and Procedures: Sixteen obese adult men and women with a mean body mass index of 35.7 ± 4.3 kg/m² were studied after 1 week on a maintenance energy lead-in diet and after 5 weeks on an identical but 40% reduced-energy diet provided by the General Clinical Research Center (GCRC). ACE activity was measured spectrophotometrically. Plasma renin activity and serum aldosterone were measured by radioimmunoassay. Results: All subjects lost weight, with a mean decrease in body weight of 7.0 ± 2.1 kg or 6 ± 3% of initial body weight (p < 0.00001). Systolic and diastolic blood pressure, supine plasma renin activity, and serum aldosterone levels decreased with weight loss (p < 0.05). Supine ACE activity decreased 23 ± 12% with weight loss (p < 0.00001). Standing ACE activity, which was significantly higher than supine ACE activity before and after weight loss (p < 0.05), also decreased 18 ± 17% with weight loss (p = 0.0007). A 75-g oral glucose load had no effect on serum ACE activity over a 3-hour period. Discussion: In obese adults, serum ACE activity declines with modest weight loss, increases with postural change, and is unaffected by an oral glucose load.     

Night Eating Syndrome Is Associated with Depression,Low Self‐Esteem,Reduced Daytime Hunger,and Less Weight Loss in Obese Outpatients

Objective: The objective of this study was to assess the relationship between the night eating syndrome (NES), measures of depression and self‐esteem, test meal intake, and weight loss in obese participants. Research Methods and Procedures: The study included 76 overweight (body mass index = 36.7 ± 6.5 SD) outpatients (53 women and 23 men; aged 43.5 ± 9.5 years) entering a weight loss program. They completed a Night Eating Questionnaire, the Zung Depression Inventory, and the Rosenberg Self‐Esteem Scale. Based on criteria by Stunkard et al. (Stunkard A, Berkowitz R, Wadden T, Tanrikut C, Reiss E, Young L. Binge eating disorder and the night eating syndrome. Int J Obes Relat Metab Disord. 1996;20:1–6), participants had NES if they reported: (1) skipping breakfast ≥4 d/wk, interpreted as morning anorexia; (2) consuming more than 50% of total daily calories after 7 pm ; and (3) difficulty falling asleep or staying asleep ≥4 d/wk. Eleven (14%) participants met the criteria for NES. After an 8‐hour fast, all participants ingested a nutritionally complete liquid meal through a straw from a large opaque cooler until extremely full. They also completed ratings of hunger and fullness before and after this meal. Results: Night eaters had higher depression (p = 0.04), lower self‐esteem (p = 0.003), and less hunger (p = 0.005), and a trend for more fullness (p = 0.06) before the daytime test meal than the others. However, there were no significant differences in test‐meal intake between groups. Nevertheless, test‐meal intake was greater later in the day only for the night eaters (p = 0.01). Over a 1‐month period, the night eaters lost less weight (4.4 ± 3.2 kg) than the others (7.3 ± 3.2 kg; p = 0.04), after controlling for body mass index. Discussion: NES is a syndrome with distinct psychopathology and increased food intake later in the day, both of which may contribute to poorer weight loss outcome. NES criteria need to be better quantified and NES deserves consideration as a diagnostic eating disorder.