Objectives: We sought to estimate the means and percentile cutoffs of PBF, TBF, and FFM and to assess the differences by sex, age, race-ethnicity, and body mass index in US adults.

Design: Data from the National Health and Nutrition Examination Survey (NHANES), which were collected during the 6-y period from 1999 to 2004 and comprise a large nationally representative sample of the US population, were analyzed (n = 6559 men and 6507 nonpregnant women). TBF and FFM were measured by using dual-energy X-ray absorptiometry. PBF was calculated as TBF divided by total mass multiplied by 100.

Results: There were large differences between men and women in unadjusted mean PBF (28.1% compared with 40.0%, P < 0.001), TBF (25.4 compared with 30.8 kg, P < 0.001), and FFM (62.3 compared with 44.0 kg, P < 0.001); the sex differences persisted across all body mass index categories after adjustment for age and race-ethnicity (all P < 0.001). The common percentile cutoffs of PBF, TBF, and FFM were estimated by sex, race-ethnicity, and age groups. Equations for the estimation of PBF (R² = 0.85), TBF (R² = 0.94), and FFM (R² = 0.94) according to demographic characteristics and simple anthropometric measures were generated.

Conclusion: The estimates of means and percentile cutoffs for PBF, TBF, and FFM, on the basis of NHANES 1999–2004 dual-energy X-ray absorptiometry data, provide a reference in the US adult population.

Objective: The objective was to study the associations of 5 CLOCK polymorphisms with MetS features by analyzing fatty acid (FA) composition from dietary and red blood cell (RBC) membrane sources.

Design: Participants (n = 1100) in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study were included. Dietary intake was estimated with a validated questionnaire. Anthropometric and biochemical measurements and genotypes were determined. Postprandial lipids and the FA composition of RBC membranes were analyzed.

Results: CLOCK single nucleotide polymorphisms were significantly associated with obesity and individual components of MetS. For single nucleotide polymorphism rs4580704, minor allele carriers had a 46% lower risk of hypertension than did noncarriers. The monounsaturated fatty acid (MUFA) content of RBC membranes, particularly oleic acid, changed according to CLOCK genetic variants (P < 0.05). We identified significant gene-diet interactions associated with MetS at the CLOCK locus. By dichotomizing MUFA intake, we found different effects across rs4580704 genotypes for glucose (P = 0.020) and insulin resistance (P = 0.026). The protective effect of the minor allele on insulin sensitivity was only present when MUFA intake was >13.2% of energy. We also found different effects across CLOCK 3111T->C genotypes for saturated fatty acid intake (% of energy) (P = 0.017). The deleterious effect of gene variants on waist circumference was only found with high saturated fatty acid intakes (>11.8%).

Conclusions: CLOCK polymorphisms interact with FAs to modulate MetS traits. The dietary source and membrane content of MUFAs are implicated in the relations between alterations in the circadian system and MetS.

Objective: We aimed to test the hypothesis that acute sleep loss decreases physical activity while increasing food intake, thereby shifting 2 crucial behavioral components of energy homeostasis toward weight gain.

Design: In 15 healthy, normal-weight men, spontaneous physical activity was registered by accelerometry during the entire experiment, and food intake as well as relevant hormones were assessed during a 15-h daytime period after 2 nights of regular sleep (bed time: 2245–0700) and after 2 nights of restricted sleep (bed time: 0245–0700). Experiments were performed in a crossover design.

Results: Sleep restriction significantly decreased physical activity during the daytime spent under free-living conditions after the first night of sleep manipulation (P = 0.008). Also, intensities of physical activity were shifted toward lower levels, with less time spent with intense activities (P = 0.046). Total energy intake, feelings of hunger, and appetite as well as ghrelin and leptin concentrations during day 2 remained unaffected by acute sleep restriction.

Conclusions: In contrast to our expectation, short-term sleep loss neither increased food intake nor affected concentrations of the hunger-regulating hormones leptin and ghrelin. However, the observed decrease in daytime physical activity may point to another potentially important behavioral mechanism for the health-impairing influence of sleep loss.

Objective: Because FTO is highly expressed in hypothalamic regions that are important for appetite, FTO genotype may affect energy balance by influencing eating behavior. Loss of control (LOC) eating, a behavior commonly reported by overweight youth, predicts excessive weight gain in children. However, the relation between FTO genotype and LOC eating has not been previously examined.

Design: Two-hundred eighty-nine youth aged 6–19 y were genotyped for rs9939609, underwent body-composition measurements, and were interviewed to determine the presence or absence of LOC eating. A subset (n = 190) participated in a lunch buffet test meal designed to model an LOC eating episode. Subjects with AA and AT genotypes were grouped together for comparison with wild-type TT subjects.

Results: Subjects with at least one A allele (67.7%) had significantly greater body mass indexes, body mass index z scores (P < 0.01), and fat mass (P < 0.05). Of the AA/AT subjects, 34.7% reported LOC compared with 18.2% of the TT subjects (P = 0.002). Although total energy intake at the test meal did not differ significantly by genotype (P = 0.61), AA/AT subjects consumed a greater percentage of energy from fat than did the TT subjects (P < 0.01).

Conclusions: Children and adolescents with 1 or 2 FTO rs9939609 obesity-risk alleles report more frequent LOC eating episodes and select foods higher in fat at a buffet meal. Both LOC eating and more frequent selection of energy-dense, palatable foods may be mechanisms through which variant FTO alleles lead to excess body weight.

Objective: The objective was to test the hypothesis that temperature in a heat-dissipating region of the hand is elevated in obese adults.

Design: Obese [body mass index (in kg/m²) ≥ 30] and normal-weight (NW; body mass index = 18–25) adults were studied under thermoneutral conditions at rest. Core body temperature was measured by using ingested telemetric capsules. The temperatures of the third fingernail bed of the right hand and of abdominal skin from an area 1.5 cm inferior to the umbilicus were determined by using infrared thermography. Abdominal skin temperatures were also measured via adhesive thermistors that were placed over a prominent skin-surface blood vessel and over an adjacent nonvessel location. The groups were compared by analysis of covariance with age, sex, race, and room temperature as covariates.

Results: Core temperature did not differ significantly between the 23 obese and 13 NW participants (P = 0.74). However, infrared thermography–measured fingernail-bed temperature was significantly higher in obese subjects than in NW subjects (33.9 ± 0.7°C compared with 28.6 ± 0.9°C; P < 0.001). Conversely, infrared thermography–measured abdominal skin temperature was significantly lower in obese subjects than in NW subjects (31.8 ± 0.2°C compared with 32.8 ± 0.3°C; P = 0.02). Nonvessel abdominal skin temperatures measured by thermistors were also lower in obese subjects (P = 0.04).

Conclusions: Greater subcutaneous abdominal adipose tissue in obese adults may provide a significant insulating layer that blunts abdominal heat transfer. Augmented heat release from the hands may offset heat retention in areas of the body with greater adiposity, thereby helping to maintain normothermia in obesity. This trial was registered at clinicaltrials.gov as NCT00266500.

Objectives: We aimed to 1) replicate previous findings that showed preferential central accumulation of adipose tissue in recently weight-restored AN women compared with control subjects, 2) describe the change within patients with longer-term (1-y) weight maintenance, and 3) compare adipose tissue distribution after 1-y maintenance with that of control subjects.

Design: Body composition and adipose tissue distribution were assessed by whole-body magnetic resonance imaging in women with AN shortly after weight normalization (n = 30) and again 1 y after hospital discharge (n = 16) and in 8 female control subjects at 2 time points.

Results: With acute weight restoration, AN patients had significantly greater visceral and intermuscular adipose tissue compared with control women [visceral: 0.75 ± 0.26 compared with 0.51 ± 0.26 kg in AN patients and controls, respectively (P = 0.02); intermuscular: 0.46 ± 0.17 compared with 0.29 ± 0.13 kg in AN patients and controls, respectively (P = 0.01)]. With maintenance of normal weight for 1 y, visceral adipose tissue distribution in AN patients was not different from that in healthy control subjects.

Conclusions: In adult women with AN, normalization of weight in the short term is associated with a distribution of adipose tissue that is consistent with a central adiposity phenotype. This abnormal distribution appears to normalize within a 1-y period of weight maintenance. This research was registered at clinicaltrials.gov as NCT 00271921 and NCT 00368667.

Objective: This study examined the effects of ADF that is administered under controlled compared with self-implemented conditions on body weight and coronary artery disease (CAD) risk indicators in obese adults.

Design: Sixteen obese subjects (12 women, 4 men) completed a 10-wk trial, which consisted of 3 phases: 1) a 2-wk control phase, 2) a 4-wk weight loss/ADF controlled food intake phase, and 3) a 4-wk weight loss/ADF self-selected food intake phase.

Results: Dietary adherence remained high throughout the controlled food intake phase (days adherent: 86%) and the self-selected food intake phase (days adherent: 89%). The rate of weight loss remained constant during controlled food intake (0.67 ± 0.1 kg/wk) and self-selected food intake phases (0.68 ± 0.1 kg/wk). Body weight decreased (P < 0.001) by 5.6 ± 1.0 kg (5.8 ± 1.1%) after 8 wk of diet. Percentage body fat decreased (P < 0.01) from 45 ± 2% to 42 ± 2%. Total cholesterol, LDL cholesterol, and triacylglycerol concentrations decreased (P < 0.01) by 21 ± 4%, 25 ± 10%, and 32 ± 6%, respectively, after 8 wk of ADF, whereas HDL cholesterol remained unchanged. Systolic blood pressure decreased (P < 0.05) from 124 ± 5 to 116 ± 3 mm Hg.

Conclusion: These findings suggest that ADF is a viable diet option to help obese individuals lose weight and decrease CAD risk. This trial was registered at clinicaltrials.gov as UIC-004-2009.

Objective: The objective of this study was to examine associations of C17A + G241A and +2138InsCAGACC MC3R variants with children's energy balance.

Design: Children aged 6–19 y were genotyped for MC3R C17A, G241A, and +2138InsCAGACC. Subjects underwent studies of energy intake from a 9835-kcal food array (n = 185), resting energy expenditure (REE) by using indirect calorimetry (n = 302), or total daily energy expenditure (TEE) by using doubly labeled water (n = 120). Linear regression was used to examine the associations between MC3R polymorphisms and the measures of energy balance.

Results: Body mass index and fat mass were greater in those with double homozygosity for C17A + G241A (P = 0.001). After accounting for covariates (including body composition), the number of minor C17A + G241A alleles was associated with significantly greater energy intake (β = +0.15, P = 0.02) but not altered REE or TEE. No significant associations were observed between +2138InsCAGACC and measures of either fat mass or energy balance.

Conclusions: C17A + G241A polymorphisms may be associated with pediatric obesity because of greater energy intake rather than because of diminished energy expenditure. +2138InsCAGACC does not appear to be associated with obesity or measures of energy balance in children.

Objective: The aim of this study was to assess the effects of 12 wk of mandatory exercise on appetite control.

Design: Fifty-eight overweight and obese men and women [mean (±SD) body mass index (in kg/m²) = 31.8 ± 4.5, age = 39.6 ± 9.8 y, and maximal oxygen intake = 29.1 ± 5.7 mL · kg^–1 · min^–1] completed 12 wk of supervised exercise in the laboratory. The exercise sessions were designed to expend 2500 kcal/wk. Subjective appetite sensations and the satiating efficiency of a fixed breakfast were compared at baseline (week 0) and at week 12. An Electronic Appetite Rating System was used to measure subjective appetite sensations immediately before and after the fixed breakfast in the immediate postprandial period and across the whole day. The satiety quotient of the breakfast was determined by calculating the change in appetite scores relative to the breakfast's energy content.

Results: Despite large variability, there was a significant reduction in mean body weight (3.2 ± 3.6 kg), fat mass (3.2 ± 2.2 kg), and waist circumference (5.0 ± 3.2 cm) after 12 wk. The analysis showed that a reduction in body weight and body composition was accompanied by an increase in fasting hunger and in average hunger across the day (P < 0.0001). Paradoxically, the immediate and delayed satiety quotient of the breakfast also increased significantly (P < 0.05).

Conclusions: These data show that the effect of exercise on appetite regulation involves at least 2 processes: an increase in the overall (orexigenic) drive to eat and a concomitant increase in the satiating efficiency of a fixed meal.

Objective: The objective was to compare the brain responses of SWLs to food pictures with those of NW and obese controls.

Design: Blood oxygen level–dependent responses to high- and low-energy food pictures were measured in 18 NW controls, 16 obese controls, and 17 SWLs.

Results: Group differences were identified in 4 regions, which indicated significant change in activation in response to the food pictures. SWLs showed greater activation in the left superior frontal region and right middle temporal region than did NW and obese controls—a pattern of results confirmed in exploratory voxel-wise analyses. Obese controls also showed greater activation in a bilateral precentral region.

Conclusions: These results suggest that SWLs show greater activation in frontal regions and primary and secondary visual cortices—a pattern consistent with greater inhibitory control in response to food cues and greater visual attention to the food cues. A greater engagement of inhibitory control regions in response to food cues as well as a greater monitoring of foods may promote control of food intake and successful weight-loss maintenance.

Objective: The objective was to assess whether beverage intake at age 5 y predicted energy intake, adiposity, and weight status across childhood and adolescence.

Design: Participants were part of a longitudinal study of non-Hispanic white girls and their parents (n = 170) who were assessed biennially from age 5 to 15 y. At each assessment, beverage intake (milk, fruit juice, and sweetened beverages) and energy intake were assessed by using three 24-h recalls. Percentage body fat and waist circumference were measured. Height and weight were measured and used to calculate body mass index. Multiple regression analyses were used to predict the girls’ adiposity. In addition, at age 5 y, girls were categorized as consuming <1, ≥1 and <2, or ≥2 servings of sweetened beverages. A mixed modeling approach was used to assess longitudinal differences and patterns of change in sweetened beverage and energy intake, adiposity, and weight status by frequency of sweetened beverage intake.

Results: Sweetened beverage intake at age 5 y, but not milk or fruit juice intake, was positively associated with adiposity from age 5 to 15 y. Greater consumption of sweetened beverages at age 5 y (≥2 servings/d) was associated with a higher percentage body fat, waist circumference, and weight status from age 5 to 15 y.

Conclusion: These findings provide new longitudinal evidence that early intake of sweetened beverages predicts adiposity and weight status across childhood and adolescence.

Objective: The objective was to identify factors associated with vitamin D status and deficiency in obese adolescents to further evaluate the relation of body fat indexes to vitamin D status and deficiency.

Design: Data from 58 obese adolescents were obtained. Visceral adipose tissue (VAT) was measured by computed tomography. Dual-energy X-ray absorptiometry was used to measure total bone mineral content, bone mineral density, body fat mass (FM), and lean mass. Relative measures of body fat were calculated. Blood tests included measurements of 25-hydroxyvitamin D [25(OH)D], parathyroid hormone (PTH), osteocalcin, type I collagen C-telopeptide, hormones, and metabolic factors. Vitamin D deficiency was defined as 25(OH)D < 20 ng/mL. PTH elevation was defined as PTH > 65 ng/mL.

Results: The mean (±SD) age of the adolescents was 14.9 ± 1.4 y; 38 (66%) were female, and 8 (14%) were black. The mean (±SD) body mass index (in kg/m²) was 36 ± 5, FM was 40.0 ± 5.5%, and VAT was 12.4 ± 4.3%. Seventeen of the adolescents were vitamin D deficient, but none had elevated PTH concentrations. Bone mineral content and bone mineral density were within 2 SDs of national standards. In a multivariate analysis, 25(OH)D decreased by 0.46 ± 0.22 ng/mL per 1% increment in FM (β ± SE, P = 0.05), whereas PTH decreased by 0.78 ± 0.29 pg/mL per 1% increment in VAT (P = 0.01).

Conclusions: To the best of our knowledge, our results show for the first time that obese adolescents with 25(OH)D deficiency, but without elevated PTH concentrations, have a bone mass within the range of national standards (±2 SD). The findings provide initial evidence that the distribution of fat may be associated with vitamin D status, but this relation may be dependent on metabolic factors. This study was registered at www.clinicaltrials.gov as NCT00209482, NCT00120146.