Autonomic Nervous System Activity and the State and Development of Obesity in Japanese School Children

Objective: The autonomic nervous system (ANS) plays an important role in regulating energy expenditure and body fat content; however, the extent to which the ANS contributes to pediatric obesity remains inconclusive. The aim of this study was to evaluate whether sympathetic and/or the parasympathetic nerve activities were altered in an obese pediatric population. We further examined a physiological association between the duration of obesity and the sympatho‐vagal activities to scrutinize the nature of ANS alteration as a possible etiologic factor of childhood obesity. Research Methods and Procedures: Forty‐two obese and 42 non‐obese healthy sedentary school children were carefully selected from 1080 participants initially recruited to this study. The two groups were matched in age, gender, and height. The clinical records of physical characteristics and development of the obese children were retrospectively reviewed to investigate the onset and progression of obesity. The ANS activities were assessed during a resting condition by means of heart rate variability power spectral analysis, which enables us to identify separate frequency components, i.e., total power (TP), low‐frequency (LF) power, and high‐frequency (HF) power. The spectral powers were then logarithmically transformed for statistical testing. Results: The obese children demonstrated a significantly lower TP (6.77 ± 0.12 vs. 7.11 ± 0.04 ln ms², p < 0.05), LF power (6.16 ± 0.12 vs. 6.42 ± 0.05 ln ms², p < 0.05), and HF power (5.84 ± 0.15 vs. 6.34 ± 0.07 ln ms², p < 0.01) compared with the non‐obese children. A partial correlation analysis revealed that the LF and HF powers among 42 obese children were negatively associated with the duration of obesity independent of age (LF: partial r = ?0.55, p < 0.001; HF: partial r = ?0.40, p < 0.01). The obese children were further subdivided into two groups based on the length of their obesity. All three spectral powers were significantly reduced in the obese group with obesity of >3 years (n = 18) compared to the group with obesity of <3 years. Discussion: Our data indicate that obese children possess reduced sympathetic as well as parasympathetic nerve activities. Such autonomic depression, which is associated with the duration of obesity, could be a physiological factor promoting the state and development of obesity. These findings further imply that preventing and treating obesity beginning in the childhood years could be an urgent and crucial pediatric public health issue.     

The Association between Plasma Adiponectin and Insulin Sensitivity in Humans Depends on Obesity

Objective: In humans, low plasma adiponectin concentrations precede a decrease in insulin sensitivity and predict type 2 diabetes independently of obesity. However, it is possible that the contribution of adiponectin to insulin sensitivity is not equally strong over the whole range of obesity. Research Methods and Procedures: We investigated the cross‐sectional association between plasma adiponectin levels and insulin sensitivity in different ranges of body fat content [expressed as percentage of body fat (PFAT)] in a large cohort of normal glucose‐tolerant subjects (n = 900). All individuals underwent an oral glucose tolerance test (OGTT), and 299 subjects additionally a euglycemic hyperinsulinemic clamp. In longitudinal analyses, the association of adiponectin at baseline with change in insulin sensitivity was investigated in a subgroup of 108 subjects. Results: In cross‐sectional analyses, the association between plasma adiponectin and insulin sensitivity, adjusted for age, gender, and PFAT, depended on whether subjects were lean or obese [p for interaction adiponectin × PFAT = <0.001 (OGTT) and 0.002 (clamp)]. Stratified by quartiles of PFAT, adiponectin did not correlate significantly with insulin sensitivity in subjects in the lowest PFAT quartile (R² = 0.10, p = 0.13, OGTT; and R² = 0.10, p = 0.57, clamp), whereas the association in the upper PFAT quartile was rather strong (R² = 0.36, p < 0.0001, OGTT; and R² = 0.48, p = 0.003, clamp). In longitudinal analyses, plasma adiponectin at baseline preceded change in insulin sensitivity in obese (n = 54, p = 0.03) but not in lean (n = 54, p = 0.68) individuals. Discussion: These data suggest that adiponectin is especially critical in sustaining insulin sensitivity in obese subjects. Thus, interventions to reduce insulin resistance by increasing adiponectin concentrations may be effective particularly in obese, insulin‐resistant individuals.     

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.     

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 Physical Training and Its Cessation on Percent Fat and Bone Density of Children with Obesity

GUTIN, BERNARD, SCOTT OWENS, TOMOKI OKUYAMA, SHARON RIGGS, MICHAEL FERGUSON, AND MARK LITAKER. Effect of physical training and its cessation on percent fat and bone density of children with obesity. Obes Res. Objective We determined the effect of 4-month periods of physical training (PT) and detraining on percent fat (percent fat) and bone density of children with obesity. Research Methods and Procedures Subjects were 79 7- to 11-year-old children with obesity; 34 were white, 44 were black, and 1 was Asian, 26 were male and 53 were female. They were randomly assigned to two groups: group 1 engaged in PT for the first 4 months, while group 2 engaged in PT during the second 4 months. Body composition was measured with dual energy absorptiometry, and diet was measured with 4 days of recall for each 4-month period. PT was offered 5 dayslweek for 40 minuteslsession, heart rate monitors were worn, and no dietary information was given; mean attendance was 80%, and mean heart rate per session was 157 bpm. Results Group by time interactions across the three time-points (from analysis of variance) were significant for percent fat (p = <0.001) and bone density (p = 0.045). Both groups declined in percent fat during the periods of PT, by an average of 1.6 %fat units; in the 4 months after cessation of PT, group 1 increased by 1.3 %fat. In both groups, bone density increased more during periods of PT (0.025 g/cm²) than during periods of no PT (0.010 g/cm²). No significant PT vs. no-PT differences were found for dietary intake of energy, macronutrients, or calcium. Discussion This study suggests that regular exercise, without dietary intervention, can enhance the body composition of children with obesity.     

Leptin Levels Are Associated with Fat Oxidation and Dietary‐Induced Weight Loss in Obesity

Objective: To examine the relationship between fasting plasma leptin and 24‐hour energy expenditure (EE), substrate oxidation, and spontaneous physical activity (SPA) in obese subjects before and after a major weight reduction compared with normal weight controls. To test fasting plasma leptin, substrate oxidations, and SPA as predictive markers of success during a standardized weight loss intervention. Research Methods and Procedures: Twenty‐one nondiabetic obese (body mass index: 33.9 to 43.8 kg/m²) and 13 lean (body mass index: 20.4 to 24.7 kg/m²) men matched for age and height were included in the study. All obese subjects were reexamined after a mean weight loss of 19.2 kg (95% confidence interval: 15.1–23.4 kg) achieved by 16 weeks of dietary intervention followed by 8 weeks of weight stability. Twenty‐four‐hour EE and substrate oxidations were measured by whole‐body indirect calorimetry. SPA was assessed by microwave radar. Results: In lean subjects, leptin adjusted for fat mass (FM) was correlated to 24‐hour EE before (r = ?0.56, p < 0.05) but not after adjustment for fat free mass. In obese subjects, leptin correlated inversely with 24‐hour and resting nonprotein respiratory quotient (r = ?0.47, p < 0.05 and r = ?0.50, p < 0.05) both before and after adjustments for energy balance. Baseline plasma leptin concentration, adjusted for differences in FM, was inversely related to the size of weight loss after 8 weeks (r = ?0.41, p = 0.07), 16 weeks (r = ?0.51, p < 0.05), and 24 weeks (r = ?0.50, p < 0.05). Discussion: The present study suggests that leptin may have a stimulating effect on fat oxidation in obese subjects. A low leptin level for a given FM was associated with a greater weight loss, suggesting that obese subjects with greater leptin sensitivities are more successful in reducing weight.     

Maternal feeding strategies, child eating behaviors, and child BMI in low-income African-American preschoolers

Objective: To test the hypothesis that low‐income African‐American preschool children would have a higher BMI if their mothers reported greater “restriction” and “control” in feeding and if mothers reported that children showed greater “food responsiveness” and “desire to drink.” In addition, to test whether higher maternal “pressure to eat” would be associated with lower child BMI. Research Methods and Procedures: A questionnaire was completed by 296 low‐income African‐American mothers of preschool children. It assessed three constructs on maternal feeding strategies (“restriction,” “pressure to eat,” and “control”) and two on child eating behaviors (“food responsiveness” and “desire to drink”). Children's BMI was measured, and mothers’ BMI was self‐reported. Results: The mean (standard deviation) BMI z‐score of the children was 0.34 (1.5), and 44% of the mothers were obese (BMI ≥30 kg/m²). Only maternal “pressure to eat” had a significant overall association with child BMI z‐score (r = ?0.16, p < 0.01). Both maternal “restriction” and “control” were positively associated with children's BMI z‐score in the case of obese mothers (r = 0.20, p = 0.03 and r = 0.24, p = 0.007, respectively), but this was not so in the case of non‐obese mothers (r = ?0.16, p = 0.05 and r = ?0.07, p = 0.39, respectively). Discussion: Among low‐income African Americans, the positive association between maternal restriction and control in feeding and their preschoolers’ BMI was limited to obese mothers. Relations between parent feeding strategies and child weight status in this population may differ on the basis of maternal weight status.     

Lipoprotein Oxidation and Plasma Vitamin E in Nondiabetic Normotensive Obese Patients

Objective: To correlate the susceptibility of low‐(LDL) and very‐low‐density lipoprotein to oxidation in vitro and the concentrations of serum antibodies against malondialdehyde‐modified LDL and plasma vitamin E with the anthropometric and laboratory characteristics of obesity. Research Methods and Procedures: A total of 75 nondiabetic, normotensive obese patients were assigned to one of four groups according to their body mass index (BMI): moderately obese (30 ≤ BMI ≤ 34.9 kg/m², n = 11), severely obese (35 ≤ BMI ≤ 39.9 kg/m², n = 20), morbidly obese (40 ≤ BMI ≤ 50 kg/m², n = 29), and very severely obese (BMI > 50 kg/m², n = 15). Results: The oxidation lag time for LDL from patients with a BMI ≥35 kg/m² was shorter than that for LDL from non‐obese controls (n = 13), whereas very‐low‐density lipoprotein oxidation lag times were not significantly different. The serum antibodies against modified LDL were similar in all groups, whereas the plasma vitamin E concentrations of obese patients were decreased (p ≤ 0.01). There was a negative correlation between LDL oxidation lag time and BMI (r = ?0.35, p = 0.0008), and between plasma vitamin E and BMI (r = ?0.53, p < 0.0001) and waist‐to‐hip ratio (r = ?0.40, p = 0.0003). Discussion: The LDL of nondiabetic, normotensive obese patients is more readily oxidized, and plasma vitamin E concentrations are low. These are both risk factors for coronary heart disease.     

The Feet of Overweight and Obese Young Children: Are They Flat or Fat?

Objective: The purpose of this study was to determine whether the flat feet displayed by young obese and overweight children are attributable to the presence of a thicker midfoot plantar fat pad or a lowering of the longitudinal arch relative to that in non‐overweight children. Research Methods and Procedures: Foot anthropometry, an arch index derived from plantar footprints, and midfoot plantar fat pad thickness measured by ultrasound were obtained for 19 overweight/obese preschool children (mean age, 4.3 ± 0.9 years; mean height, 1.07 ± 0.1 m; mean BMI, 18.6 ± 1.2 kg/m²) and 19 non‐overweight children matched for age, height, and sex (mean age, 4.3 ± 0.7 years; mean height, 1.05 ± 0.1 m; mean BMI, 15.7 ± 0.7 kg/m²). Results: Independent t tests revealed no significant between‐subject group differences (p = 0.39) in the thickness of the midfoot plantar fat pad. However, the overweight/obese children had a significantly lower plantar arch height (0.9 ± 0.3 cm) than their non‐overweight counterparts (1.1 ± 0.2 cm; p = 0.04). Discussion: The lower plantar arch height found in the overweight/obese children suggests that the flatter feet characteristic of overweight/obese preschool children may be caused by structural changes in their foot anatomy. It is postulated that these structural changes, which may adversely affect the functional capacity of the medial longitudinal arch, might be exacerbated if excess weight bearing continues throughout childhood and into adulthood.     

Insulin‐ and Exercise‐Stimulated Skeletal Muscle Blood Flow and Glucose Uptake in Obese Men

Objective: Insulin resistance in obese subjects results in the impaired use of glucose by insulin‐sensitive tissues, e.g., skeletal muscle. In the present study, we determined whether insulin resistance in obesity is associated with an impaired ability of exercise to stimulate muscle blood flow, oxygen delivery, or glucose uptake. Research Methods and Procedures: Nine obese (body mass index = 36 ± 2 kg/m²) and 11 age‐matched nonobese men (body mass index = 22 ± 1 kg/m²) performed one‐legged isometric exercise during hyperinsulinemia. Rates of femoral muscle blood flow, oxygen consumption, and glucose uptake were measured simultaneously in both legs using [¹⁵O]H₂O, [¹⁵O]O₂, [¹⁸F]fluoro‐deoxy‐glucose, and positron emission tomography. Results: The obese subjects exhibited resistance to insulin stimulation of glucose uptake in resting muscle, regardless of whether glucose uptake was expressed per kilogram of femoral muscle mass (p = 0.001) or per the total mass of quadriceps femoris muscle. At similar workloads, oxygen consumption, blood flow, and glucose uptake were lower in the obese than the nonobese subjects when expressed per kilogram of muscle, but similar when expressed per quadriceps femoris muscle mass. Discussion: We conclude that obesity is characterized by insulin resistance of glucose uptake in resting skeletal muscle regardless of how glucose uptake is expressed. When compared with nonobese individuals at similar absolute workloads and under identical hyperinsulinemic conditions, the ability of exercise to increase muscle oxygen uptake, blood flow, and glucose uptake per muscle mass is blunted in obese insulin‐resistant subjects. However, these defects are compensated for by an increase in muscle mass.     

Twenty-four-hour ghrelin is elevated after calorie restriction and exercise training in non-obese women

Objective: The purpose of this study was to determine whether chronic energy deficiency achieved with caloric restriction combined with exercise is associated with changes in the 24‐hour profile of ghrelin in non‐obese, pre‐menopausal women. Research Methods and Procedures: Twelve non‐obese (BMI = 18 to 25 kg/m²), non‐exercising women (age, 18 to 24 years) were randomly assigned to a non‐exercising control group or a diet and exercise group. The 3‐month diet and exercise intervention yielded a daily energy deficit of ?45.7 ± 12.4%. Serial measurements were made of body composition, energy balance, and feelings of fullness. Repeated blood sampling over 24 hours to measure ghrelin occurred before and after the study. Results: Significant decreases in body weight, body fat, and feelings of fullness were observed in only the energy‐deficit group (p < 0.05); significant changes in the following ghrelin features were found in only the deficit group (p < 0.05): elevations in baseline (+353 ± 118 pg/mL), lunch peak (+370 ± 102 pg/mL), dinner peak (+438 ± 149 pg/mL), nocturnal rise (+269 ± 77 pg/mL), and nocturnal peak (+510 ± 143 pg/mL). In addition, we found a larger dinner decline (?197 ± 52 pg/mL) and negative correlations between changes in the ghrelin dinner profile and changes in body weight (R = 0.784), 24‐hour intake (R = 0.67), energy deficiency (R = 0.762), and feelings of fullness (R = 0.648; p < 0.05). Discussion: Changes in ghrelin concentrations across the day after weight loss are closely associated with other physiological adaptations to energy deficiency, further supporting the role of ghrelin as a countermeasure to restore energy balance.     

Stigmatized Students: Age,Sex, and Ethnicity Effects in the Stigmatization of Obesity

Objective: To assess the stigmatization of obesity relative to the stigmatization of various disabilities among young men and women. Attitudes across ethnic groups were compared. In addition, these findings were compared with data showing severe stigmatization of obesity among children. Research Methods and Procedures: Participants included 356 university students (56% women; mean age, 20.6 years; mean BMI, 23.3 kg/m²; range, 14.4 to 45.0 kg/m²) who ranked six drawings of same‐sex peers in order of how well they liked each person. The drawings showed adults with obesity, various disabilities, or no disability. These rankings were compared with those obtained through a similar procedure with 458 fifth‐ and sixth‐grade children. Results: Obesity was highly stigmatized relative to physical disabilities. African‐American women liked obese peers more than did African‐American men, white men, or white women [F (1, 216) = 4.02, p < 0.05]. Overweight and obese participants were no less stigmatizing of obesity than normal weight participants. Adults were more accepting than children of their obese peers [t (761) = 9.16, p < 0.001]. Discussion: Although the stigmatization of obesity was high among participants overall, African‐American women seemed to have more positive attitudes toward obesity than did white women, white men, or African‐American men. Participants’ weight did not affect their stigmatization of obesity: obese and overweight adults were as highly stigmatizing of obesity as non‐overweight adults. Such internalized stigmatization could help to explain the low self‐esteem and poor body image among obese young adults. However, adults seemed to have more positive attitudes about obesity than children. An understanding of the factors that limit the stigma of obesity among African‐American women could help efforts to reduce stigma.     

Skeletal muscle fat oxidation is increased in African-American and white women after 10 days of endurance exercise training

Objective: Obesity is associated with lower rates of skeletal muscle fatty acid oxidation (FAO), which is linked to insulin resistance. FAO is reduced further in obese African‐American (AAW) vs. white women (CW) and may also be lower in lean AAW vs. CW. In lean CW, endurance exercise training (EET) elevates the oxidative capacity of skeletal muscle. Therefore, we determined whether EET would elevate skeletal muscle FAO similarly in AAW and CW with a lower lipid oxidative capacity. Research Methods and Procedures: In vitro rates of FAO were assessed in rectus abdominus muscle strips using [1‐¹⁴C] palmitate (Pal) from lean AAW [BMI = 24.2 ± 0.9 (standard error) kg/m²] and CW (23.6 ± 0.8 kg/m²) undergoing voluntary abdominal surgery. Lean AAW (22 ± 0.9 kg/m²) and CW (24 ± 0.8 kg/m²) and obese AAW (36 ± 1.2 kg/m²) and CW (40 ± 1.3 kg/m²) underwent 10 consecutive days of EET on a cycle ergometer (60 min/d, 75% peak oxygen uptake). FAO was measured in vastus lateralis homogenates as captured ¹⁴CO₂ using [1‐¹⁴C] Pal, palmitoyl‐CoA (Pal‐CoA), and palmityl‐carnitine (Pal‐Car). Results: Muscle strip experiments showed suppressed rates of FAO (p = 0.03) in lean AAW vs. CW. EET increased the rates of skeletal muscle Pal oxidation (p = 0.05) in both lean AAW and CW. In obese subjects, Pre‐EET Pal (but not Pal‐CoA or Pal‐Car) oxidation was lower (p = 0.05) in AAW vs. CW. EET increased Pal oxidation 100% in obese AAW (p < 0.05) and 59% (p < 0.05) in obese CW. Similar increases (p < 0.05) in post‐EET FAO were observed for Pal‐CoA and Pal‐Car in both groups. Discussion: Both lean and obese AAW possess a lower capacity for skeletal muscle FAO, but EET increases FAO similarly in both AAW and CW. These data suggest the use of EET for treatment against obesity and diabetes for both AAW and CW.     

Body Weight Modulates Cholesterol Metabolism in Non‐Insulin Dependent Type 2 Diabetics

Objective: Cholesterol metabolism was studied in 64 subjects with type 2 diabetes who had body weight ranging from normal to obese, to find out whether weight interferes with cholesterol metabolism in diabetes. Research Methods and Procedures: Cholesterol absorption was measured with peroral isotopes and by assaying serum plant sterol and cholestanol to cholesterol ratios, cholesterol synthesis with sterol balance, and measuring serum cholesterol precursor ratios. Results: The study population was divided into normal‐weight (body mass index, 24.1 ± 0.4 kg/m²; mean ± SEM; n = 20) and obese (31.0 ± 0.5 kg/m²; n = 44) groups. Despite similar serum cholesterol and blood glucose values, fecal neutral sterol excretion, cholesterol and bile acid synthesis, cholesterol turnover (1649 ± 78 vs. 1077 ± 52 mg/d; p < 0.001), and serum cholesterol precursors were higher, and cholesterol absorption % (32 ± 1 vs. 40 ± 2%; p < 0.05), serum cholestanol, and plant sterols were lower in the obese vs. the non‐obese groups. Serum sex hormone‐binding globulin was positively associated with variables of cholesterol absorption, whereas blood glucose, serum insulin, and body mass index were associated with variables of cholesterol synthesis. In multiple stepwise regression analysis, cholesterol absorption percentage (R² = 24%) and body mass index (R² = 15%) were the only variables explaining the variability of cholesterol synthesis. Discussion: Body weight, through its entire range, regulates cholesterol metabolism in type 2 diabetes such that with increasing insulin resistance, cholesterol absorption is lowered and cholesterol synthesis increased.     

Effect of sarcopenia on cardiovascular disease risk factors in obese postmenopausal women

Objective: To compare sarcopenic‐obese and obese postmenopausal women for risk factors predisposing to cardiovascular disease (CVD) and determine whether there may be a relationship between muscle mass and metabolic risk in obese postmenopausal women. Research Methods and Procedures: In this cross‐sectional study, 22 healthy obese postmenopausal women (mean age, 66 ± 5 years; mean BMI, 27 ± 3 kg/m²) were divided into two groups matched for age (±2 years) and fat mass (FM) (±2%). Sarcopenia was defined as a muscle mass index of <14.30 kg fat‐free mass (FFM)/m² (which corresponds to 1 standard deviation below the values of a young reference population), and obesity was defined as an FM of >35% (which corresponds to the World Health Organization guidelines). FM, FFM (measured by DXA), daily energy expenditure (accelerometry), dietary intake (3‐day dietary record), and blood biochemical analyses (lipid profile, insulin, glucose, and C‐reactive protein) were obtained. Visceral fat mass (VFM) was calculated by the equation of Bertin, which estimates VFM from DXA measurements. Results: Obese women had more FFM (p = 0.006), abdominal FM (p = 0.047), and VFM (p = 0.041) and a worse lipid profile [p = 0.040 for triglycerides; p = 0.004 for high‐density lipoprotein (HDL); p = 0.026 for total cholesterol/HDL] than sarcopenic‐obese postmenopausal women. Obese women also ingested significantly more animal (p = 0.001) and less vegetal proteins (p = 0.013), although both groups had a similar total protein intake (p = 0.967). Discussion: Sarcopenia seems to be associated with lower risk factors predisposing to CVD in obese postmenopausal women. With the increase in the number of aging people, the health implications of being sarcopenic‐obese merit more attention.     

Ghrelin Does Not Influence Gastric Emptying in Obese Subjects

Objective: To evaluate the relationship between fasting plasma concentrations of ghrelin and gastric emptying in obese individuals compared with lean subjects. Research Methods and Procedures: We included 20 obese patients (9 men and 11 women, BMI > 30 kg/m²) and 16 nonobese control subjects (7 men and 9 women, BMI ≤ 25 kg/m²). Gastric emptying of solids (egg sandwich labeled with radionuclide) was measured at 120 minutes with (99m)Tc‐single photon emission computed tomography imaging. Ghrelin and leptin were analyzed by radioimmunoassay and ELISA methods, respectively. Results: The gastric half‐emptying time was similar in obese men and women (67.8 ± 14.79 vs. 66.6 ± 13.56 minutes) but significantly shorter (p < 0.001) than in the control population (men: 88.09 ± 11.72 minutes; women: 97.25 ± 10.31 minutes). Ghrelin levels were significantly lower in obese subjects (131.37 ± 47.67 vs. 306.3 ± 45.52 pg/mL; p < 0.0001 in men and 162.13 ± 32.95 vs. 272.8 ± 47.77 pg/mL; p < 0.0001 in women). A negative correlation between gastric emptying and fasting ghrelin levels was observed only in lean subjects (y = ?0.2391x + 157.9; R² = 0.95). Also, in the lean group, ghrelin was the only significant independent determinant of gastric emptying, explaining 98% of the variance (adjusted R²) in a multiple regression analysis. Discussion: This report shows that, in humans, gastric emptying is faster in obese subjects than in lean controls and that, whereas ghrelin is the best determinant of gastric kinetics in healthy controls, this action is lost in obesity.     

Lifestyle factors and incident mobility limitation in obese and non-obese older adults

Objective: This study examines the association between incident mobility limitation and 4 lifestyle factors: smoking, alcohol intake, physical activity, and diet in well‐functioning obese (n = 667) and non‐obese (n = 2027) older adults. Research Methods and Procedures: Data were from men and women, 70 to 79 years of age from Pittsburgh, PA and Memphis, TN, participating in the Health, Aging and Body Composition (Health ABC) study. In addition to individual lifestyle practices, a high‐risk lifestyle score (0 to 4) was calculated indicating the total number of unhealthy lifestyle practices per person. Mobility limitation was defined as reported difficulty walking 1/4 mile or climbing 10 steps during two consecutive semiannual assessments over 6.5 years. Results: In non‐obese older persons, significant risk factors for incident mobility limitation after adjustment for socio‐demographics and health‐related variables were current and former smoking [hazard ratio (HR) = 1.51; 95% confidence interval (CI), 1.20 to 1.89; HR = 1.40; 95% CI, 1.12 to 1.74), former alcohol intake (HR = 1.30; 95% CI, 1.05 to 1.60), low and medium physical activity (HR = 1.78; 95% CI, 1.45 to 2.18; HR = 1.29, 95% CI, 1.07 to 1.54), and eating an unhealthy diet (HR = 1.57; 95% CI, 1.17 to 2.10). In the obese, only low physical activity was associated with a significantly increased risk of mobility limitation (HR = 1.44; 95% CI, 1.08 to 1.92). Having two or more unhealthy lifestyle factors was a strong predictor of mobility limitation in the non‐obese only (HR = 1.98; 95% CI, 1.61 to 2.43). Overall, obese persons had a significantly higher risk of mobility limitation compared with non‐obese persons, independent of lifestyle factors (HR = 1.73; 95% CI, 1.52 to 1.96). Conclusions: These results underscore the importance of a healthy lifestyle for maintaining function among non‐obese older adults. However, a healthy lifestyle cannot overcome the effect of obesity in obese older adults; this stresses the importance of preventing obesity to protect against mobility loss in older persons.     

Low Plasma Leptin Concentration and Low Rates of Fat Oxidation in Weight‐Stable Post‐Obese Subjects

Objective: A low resting metabolic rate for a given body size and composition, a low rate of fat oxidation, low levels of physical activity, and low plasma leptin concentrations are all risk factors for body weight gain. The aim of the present investigation was to compare resting metabolic rate (RMR), respiratory quotient (RQ), levels of physical activity, and plasma leptin concentrations in eight post‐obese adults (2 males and 6 females; 48.9 ± 12.2 years; body mass index [BMI]: 24.5 ± 1.0 kg/m²; body fat 33 ± 5%; mean ± SD) who lost 27.1 ± 21.3 kg (16 to 79 kg) and had maintained this weight loss for ≥2 months (2 to 9 months) to eight age‐ and BMI‐matched control never‐obese subjects (1 male and 7 females; 49.1 ± 5.2 years; BMI 24.4 ± 1.0 kg/m²; body fat 33 ± 7%). Research Methods and Procedures: Following 3 days of weight maintenance diet (50% carbohydrate and 30% fat), RMR and RQ were measured after a 10‐hour fast using indirect calorimetry and plasma leptin concentrations were measured using radioimmunoassay. Levels of physical activity were estimated using an accelerometer over a 48‐hour period in free living conditions. Results: After adjustment for fat mass and fat‐free mass, post‐obese subjects had, compared with controls, similar levels of physical activity (4185 ± 205 vs. 4295 ± 204 counts) and similar RMR (1383 ± 268 vs. 1430 ± 104 kcal/day) but higher RQ (0.86 ± 0.04 vs. 0.81 ± 0.03, p < 0.05). Leptin concentration correlated positively with percent body fat (r = 0.57, p < 0.05) and, after adjusting for fat mass and fat‐free mass, was lower in post‐obese than in control subjects (4.5 ± 2.1 vs. 11.6 ± 7.9 ng/mL, p < 0.05). Discussion: The low fat oxidation and low plasma leptin concentrations observed in post‐obese individuals may, in part, explain their propensity to relapse.     

Additive Interactions of Maternal Prepregnancy BMI and Breast‐feeding on Childhood Overweight

Objective: To examine the interactions of maternal prepregnancy BMI and breast‐feeding on the risk of overweight among children 2 to 14 years of age. Research Methods and Procedures: The 1996 National Longitudinal Survey of Youth, Child and Young Adult data in the United States were analyzed (n = 2636). The weighted sample represented 51.3% boys, 78.0% whites, 15.0% blacks, and 7.0% Hispanics. Childhood overweight was defined as BMI ≥95th percentile for age and sex. Maternal prepregnancy obesity was determined as BMI ≥30 kg/m². The duration of breast‐feeding was measured as the weeks of age from birth when breast‐feeding ended. Results: After adjusting for potential confounders, children whose mothers were obese before pregnancy were at a greater risk of becoming overweight [adjusted odds ratio (OR), 4.1; 95% confidence interval (CI), 2.6, 6.4] than children whose mothers had normal BMI (<25 kg/m²; p < 0.001 for linear trend). Breast‐feeding for ≥4 months was associated with a lower risk of childhood overweight (OR, 0.6; 95% CI, 0.4, 1.0; p = 0.06 for linear trend). The additive interaction between maternal prepregnancy obesity and lack of breast‐feeding was detected (p < 0.05), such that children whose mothers were obese and who were never breast‐fed had the greatest risk of becoming overweight (OR, 6.1; 95% CI, 2.9, 13.1). Discussion: The combination of maternal prepregnancy obesity and lack of breast‐feeding may be associated with a greater risk of childhood overweight. Special attention may be needed for children with obese mothers and lack of breast‐feeding in developing childhood obesity intervention programs.