Effects of Dinner Composition on Postprandial Macronutrient Oxidation in Prepubertal Girls

Objective: To see whether a fat‐rich (50%) evening meal promoted fat oxidation and a different spontaneous food intake on the following day at breakfast than a meal with a lower fat content (20%) in 10 prepubertal obese girls. Research Methods and Procedures: The postabsorptive and postprandial (10.5 hours) energy expenditure after a low‐fat (LF) (20% fat, 68% carbohydrate, 12% protein) and an isocaloric (2.1 MJ) and isoproteic high‐fat (HF; 50% fat, 38% carbohydrate, 12% protein) meal were measured by in direct calorimetry. Results: Fat oxidation was not significantly different after the two meals [LF, 31 ± 9 vs. HF, 35 ± 9 g/10.5 hours, p = not significant (NS)]. The girls oxidized 1.8 ± 0.9 times more fat than that ingested (11.1 grams) with the LF meal vs. 0.3 ± 0.3 times more fat than that ingested (27.1 grams) with the HF meal (p < 0.001). Carbohydrate oxidation was significantly higher after an LF than an HF meal (39 ± 12 vs. 29 ± 9 g/10.5 hours, p < 0, 05). At breakfast, the girls spontaneously ingested a similar amount of energy (1.5 ± 0.7 vs. 1.5 ± 0.6 MJ, p = NS) and macronutrient proportions (fat, 23% vs. 26%, p = NS; protein, 9% vs. 10%; carbohydrate, 68% vs. 64%,) independently of their having eaten an HF or an LF dinner. Discussion: An HF dinner did not stimulate fat oxidation, and no compensatory effect in spontaneous food intake was observed during breakfast the following morning. Cumulated total fat oxidation after dinner was higher than total fat ingested at dinner, but a much larger negative fat balance was observed after the LF meal. Spontaneous energy and nutrient intakes at breakfast were similar after LF and HF isocaloric, isoproteic dinners. This study points out the lack of sensitivity of short‐term fat balance to subsequently readjust fat intake and emphasizes the importance of an LF meal to avoid transient positive fat imbalance.     

Relationship Between Birth Weight and Body Composition,Energy Metabolism,and Sympathetic Nervous System Activity Later in Life

Objective: Epidemiological studies suggest that high birth weight might be associated with an increased risk of obesity later in life. Programming of metabolic, endocrine, and/or autonomic pathways during intrauterine development has been proposed to explain this association. Research Methods and Procedures: To determine the relationship between birth weight and body composition and energy metabolism later in life, we measured fat mass and fat‐free mass (hydrodensitometry or double‐energy X‐ray absorptiometry), 24‐hour energy expenditure, sleeping metabolic rate, and 24‐hour respiratory quotient (respiratory chamber) in 272 adult nondiabetic Pima Indians (161 males/111 females, age 25 ± 5 years, mean ± SD). In these subjects, birth weight varied over a wide range (2000 to 5000 g). Individuals known to be offspring of diabetic pregnancies were excluded. In 44 of the 272 subjects, muscle sympathetic nerve activity was assessed by microneurography. Results: Birth weight was positively correlated with adult height (r = 0.20, p < 0.001) and fat‐free mass (r = 0.21, p < 0.001), but not with fat mass (r = 0.01, not significant). Sleeping metabolic rate, adjusted for age, sex, fat‐free mass, and fat mass, was negatively related to birth weight (r = ?0.13, p < 0.05), whereas adjusted 24‐hour energy expenditure (r = 0.07, not significant) and 24‐hour respiratory quotient (r = ?0.09, not significant) were not. There was no relationship between birth weight and muscle sympathetic nerve activity (r = 0.12, not significant, n = 44). Discussion: In Pima Indians who are not offspring of diabetic pregnancies, high birth weight is associated with increased height and lean body mass, but not with increased adiposity later in life. Although high birth weight may be associated with relatively low resting energy expenditure, it is not associated with major abnormalities in 24‐hour energy metabolism or with low muscle sympathetic nerve activity later in life.     

Total and Regional Fat and Serum Cardiovascular Disease Risk Factors in Lean and Obese Children and Adolescents

Objective: This study was conducted to evaluate the association of total and central adiposity with serum cardiovascular disease (CVD) risk factors in lean and obese Portuguese children and adolescents. Research Methods and Procedures: A total of 87 girls (13.2 ± 1.6 years old, 29.9 ± 6.4% body fat [mean ± SD]) and 72 boys (13.2 ± 1.6 years old, 20.8 ± 9.9% body fat) volunteered for the study. Whole‐body composition and fat distribution, from DXA and anthropometry, and serum lipids, lipoproteins, and apolipoproteins were evaluated. Results: The sum of three trunk skinfolds (STS) was highly correlated with total trunk fat mass measured by DXA (p < 0.001). Body mass index, DXA‐measured percentage of body fat, trunk fat mass, STS, and the waist‐to‐height ratio were generally found to be associated with triacylglycerol, the ratio of total cholesterol (TC) to high density lipoprotein‐cholesterol (HDL‐C), low density lipoprotein‐cholesterol (LDL‐C), and apolipoprotein B levels, (significant age‐adjusted r between 0.16 and 0.27, p < 0.05). Body mass index, STS, and the waist circumference were also associated with HDL‐C (p < 0.05), whereas no body composition variable significantly correlated with TC or apolipoproteins A‐I. The STS was significantly correlated with HDL‐C (p < 0.01), TC/HDL‐C (p < 0.05), and apolipoproteins A‐I (p < 0.05) independently of whole‐body fatness. Obese subjects (n = 73) had higher TC, LDL‐C, TC/HDL‐C, and apolipoprotein B than did non‐obese subjects (n = 86), and significant associations between central adiposity and some lipid variables (triacylglycerol and HDL‐C) were found in obese children and adolescents that were not present in leaner individuals. Discussion: DXA‐ and anthropometry‐based whole‐body and central fat measures are associated with serum CVD risk factors in Portuguese boys and girls. Obese children and adolescents have a poorer lipid profile than do their leaner counterparts. Trunk skinfolds, which are easy to obtain even in large samples, predict CVD risk factors to the same extent as DXA‐based variables, in some cases, independently of total fatness.     

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.     

Human adenovirus 36 induces adiposity, increases insulin sensitivity, and alters hypothalamic monoamines in rats

Objective: Human adenovirus 36 (Ad‐36) increases adiposity and reduces serum lipids in chicken, mouse, and non‐human primate models, and it is linked to obesity in sero‐epidemiological studies in humans. Involvement of the central nervous system (CNS) or adipose tissue in the mechanism of Ad‐36‐induced adiposity is unknown. The effects of Ad‐36 on adiposity and on the neuroendocrine system were investigated in a rat model. Research Methods and Procedures: Five‐week‐old male Wistar rats were inoculated intraperitoneally with Ad‐36 or medium. Results: Despite similar food intakes, infected rats attained significantly greater body weight and fat pad weight by 30 weeks post‐inoculation. Epididymal‐inguinal, retroperitoneal, and visceral fat pad weights of the infected group were greater by 60%, 46%, and 86%, respectively (p < 0.00001). The fasting serum insulin level and homeostasis model assessment index indicated greater insulin sensitivity in the infected group. Visceral adipose tissue expression of glycerol 3‐phosphate dehydrogenase, peroxisome proliferator‐activated receptor γ, and CCAAT/enhancer‐binding protein α and β was markedly increased in the infected animals compared with controls. Ad‐36 decreased norepinephrine levels significantly in the paraventricular nucleus in infected vs. control rats (mean ± standard error, 8.9 ± 1.1 vs. 12.8 ± 1.2 pg/μg protein; p < 0.05). Ad‐36 markedly decreased serum corticosterone in infected vs. control rats (mean ± standard error, 97 ± 41.0 vs. 221 ± 111 ng/mL; p < 0.005). Discussion: The results suggest that the pro‐adipogenic effect of Ad‐36 may involve peripheral as well as central effects. The male Wistar rat is a good model for the elucidation of metabolic and molecular mechanisms of Ad‐36‐induced adiposity.     

Obese reproductive-age women exhibit a proatherogenic inflammatory response during hyperglycemia

Objective: The objective was to determine if physiological hyperglycemia induces a proatherogenic inflammatory response in mononuclear cells (MNCs) in obese reproductive‐age women. Research Methods and Procedures: Seven obese and 6 age‐matched lean women (20 to 39 years of age) underwent a 2‐hour 75‐g oral glucose tolerance test. The release of interleukin‐6 (IL‐6) and interleukin‐1β (IL‐1β) from MNCs cultured in the presence of lipopolysaccharide (LPS) was measured after isolation from blood samples drawn fasting and 2 hours after glucose ingestion. Reactive oxygen species (ROS) generation and intra‐nuclear nuclear factor κB (NFκB) from MNCs were quantified from the same blood samples. Insulin resistance was estimated by homeostasis model assessment of insulin resistance (HOMA‐IR). Total body fat and truncal fat were determined by DXA. Results: Obese women had a higher (p < 0.03) total body fat (42.2 ± 1.1 vs. 27.7 ± 2.0%), truncal fat (42.1 ± 1.2 vs. 22.3 ± 2.4%), and HOMA‐IR (3.3 ± 0.5 vs. 1.8 ± 0.2). LPS‐stimulated IL‐6 release from MNCs was suppressed during hyperglycemia in lean subjects (1884 ± 495 vs. 638 ± 435 pg/mL, p < 0.05) but not in obese women (1184 ± 387 vs. 1403 ± 498 pg/mL). There was a difference (p < 0.05) between groups in the hyperglycemia‐induced MNC‐mediated release of IL‐6 (?1196 ± 475 vs. 219 ± 175 pg/mL) and IL‐1β (?79 ± 43 vs. 17 ± 12 pg/mL). In addition, the obese group exhibited increased (p < 0.05) MNC‐derived ROS generation (39.3 ± 9.9 vs. ?1.0 ± 12.8%) and intra‐nuclear NFκB (9.4 ± 7.3 vs. ?23.5 ± 13.5%). Truncal fat was positively correlated with the MNC‐derived IL‐6 response (ρ = 0.58, p < 0.05) and intra‐nuclear NFκB (ρ = 0.64, p < 0.05). Discussion: These data suggest that obese reproductive‐age women are unable to suppress proatherogenic inflammation during physiological hyperglycemia. Increased adiposity may be a significant contributor to this pro‐inflammatory susceptibility.     

The Peroxisome Proliferator‐Activated Receptor α L162V Mutation Is Associated with Reduced Adiposity

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

Effects of acute and chronic protein intake on metabolism, appetite, and ghrelin during weight loss

Objective: This study evaluated the effects of acute and chronic consumption of higher dietary protein on energy expenditure, macronutrient use, appetite, and appetite‐regulating hormones during weight loss in women. Research Methods and Procedures: Thirty‐eight women chronically consuming a 750 kcal/d energy‐deficit diet with a protein content of 30% (higher protein‐chronic diet, HP‐CD, n = 21) or 18% (normal protein‐chronic diet, NP‐CD, n = 17) for 9 weeks were tested. On separate days, metabolic, appetite, and hormonal responses were measured over 4 hours when the women consumed a higher protein‐acute meal (HP‐AM) (30% of energy as protein) or a normal protein‐acute meal (NP‐AM) (18% of energy as protein). Results: With chronic diet groups combined, HP‐AM led to lower respiratory exchange ratio (0.829 ± 0.005 vs. 0.843 ± 0.008; p < 0.05), lower carbohydrate oxidation (p < 0.05), and higher fat oxidation (p < 0.05) compared with NP‐AM. HP‐AM also led to reduced self‐reported postprandial hunger (p < 0.001) and desire to eat (p < 0.001) and lower postprandial ghrelin (252 ± 16 vs. 274 ± 18 ng/mL · 240 minutes, p < 0.05) compared with NP‐AM. No differences in postprandial energy expenditure (PPEE) occurred between meals. When combining acute meals, respiratory exchange ratio was lower (p < 0.05) and protein oxidation (p < 0.001) was higher in the HP‐CD vs. NP‐CD. An acute meal‐by‐chronic diet interaction was observed with PPEE such that HP‐AM led to greater PPEE in the HP‐CD vs. NP‐CD (28.7 ± 2.7 vs. 19.9 ± 2.7 kcal/min for 195 minutes; p < 0.05). Conclusions: During weight loss, thermogenesis and protein use appear to be influenced by chronic protein intake, while appetite and ghrelin are more responsive to acute protein intake.     

Low-dose pramlintide reduced food intake and meal duration in healthy, normal-weight subjects

Objective: We previously reported that a single preprandial injection (120 μg) of pramlintide, an analog of the β‐cell hormone amylin, reduced ad libitum food intake in obese subjects. To further characterize the meal‐related effects of amylin signaling in humans, we studied a lower pramlintide dose (30 μg) in normal‐weight subjects. Research Methods and Procedures: In a randomized, double‐blind, placebo‐controlled, cross‐over study, 15 healthy men (age, 24 ± 7 years; BMI, 22.2 ± 1.8 kg/m²) underwent a standardized buffet meal test on two occasions. After an overnight fast, subjects received a single subcutaneous injection of pramlintide (30 μg) or placebo, followed immediately by a standardized pre‐load meal. After 1 hour, subjects were offered an ad libitum buffet meal, and total caloric intake and meal duration were measured. Results: Compared with placebo, pramlintide reduced total caloric intake (1411 ± 94 vs. 1190 ± 117 kcal; Δ, ?221 ± 101 kcal; ?14 ± 9%; p = 0.05) and meal duration (36 ± 2 vs. 31 ± 3 minutes; Δ, ?5.1 ± 1.4 minutes; p < 0.005). Visual analog scale profiles of hunger trended lower and fullness higher during the first hour after pramlintide administration. In response to the buffet, hunger and fullness changed to a similar degree after pramlintide and placebo, despite subjects on pramlintide consuming 14% fewer kilocalories. Visual analog scale nausea ratings remained near baseline, without differences between treatments. Plasma peptide YY, cholecystokinin, and ghrelin concentrations did not differ with treatment, whereas glucagon‐like peptide‐1 concentrations after meals were lower in response to pramlintide than to placebo. Discussion: These observations add support to the concept that amylin agonism may have a role in human appetite control.     

Insulin Action,Regional Fat,and Myocyte Lipid: Altered Relationships with Increased Adiposity

Objective: Abdominal fat and myocyte triglyceride levels relate negatively to insulin sensitivity, but their interrelationships are inadequately characterized in the overweight. Using recent methods for measuring intramyocyte triglyceride, these relationships were studied in men with a broad range of adiposity. Research Methods and Procedures: Myocyte triglyceride content (¹H‐magnetic resonance spectroscopy of soleus and tibialis anterior muscles and biochemical assessment of vastus lateralis biopsies), regional fat distribution (DXA and abdominal magnetic resonance imaging), serum lipids, insulin action (euglycemic hyperinsulinemic clamp), and substrate oxidation rates (indirect calorimetry) were measured in 39 nondiabetic men (35.1 ± 7.8 years) with a broad range of adiposity (BMI 28.6 ± 4.1 kg/m², range 20.1 to 37.6 kg/m²). Results: Relationships between insulin‐stimulated glucose disposal and regional body fat depots appeared more appropriately described by nonlinear than linear models. When the group was subdivided using median total body fat as the cut‐point, insulin‐stimulated glucose disposal correlated negatively to all regional body fat measures (all p ≤ 0.004), serum triglycerides and free fatty acids (p < 0.02), and both soleus intramyocellular lipid (p = 0.003) and vastus lateralis triglyceride (p = 0.04) in the normal/less overweight group. In contrast, only visceral abdominal fat showed significant negative correlation with insulin‐stimulated glucose disposal in more overweight men (r = ?0.576, p = 0.01), some of whom surprisingly had lower than expected myocyte lipid levels. These findings persisted when the group was subdivided using different cut‐points or measures of adiposity. Discussion: Interrelationships among body fat depots, myocyte triglyceride, serum lipids, and insulin action are generally absent with increased adiposity. However, visceral abdominal fat, which corresponds less closely to total adiposity, remains an important predictor of insulin resistance in men with both normal and increased adiposity.     

Correlation between Serum Resistin Level and Adiposity in Obese Individuals

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

Increased Susceptibility to Insulin Resistance Associated with Abdominal Obesity in Aging Rats**

Objective: Recent data have suggested that the insulin resistance observed with aging may be more related to adiposity than aging per se. We asked whether the insulin resistance observed in aged rats was comparable (both in magnitude and location) to that of fat‐fed rats. Research Methods and Procedures: We performed hyperinsulinemic (5 mU/min per kg) euglycemic clamps with tracer in conscious, 6‐hour fasted young (YL), fat‐fed young (YF), fat‐fed old (OF), and calorically restricted old (OL) rats. Results: Intraabdominal fat measurements showed that OF and YF rats were more obese than YL (p ≤ 0.001; YF > OF > YL). Caloric restriction not only prevented age‐related obesity but also reduced the ratio of intraabdominal fat to lean body mass (LBM) compared with YL (OL: 0.59 ± 0.05 vs. YL: 1.07 ± 0.04; p = 0.017). Despite similar incremental insulin, YF and OF rats required 40% less infused glucose to maintain euglycemia than YL and OL rats (p < 0.001). Insulin‐stimulated glucose uptake (Si_Rd: ΔRd/(ΔInsulin × Glucose_SS) was impaired in OF rats (OF: 14.03 ± 1.79 vs. YL: 23.08 ± 1.87 × 10³ dL/min × kg LBM per pM; p = 0.004) and improved in OL rats (29.41 ± 1.84 × 10³ dL/min × kg LBM per pM; p = 0.031) compared with YL. Despite greater obesity, YF rats did not exhibit lower Si_Rd compared with OF rats (p = 0.58). In contrast, the ability of insulin to suppress endogenous glucose production (EGP; Si_EGP: ΔEGP/(ΔInsulin × Glucose_SS) was not impaired in OF rats (OF vs. YL; p = 0.61) but was markedly impaired in YF rats by ～75% (1.72 ± 0.66 × 10³ dL/min × kg per pM; p = 0.013). Surprisingly, separate regression analysis for old and young animals revealed that old rats exhibited a significantly steeper regression between Si (Rd and EGP) and adiposity than young rats (p < 0.05). Thus, older rats showed a proportionately greater decrement in insulin sensitivity with an equivalent increase in adiposity. Discussion: These data suggest that, in rodents, youth affords significant protection against obesity‐induced insulin resistance.     

Effect of Rosiglitazone on Insulin Sensitivity and Body Composition in Type 2 Diabetic Patients

Objective: To investigate the effects of rosiglitazone (RSG) on insulin sensitivity and regional adiposity (including intrahepatic fat) in patients with type 2 diabetes. Research Methods and Procedures: We examined the effect of RSG (8 mg/day, 2 divided doses) compared with placebo on insulin sensitivity and body composition in 33 type 2 diabetic patients. Measurements of insulin sensitivity (euglycemic hyperinsulinemic clamp), body fat (abdominal magnetic resonance imaging and DXA), and liver fat (magnetic resonance spectroscopy) were taken at baseline and repeated after 16 weeks of treatment. Results: There was a significant improvement in glycemic control (glycosylated hemoglobin −0.7 ± 0.7%, p ≤ 0.05) and an 86% increase in insulin sensitivity in the RSG group (glucose-disposal rate change from baseline: 17.5 ± 14.5 μmol glucose/min/kg free fat mass, p < 0.05), but no significant change in the placebo group compared with baseline. Total body weight and fat mass increased (p ≤ 0.05) with RSG (2.1 ± 2.0 kg and 1.4 ± 1.6 kg, respectively) with 95% of the increase in adiposity occurring in nonabdominal regions. In the abdominal region, RSG increased subcutaneous fat area by 8% (25.0 ± 28.7 cm², p = 0.02), did not alter intra-abdominal fat area, and reduced intrahepatic fat levels by 45% (−6.7 ± 9.7%, concentration relative to water). Discussion: Our data indicate that RSG greatly improves insulin sensitivity in patients with type 2 diabetes and is associated with an increase in adiposity in subcutaneous but not visceral body regions.     

Body Weight Loss and Weight Maintenance in Relation to Habitual Caffeine Intake and Green Tea Supplementation

Objective: Investigation of the effect of a green tea‐caffeine mixture on weight maintenance after body weight loss in moderately obese subjects in relation to habitual caffeine intake. Research Methods and Procedures: A randomized placebo‐controlled double blind parallel trial in 76 overweight and moderately obese subjects, (BMI, 27.5 ± 2.7 kg/m²) matched for sex, age, BMI, height, body mass, and habitual caffeine intake was conducted. A very low energy diet intervention during 4 weeks was followed by 3 months of weight maintenance (WM); during the WM period, the subjects received a green tea‐caffeine mixture (270 mg epigallocatechin gallate + 150 mg caffeine per day) or placebo. Results: Subjects lost 5.9 ±1.8 (SD) kg (7.0 ± 2.1%) of body weight (p < 0.001). At baseline, satiety was positively, and in women, leptin was inversely, related to subjects’ habitual caffeine consumption (p < 0.01). High caffeine consumers reduced weight, fat mass, and waist circumference more than low caffeine consumers; resting energy expenditure was reduced less and respiratory quotient was reduced more during weight loss (p < 0.01). In the low caffeine consumers, during WM, green tea still reduced body weight, waist, respiratory quotient and body fat, whereas resting energy expenditure was increased compared with a restoration of these variables with placebo (p < 0.01). In the high caffeine consumers, no effects of the green tea‐caffeine mixture were observed during WM. Discussion: High caffeine intake was associated with weight loss through thermogenesis and fat oxidation and with suppressed leptin in women. In habitual low caffeine consumers, the green tea‐caffeine mixture improved WM, partly through thermogenesis and fat oxidation.     

Circadian Eating and Sleeping Patterns in the Night Eating Syndrome

Objective: To compare the eating and sleep‐wake patterns of persons with the night eating syndrome (NES) with those of matched control subjects. Research Methods and Procedures: Forty‐six overweight/obese NES subjects (mean age 43.3 ± 9.8 years; 32 women) and 43 similar controls (mean age 39.0 ± 11.0 years; 28 women) wore wrist actigraphs for 7 days and completed sleep and food diaries at home. Results: There was no difference between the total energy intake of the NES and the control subjects, but the pattern of energy intake differed greatly. Relative to control subjects, the temporal pattern of food intake of night eaters was delayed. Food intake after the evening meal, as a proportion of the 24‐hour intake, was more than 3‐fold greater in NES subjects than in controls (34.6 ± 10.1% vs. 10.0 ± 6.9%, p = 0.001). NES subjects had sleep onset, offset, and total sleep duration times comparable with those of controls. NES subjects reported more nocturnal awakenings than did controls (1.5 ± 1.0 per night vs. 0.5 ± 0.5; p < 0.001), and their actigraphically monitored arousals occurred earlier during sleep (at 128 minutes after sleep onset vs. 193 minutes, p = 0.01). NES subjects consumed food on 74% of the awakenings vs. 0% for the controls. Discussion: The pattern of cumulative energy intake of the night eaters suggests a phase delay in energy consumption relative to sleep‐wake times. NES may involve a dissociation of the circadian control of eating relative to sleep.     

Morning Versus Evening Power Output and Repeated‐Sprint Ability

We investigated the effect of time‐of‐day on both maximal sprint power and repeated‐sprint ability (RSA). Nine volunteers (22±4 yrs) performed a RSA test both in the morning (07:00 to 09:00 h) and evening (17:00 to 19:00 h) on different days in a random order. The RSA cycle test consisted of five, 6 sec maximal sprints interspersed by 24 sec of passive recovery. Both blood lactate concentration and heart rate were higher in the evening than morning RSA (lactate values post exercise: 13±3 versus 11±3 mmol/L^?1, p<0.05). The peak power developed during the first sprint was higher in the evening than morning (958±112 vs. 915±133 W, p<0.05), but this difference was not apparent in subsequent sprints, leading to a higher power decrement across the 5×6 sec test in the evening (11±2 vs. 7±3%, p<0.05). Both the total work during the RSA cycle test and the power developed during bouts 2 to 5 failed to be influenced by time‐of‐day. This suggests that the beneficial effect of time‐of‐day may be limited to a single expression of muscular power and fails to advantage performance during repeated sprints.     

Post‐Exercise Substrate Utilization after a High Glucose vs. High Fructose Meal During Negative Energy Balance in the Obese

Objective: To assess the effects of negative energy balance on the metabolic response of a meal containing either glucose or fructose as the primary source of carbohydrate after exercise in obese individuals in energy balance, or negative energy balance. Research Methods and Procedures: Fourteen adults with mean body mass index (BMI) 30.3 ± 1 kg/m², age 26 ± 2 years, and weight 93.5 ± 5.4 kg, adhered to an energy‐balanced (EB) or a negative energy‐balanced (NEB) diet for 6 days. On Day 7, subjects exercised at 70% VO_2peak for 40 minutes then consumed either high glucose (50 g of glucose, HG) or high fructose (50 g of fructose, HF) liquid meal. Substrate utilization was measured by indirect calorimetry for 3 hours. Blood samples were collected before exercise and 0, 30, 60, 120, and 180 minutes after consuming the meal. Results: The HG produced 15.9% greater glycemic (p < 0.05) and 30.9% larger insulinemic (p < 0.05) responses than the HF under both EB and NEB conditions. After the NEB diet, carbohydrate and fat oxidation did not differ for HG and HF. In contrast, carbohydrate oxidation increased 31%, and fat oxidation decreased 39% with HF compared with HG after the EB diet. Thus, HF and HG consumed after exercise produced marked differences in macronutrient oxidation when obese subjects followed an EB diet, but no difference when adhering to a NEB diet. Discussion: The data suggest that the use of fructose in supplements/meals may provide no additional benefit in terms of substrate utilization during a weight loss program involving diet and exercise.     

Acute and delayed responses of C-reactive protein,malondialdehyde and antioxidant markers after resistance training session in elite weightlifters: Effect of time of day

The aim of this study was to investigate the effect of an Olympic-Weightlifting-session followed by 48-h recovery period on the oxidative and antioxidant parameters’ diurnal variation. Nine weightlifters (21?±?0.5 years) performed, in randomized order, three Olympic-Weightlifting-sessions at 08?h:00, 14?h:00 and 18?h:00. Blood samples were collected: at rest and 3?min and 48?h after each session. C-reactive protein (CRP), rate of lipid peroxidation and antioxidant activities were assessed. At rest, analysis of variance showed a significant time of day (TOD) effect (p?<?0.05) for uric acid, catalase and glutathione peroxidase with higher values at 14?h:00 and 18?h:00 compared with 08?h:00. However, no significant TOD effect for malondialdehyde, total bilirubin and CRP was observed. Given the profound changes (p?<?0.001) in the post-training session values, these diurnal variations have been altered immediately and even 48?h after the training sessions. Despite the significant decreases in the post-training values after the 48-h recovery period (p?<?0.05), levels of lipid peroxidation and enzymatic defense remained elevated (p?<?0.05) 48?h after the morning training session. However, after the afternoon and evening sessions, the same period was sufficient to return values to the baseline levels. In conclusion, the morning session seems to generate the most important acute and delayed lipid peroxidation responses. Therefore, weightlifting coaches should avoid scheduling their training sessions in the morning-hours.     

Successful long-term weight maintenance: a 2-year follow-up

Objective: To find factors associated with successful weight maintenance (WM) in overweight and obese subjects after a very low‐calorie diet (VLCD). Research Methods and Procedures: Subjects (133) followed a VLCD (2.1 MJ/d) for 6 weeks in a free‐living situation. Of these, 103 subjects (age, 49.6 ± 9.7 years; BMI, 30.9 ± 3.8 kg/m²) completed the following 2‐year WM period. Body weight (BW), body composition, leptin concentration, attitude toward eating, and physical activity were determined right before (t0) and after (t1) the VLCD, after 3 months (t2), after 1 year (t3), after 1.5 years (t4), and after 2 years (t5). Results: BW loss during VLCD was 7.2 ± 3.1 kg. After 2 years, follow‐up BW regain was 69.0 ± 98.4%. After 2 years of WM, 13 subjects were successful (<10% BW regain), and 90 were unsuccessful (>10% BW regain). At baseline, these groups were significantly different in BMI (33.7 ± 4.7 vs. 30.5 ± 3.5 kg/m², respectively; p < 0.05) and fat mass (38.3 ± 9.8 vs. 32.1 ± 8.3 kg, p < 0.05). Successful subjects increased their dietary restraint significantly more during the whole study period (dietary restraint score, ?4.9 ± 4.4 vs. ?2.1 ± 3.8). Furthermore, %BW regain was associated with the amount of percentage body fat lost during VLCD, which indicates that the more fat lost, the better the WM, suggesting a fat free mass‐sparing effect. Discussion: Characteristics such as the ability to increase dietary restraint and maintain this high level of restraint, fat free mass sparing, and a relatively high baseline BMI and fat mass were associated with successful long‐term WM (<10% regain after 2 years).