Effect of Energy‐Reduced Diets High in Dairy Products and Fiber on Weight Loss in Obese Adults

Objective: Studies suggest that high‐dairy and high‐fiber/low‐glycemic index diets may facilitate weight loss, but data are conflicting. The effects on weight loss and body fat of a high‐dairy diet and a diet high in dairy and fiber and low in glycemic index were compared with a standard diet. Research Methods and Procedures: Ninety obese subjects were recruited into a randomized trial of three diets designed to provide a calorie deficit of 500 calories/d over a 48‐week period. The study compared a moderate (not low)‐calcium diet with a high‐calcium diet. Results: Seventy‐two subjects completed the study. Significant weight and fat loss occurred with all three diets. A diet with 1400 mg of calcium did not result in greater weight (11.8 ± 6.1 kg) or fat (9.0 ± 6.0 kg) loss than a diet with 800 mg of calcium (10.0 ± 6.8 and 7.5 ± 6.6 kg, respectively). A diet with 1400 mg of calcium, increased fiber content, and fewer high‐glycemic index foods did not result in greater weight (10.6 ± 6.8 kg) or fat (8.5 ± 7.8 kg) loss than the standard diet with 800 mg of calcium. Lipid profile, high‐sensitivity C‐reactive protein, leptin, fasting glucose, and insulin improved significantly, but there were no significant differences between the experimental diets and the control diet. Discussion: We found no evidence that diets higher than 800 mg of calcium in dairy products or higher in fiber and lower in glycemic index enhance weight reduction beyond what is seen with calorie restriction alone.     

Long-term effects of dietary glycemic index on adiposity, energy metabolism, and physical activity in mice

A high-glycemic index (GI) diet has been shown to increase adiposity in rodents; however, the long-term metabolic effects of a low- and high-GI diet have not been examined. In this study, a total of 48 male 129SvPas mice were fed diets high in either rapidly absorbed carbohydrate (RAC; high GI) or slowly absorbed carbohydrate (SAC; low GI) for up to 40 wk. Diets were controlled for macronutrient and micronutrient content, differing only in starch type. Body composition and insulin sensitivity were measured longitudinally by DEXA scan and oral glucose tolerance test, respectively. Food intake, respiratory quotient, physical activity, and energy expenditure were assessed using metabolic cages. Despite having similar mean body weights, mice fed the RAC diet had 40% greater body fat by the end of the study and a mean 2.2-fold greater insulin resistance compared with mice fed the SAC diet. Respiratory quotient was higher in the RAC group, indicating comparatively less fat oxidation. Although no differences in energy expenditure were observed throughout the study, total physical activity was 45% higher for the SAC-fed mice after 38 wk of feeding. We conclude that, in this animal model, 1) the effect of GI on body composition is mediated by changes in substrate oxidation, not energy intake; 2) a high-GI diet causes insulin resistance; and 3) dietary composition can affect physical activity level.     

The Effect of Dietary Glycemic Index on Weight Maintenance in Overweight Subjects: A Pilot Study

Evidence suggests that a low‐glycemic index (LGI) diet has a satiating effect and thus may enhance weight maintenance following weight loss. This study was conducted at Hammersmith Hospital, London, UK, and assessed the effect of altering diet GI on weight‐loss maintenance. It consisted of a weight‐loss phase and a 4‐month randomized weight maintenance phase. Subjects were seen monthly to assess dietary compliance and anthropometrics. Appetite was assessed bimonthly by visual analogue scales while meal challenge postprandial insulin and glucose concentrations were assessed before and after the intervention. Following a median weight loss of 6.1 (interquartile range: 5.2–7.1) % body weight, subjects were randomized to a high‐glycemic index (HGI) (n = 19) or LGI (n = 23) diet. Dietary composition differed only in GI (HGI group: 63.7 ± 9.4; LGI group: 49.7 ± 5.7, P < 0.001) and glycemic load (HGI group: 136.8 ± 56.3; LGI group: 89.7 ± 27.5, P < 0.001). Groups did not differ in body weight (weight change over 4 months, HGI group: 0.3 ± 1.9 kg; LGI group: −0.7 ± 2.9 kg, P = 0.3) or other anthropometric measurements. This pilot study suggests that in the setting of healthy eating, changing the diet GI does not appear to significantly affect weight maintenance.     

Modest Lifestyle Intervention and Glucose Tolerance in Obese African Americans

Objective: Previous studies have demonstrated the benefit of short‐term diets on glucose tolerance in obese individuals. The purpose of this study was to evaluate the effectiveness of modest lifestyle changes in maintaining improvements in glucose tolerance induced by short‐term energy restriction in obese African Americans with impaired glucose tolerance or type 2 diabetes mellitus. Research Methods and Procedures: An intervention group (n = 45; 47 ± 1 year [mean ± SE]), 105 ± 4 kg; body mass index: 39 ± 1 kg/m²) received an energy‐restricted diet (943 ± 26 kcal/d) for 1 week, followed by a lifestyle program of reduced dietary fat (?125 kcal/d) and increased physical activity (+125 kcal/d) for 1 year. Body weight and plasma concentrations of glucose, insulin, and C‐peptide during an oral glucose tolerance test were measured at baseline, 1‐week, and 4‐month intervals. A control group (n = 24; 48 ± 1 year; 110 ± 5 kg; body mass index: 41 ± 2 kg/m²) underwent these measurements at 4‐month intervals. Results: No changes in weight or glucose tolerance were observed in the control group. The intervention group had significant (p < 0.05) improvements in body weight and glucose tolerance in response to the 1‐week diet, which persisted for 4 months (p < 0.001 vs. control for change in weight). A total of 19 subjects (42%) continued the intervention program for 1 year, with sustained improvements (weight: ?4.6 ± 1.0 kg; p < 0.001 vs. control; oral glucose tolerance test glucose area: ?103 ± 44 mM · min; p < 0.05 vs. control). Discussion: A modest lifestyle program facilitates weight loss and enables improvements in glucose tolerance to be maintained in obese individuals with abnormal glucose tolerance. However, attrition was high, despite the mild nature of the program.     

非酒精性脂肪性肝病大鼠肠粘膜紧密连接蛋白ZO-1及肌球蛋白轻链激酶的变化

目的:研究不同阶段非酒精性脂肪性肝病(NAFLD)大鼠肠粘膜紧密连接蛋白ZO-1及肌球蛋白轻链激酶(MLCK)的变化。方法:将60只雄性清洁级SD大鼠随机分为两组:正常饮食组(NDG)和高脂饮食组(FDG)。于4周、8周、12周时观察各组大鼠肝脏病理学改变;应用ELISA方法测定各阶段大鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、甘油三酯(TG)、胆固醇(CHOL)的变化;应用鲎实验测定各阶段大鼠门静脉血中内毒素(ET)水平;应用免疫组化方法检测肠道粘膜肌球蛋白轻链激酶(MLCK)及紧密连接蛋白(ZO-1)的表达及分布情况。结果:随着高脂饮食时间增长,高脂饮食组大鼠肝脏脂肪变性程度逐渐加重;血清ALT、AST、TG、CHOL水平逐渐升高(4周时,P0.05,8周和12周时P0.05);大鼠血浆内毒素的水平逐渐上升(0.11±0.01比0.11±0.01,P0.05;0.36±0.01比0.11±0.01,P0.05;0.44±0.15比0.18±0.03,P0.05);高质饮食组较正常饮食组大鼠紧密连接蛋白ZO-1表达逐渐下降(3.6±0.7比3.9±0.32,P0.05;2.8±0.63比3.8±0.42,P0.05;1.8±0.79比3.7±0.48,P0.05),MLCK表达逐渐增多(0.5±0.53比0.3±0.48,P0.05;1.3±0.48比0.4±0.52,P0.05;1.9±0.74比0.5±0.53,P0.05)。结论:肠粘膜紧密连接蛋白ZO-1及MLCK可通过影响肠粘膜屏障功能,改变肠粘膜的通透性,促进非酒精性脂肪肝病发生发展。     

Serum Leptin Concentrations and Weight Gain in Postobese,Postmenopausal Women

Objective : This study was designed to determine if serum leptin concentrations (adjusted for fat mass) after weight loss on a low-calorie diet predict subsequent weight gain. Research Methods and Procedures : Body composition and serum leptin concentrations were determined on 14 moderately obese, postmenopausal, nondiabetic women with a familial predisposition to obesity. Assessments were obtained under tightly controlled metabolic ward conditions of macronutrient intake and weight maintenance both before (obese state) and after a mean weight loss of 12.0 kg to normal body weight (postobese state). Four years later, without intervention, body weight and body composition were reassessed. Results : Weight loss resulted in significant decreases in fat mass (29.7 ± 5.4 vs. 20.3 ± 4.7; kg), body mass index (27.7 ± 1.6 vs. 23.0 ± 1.5; kg/m2), percent body fat (40.7 ± 4.3 vs. 33.1 ± 5.0), and serum leptin concentrations (31.8 ± 16.0 vs. 11.5 ± 5.4; ng/mL). Serum leptin concentrations were positively correlated (p<<0.05) with fat mass in both the obese and postobese states (r = 0.67 and r = 0.56, respectively). However, residual serum leptin concentrations (adjusted for fat mass) in the obese and postobese states were not related to changes in body weight (p<= 0.61 and 0.52), fat mass (p = 0.72 and 0.42), body mass index (p = 0.59 and 0.33), or percent body fat (p = 0.84 and 0.46) over the follow-up period. Discussion : These finding do not support the hypothesis that relatively low concentrations of leptin predict weight regain after weight loss. However, because the number of subjects in this study was limited, further studies are warranted.     

Intensive weight loss program improves physical function in older obese adults with knee osteoarthritis

Objective: Physical function and body composition in older obese adults with knee osteoarthritis (OA) were examined after intensive weight loss. Research Methods and Procedures: Older obese adults (n = 87; ≥60 years; BMI ≥ 30.0 kg/m²) with symptomatic knee OA and difficulty with daily activities were recruited for a 6‐month trial. Participants were randomized into either a weight stable (WS) or weight loss (WL) program. Participants in WL (10% weight loss goal) were prescribed a 1000 kcal/d energy deficit diet with exercise 3 d/wk. WS participants attended health information sessions. Body composition and physical function (Western Ontario and McMaster University Osteoarthritis Index, 6‐minute walking distance, and stair climb time) were assessed at baseline and 6 months. Statistical analysis included univariate analysis of covariance on 6‐month measurements using baseline values as covariates. Associations between physical function and body composition were performed. Results: Body weight decreased 8.7 ± 0.8% in WL and 0.0 ± 0.7% in WS. Body fat and fat‐free mass were lower for WL than WS at 6 months (estimated means: fat = 38.1 ± 0.4% vs. 40.9 ± 0.4%, respectively; fat‐free mass = 56.7 ± 0.4 vs. 58.8 ± 0.4 kg, respectively). WL had better function than WS, with lower Western Ontario and McMaster University Osteoarthritis Index scores, greater 6‐minute walk distance, and faster stair climb time (p < 0.05). Changes in function were associated with weight loss in the entire cohort. Discussion: An intensive weight loss intervention incorporating energy deficit diet and exercise training improves physical function in older obese adults with knee OA. Greater improvements in function were observed in those with the most weight loss.     

Metabolic and Weight Loss Effects of Long‐Term Dietary Intervention in Obese Patients: Four‐Year Results

Objective: To investigate the contribution of meal and snack replacements for long‐term weight maintenance and risk factor reduction in obese patients. Research Methods and Procedures: Prospective, randomized, two‐arm, parallel intervention for 12 weeks followed by a prospective single‐arm 4‐year trial in a University Hospital clinic. One hundred patients, >18 years old and with a body mass index > 25 and ≤ 40 kg/m², were prescribed a 1200 to 1500 kcal/d control diet (Group A) or an isoenergetic diet, including two meal and snack replacements (vitamin‐ and mineral‐fortified shakes, soups, and bars) and one meal high in fruits and vegetables (Group B). Following a 3 months of weight loss, all patients were prescribed the same energy‐restricted diet (1200 to 1500 kcal) with one meal and one snack replacement for an additional 4 years. Results: All 100 patients were evaluated at 12 weeks. Mean percentage weight loss was 1.5 ± 0.4% and 7.8 ± 0.5% (mean ± SEM) for Groups A and B, respectively. At 12 weeks systolic blood pressure, plasma triacylglycerol, glucose, and insulin concentrations were significantly reduced in Group B, whereas no changes occurred in Group A. After 4 years, 75% of the patients were evaluated. Total mean weight loss was 3.2 ± 0.8% for Group A and 8.4 ± 0.8% (mean ± SEM) for Group B. Both groups showed significant improvement in blood glucose and insulin (p < 0.001), but only Group B showed significant improvement in triacylglycerol and systolic blood pressure compared to baseline values (p < 0.001). Discussion: Providing a structured meal plan via vitamin‐ and mineral‐fortified liquid meal replacements is a safe and effective dietary strategy for obese patients. Long‐term maintenance of weight loss with meal replacements can improve certain biomarkers of disease risk.     

Weight loss therapy improves pancreatic endocrine function in obese older adults

Objective: Obesity and aging increase the risk of type 2 diabetes (T2D). We evaluated whether weight loss therapy improves pancreatic endocrine function and insulin sensitivity in obese older adults. Methods and Procedures: Twenty‐four obese (BMI: 38 ± 2 kg/m²) older (age: 70 ± 2 years) adults completed a 6‐month randomized, controlled trial. Participants were randomized to diet and exercise (treatment group) or no therapy (control group). β‐Cell function (assessed using the C‐peptide minimal model), α‐cell function (assessed by the glucagon response to an oral glucose load), insulin sensitivity (assessed using the glucose minimal model), and insulin clearance rate were evaluated using a 5‐h modified oral glucose tolerance test. Results: Body weight decreased in the treatment group, but did not change in the control group (?9 ± 1% vs. 0 ± 1%; P < 0.001). Insulin sensitivity doubled in the treatment group and did not change in the control group (116 ± 49% vs. ?11 ± 13%; P < 0.05). Even though indices of β‐cell responsivity to glucose did not change (P > 0.05), the disposition index (DI), which adjusts β‐cell insulin response to changes in insulin sensitivity, improved in the treatment group compared with the control group (100 ± 47% vs. ?22 ± 9%; P < 0.05). The glucagon response decreased in the treatment but not in the control group (?5 ± 2% vs. 4 ± 4%; P < 0.05). Insulin secretion rate did not change (P > 0.05), but insulin clearance rate increased (51 ± 25%; P < 0.05), resulting in lower plasma insulin concentrations. Discussion: Weight loss therapy concomitantly improves β‐cell function, lowers plasma glucagon concentrations, and improves insulin action in obese older adults. These metabolic effects are likely to reduce the risk of developing T2D in this population.     

Alterations in fatty acid kinetics in obese adolescents with increased intrahepatic triglyceride content

Objective: It has been hypothesized that excessive fatty acid availability contributes to steatosis and the metabolic abnormalities associated with nonalcoholic fatty liver disease (NAFLD). The purpose of this study was to evaluate whether adipose tissue lipolytic activity and the rate of fatty acid release into plasma are increased in obese adolescents with NAFLD. Methods: Palmitate kinetics were determined in obese adolescents with normal (n = 9; BMI = 37 ± 2 kg/m²; intrahepatic triglyceride (IHTG) ≤5.5% of liver volume) and increased (n = 9; BMI = 36 ± 2 kg/m²; IHTG ≥ 10% of liver volume) IHTG content during the basal state (postabsorptive condition) and during physiological hyperinsulinemia (postprandial condition). Both groups were matched on body weight, BMI, percent body fat, age, sex, and Tanner stage. The hyperinsulinemic‐euglycemic clamp procedure, in conjunction with a deuterated palmitate tracer infusion, was used to determine free‐fatty acid (FFA) kinetics, and magnetic resonance spectroscopy was used to determine IHTG content. Results: The rate of whole‐body palmitate release into plasma was greater in subjects with NAFLD than those with normal IHTG content during basal conditions, (87 ± 7 vs. 127 ± 13 µmol/min; P < 0.01) and during physiological hyperinsulinemia, (24 ± 2 vs. 44 ± 8 µmol/min; P < 0.01). Discussion: These results demonstrate that adipose tissue lipolytic activity is increased in obese adolescents with NAFLD and results in an increase in the rate of fatty acid release into plasma throughout the day. This continual excess in fatty acid flux supports the hypothesis that adipose insulin resistance is involved in the pathogenesis of steatosis and contributes to the metabolic complications associated with NAFLD.     

The effects of Goami No. 2 rice, a natural fiber-rich rice, on body weight and lipid metabolism

Objective : Increased intake of dietary fiber reduces the risk of obesity and type 2 diabetes. We assessed the effects of a fiber‐rich diet on body weight, adipokine concentrations, and the metabolism of glucose and lipids in non‐obese and obese subjects in Korea, where rice is the main source of dietary carbohydrates. Research Methods and Procedures : Eleven healthy, non‐obese and 10 obese subjects completed two 4‐week phases of individual isoenergetic food intake. During the control diet phase, subjects consumed standard rice; during the modified diet phase, subjects consumed equal proportions of fiber‐rich Goami No. 2 rice and standard rice. We used a randomized, controlled, crossover study design with a washout period of 6 weeks between the two phases. Results : After the modified diet phase, body weight was significantly lower in both the non‐obese and obese subjects (non‐obese, 57.0 ± 2.9 vs. 56.1 ± 2.8 kg, p = 0.001; obese, 67.7 ± 2.1 vs. 65.7 ± 2.0 kg, p < 0.001 for before vs. after). The BMI was significantly lower in obese subjects (26.9 ± 0.5 vs. 26.0 ± 0.6 kg/m², p < 0.001). The modified diet was associated with lower serum triacylglycerol (p < 0.01), total cholesterol (p < 0.01), low‐density lipoprotein cholesterol (p < 0.05), and C‐peptide (p < 0.05) concentrations in the obese subjects. Discussion : These results indicate that fiber‐rich Goami No. 2 rice has beneficial effects and may be therapeutically useful for obese subjects.     

Three-year weight change in successful weight losers who lost weight on a low-carbohydrate diet

Objective: The purpose of this study was to evaluate long‐term weight loss and eating and exercise behaviors of successful weight losers who lost weight using a low‐carbohydrate diet. Research Methods and Procedures: This study examined 3‐year changes in weight, diet, and physical activity in 891 subjects (96 low‐carbohydrate dieters and 795 others) who enrolled in the National Weight Control Registry between 1998 and 2001 and reported ≥30‐lb weight loss and ≥1 year weight loss maintenance. Results: Only 10.8% of participants reported losing weight after a low‐carbohydrate diet. At entry into the study, low‐carbohydrate diet users reported consuming more kcal/d (mean ± SD, 1895 ± 452 vs. 1398 ± 574); fewer calories in weekly physical activity (1595 ± 2499 vs. 2542 ± 2301); more calories from fat (64.0 ± 7.9% vs. 30.9 ± 13.1%), saturated fat (23.8 ± 4.1 vs. 10.5 ± 5.2), monounsaturated fat (24.4 ± 3.7 vs. 11.0 ± 5.1), and polyunsaturated fat (8.6 ± 2.7 vs. 5.5 ± 2.9); and less dietary restraint (10.8 ± 2.9 vs. 14.9 ± 3.9) compared with other Registry members. These differences persisted over time. No differences in 3‐year weight regain were observed between low‐carbohydrate dieters and other Registry members in intent‐to‐treat analyses (7.0 ± 7.1 vs. 5.7 ± 8.7 kg). Discussion: It is possible to achieve and maintain long‐term weight loss using a low‐carbohydrate diet. The long‐term health effects of weight loss associated with a high‐fat diet and low activity level merits further investigation.     

Diet and Exercise Interventions Reduce Intrahepatic Fat Content and Improve Insulin Sensitivity in Obese Older Adults

Both obesity and aging increase intrahepatic fat (IHF) content, which leads to nonalcoholic fatty liver disease (NAFLD) and metabolic abnormalities such as insulin resistance. We evaluated the effects of diet and diet in conjunction with exercise on IHF content and associated metabolic abnormalities in obese older adults. Eighteen obese (BMI ≥30 kg/m²) older (≥65 years old) adults completed a 6‐month clinical trial. Participants were randomized to diet (D group; n = 9) or diet + exercise (D+E group; n = 9). Primary outcome was IHF quantified by magnetic resonance spectroscopy (MRS). Secondary outcomes included insulin sensitivity (assessed by oral glucose tolerance), body composition (assessed by dual‐energy X‐ray absorptiometry), physical function (VO_2peak and strength), glucose, lipids, and blood pressure (BP). Body weight (D: ?9 ± 1%, D+E: ?10 ± 2%, both P < 0.05) and fat mass (D: ?13 ± 3%, D+E ?16 ± 3%, both P < 0.05) decreased in both groups but there was no difference between groups. IHF decreased to a similar extent in both groups (D: ?46 ± 11%, D+E: ?45 ± 8%, both P < 0.05), which was accompanied by comparable improvements in insulin sensitivity (D: 66 ± 25%, D+E: 68 ± 28%, both P < 0.05). The relative decreases in IHF correlated directly with relative increases in insulin sensitivity index (ISI) (r = ?0.52; P < 0.05). Improvements in VO_2peak, strength, plasma triglyceride (TG), and low‐density lipoprotein–cholesterol concentration, and diastolic BP occurred in the D+E group (all P < 0.05) but not in the D group. Diet with or without exercise results in significant decreases in IHF content accompanied by considerable improvements in insulin sensitivity in obese older adults. The addition of exercise to diet therapy improves physical function and other obesity‐ and aging‐related metabolic abnormalities.     

Effects of combined exenatide and pioglitazone therapy on hepatic fat content in type 2 diabetes

We examined the effects of combined pioglitazone (peroxisome proliferator‐activated receptor‐γ (PPAR‐γ) agonist) and exenatide (GLP‐1 receptor agonist) therapy on hepatic fat content and plasma adiponectin levels in patients with type 2 diabetes (T2DM). Twenty‐one T2DM patients (age = 52 ± 3 years, BMI = 32.0 ± 1.5, hemoglobin A_1c (HbA_1c) = 8.2 ± 0.4%) on diet and/or metformin received additional treatment with either pioglitazone 45 mg/day for 12 months (n = 10) or combined therapy with pioglitazone (45 mg/day) and exenatide (10 µg subcutaneously twice daily) for 12 months (n = 11). At baseline, hepatic fat content and plasma adiponectin levels were similar between the two treatment groups. Pioglitazone reduced fasting plasma glucose (FPG) (P < 0.05), fasting free fatty acid (FFA) (P < 0.05), and HbA_1c (Δ = 1.0%, P < 0.01), while increasing plasma adiponectin concentration by 86% (P < 0.05). Hepatic fat (magnetic resonance spectroscopy (MRS)) was significantly reduced following pioglitazone treatment (11.0 ± 3.1 to 6.5 ± 1.9%, P < 0.05). Plasma triglyceride concentration decreased by 14% (P < 0.05) and body weight increased significantly (Δ = 3.7 kg). Combined pioglitazone and exenatide therapy was associated with a significantly greater increase in plasma adiponectin (Δ = 193%) and a significantly greater decrease in hepatic fat (12.1 ± 1.7 to 4.7 ± 1.3%) and plasma triglyceride (38%) vs. pioglitazone therapy despite the lack of a significant change in body weight (Δ = 0.2 kg). Hepatic injury biomarkers aspartate aminotransferase and alanine aminotransferase (ALT) were significantly decreased by both treatments; however, the reduction in ALT was significantly greater following combined pioglitazone and exenatide therapy. We conclude that combined in patients with T2DM, pioglitazone and exenatide therapy is associated with a greater reduction in hepatic fat content as compared to the addition of pioglitazone therapy (Δ = 61% vs. 41%, P < 0.05).     

Weight loss strategies for obese adults: personalized weight management program vs. standard care

Objective: The objective of this study was to evaluate the effect of a 32‐week personalized Polar weight management program (PWMP) compared with standard care (SC) on body weight, body composition, waist circumference, and cardiorespiratory fitness in overweight or obese adults. Research Methods and Procedures: Overweight or obese (29 ± 2 kg/m²) men and women (n = 74) 38 ± 5 years of age were randomly assigned into either PWMP (men = 20, women = 21) or SC (men = 15, women = 18). Both groups managed their own diet and exercise program after receiving the same standardized nutrition and physical activity advice. PWMP also received a weight management system with literature to enable the design of a personalized diet and exercise weight loss program. Body weight and body composition, waist circumference, and cardiorespiratory fitness were measured at weeks 0, 16, and 32. Results: Eighty percent of participants completed the 32‐week intervention, with a greater proportion of the dropouts being women (PWMP: 2 men vs. 7 women; SC: 2 men vs. 4 women). At 32 weeks, PWMP completers had significantly (p < 0.001) greater losses in body weight [6.2 ± 3.4 vs. 2.6 ± 3.6 (standard deviation) kg], fat mass (5.9 ± 3.4 vs. 2.2 ± 3.6 kg), and waist circumference (4.4 ± 4.5 vs. 1.0 ± 3.6 cm). Weight loss and fat loss were explained by the exercise energy expenditure completed and not by weekly exercise duration. Discussion: More effective weight loss was achieved after treatment with the PWMP compared with SC. The results suggest that the PWMP enables effective weight loss through tools that support self‐monitoring without the requirement of more costly approaches to program supervision.     

Acute Effects of Dietary Glycemic Index on Antioxidant Capacity in a Nutrient‐controlled Feeding Study

Oxidative stress, caused by an imbalance between antioxidant capacity and reactive oxygen species, may be an early event in a metabolic cascade elicited by a high glycemic index (GI) diet, ultimately increasing the risk for cardiovascular disease and diabetes. We conducted a feeding study to evaluate the acute effects of low‐GI compared with high‐GI diets on oxidative stress and cardiovascular disease risk factors. The crossover study comprised two 10‐day in‐patient admissions to a clinical research center. For the admissions, 12 overweight or obese (BMI: 27–45 kg/m²) male subjects aged 18–35 years consumed low‐GI or high‐GI diets controlled for potentially confounding nutrients. On day 7, after an overnight fast and then during a 5‐h postprandial period, we assessed total antioxidant capacity (total and perchloric acid (PCA) protein‐precipitated plasma oxygen radical absorbance capacity (ORAC) assay) and oxidative stress status (urinary F_2α‐isoprostanes (F₂IP)). On day 10, we measured cardiovascular disease risk factors. Under fasting conditions, total antioxidant capacity was significantly higher during the low‐GI vs. high‐GI diet based on total ORAC (11,736 ± 668 vs. 10,381 ± 612 µmol Trolox equivalents/l, P = 0.002) and PCA‐ORAC (1,276 ± 96 vs. 1,210 ± 96 µmol Trolox equivalents/l, P = 0.02). Area under the postprandial response curve also differed significantly between the two diets for total ORAC and PCA‐ORAC. No diet effects were observed for the other variables. Enhancement in plasma total antioxidant capacity occurs within 1 week on a low‐GI diet, before changes in other risk factors, raising the possibility that this phenomenon may mediate, at least in part, the previously reported effects of GI on health.     

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.     

A high-fat diet has a tissue-specific effect on adiponectin and related enzyme expression

Objective: This study was designed to test whether adiponectin plays a role in diet‐induced obesity and insulin resistance and acts as a mediator to induce or inhibit specific metabolic pathways involved in lipid metabolism Research Methods and Procedures: Forty C57BL/6J male mice were fed either a high‐fat (HF) or control diet for 4 months, and adiponectin, its receptors, and enzyme expression in liver and muscle tissue were measured. Results: Mice fed the HF diet exhibited significantly greater weight gain, abnormal oral glucose tolerance test curves, and elevated homeostasis model assessment of insulin resistance (5.3 ± 0.89 vs. 2.8 ± 0.39). A significant reduction of adiponectin RNA expression (51%) and protein levels (15%) was observed in the adipose tissue of HF animals; however, serum adiponectin levels did not differ between groups (7.12 ± 0.34 μg/mL vs. 6.44 ± 0.38 μg/mL). Expression of hepatic mRNA of AdipoR1 and AdipoR2 was reduced by 15% and 25%, respectively, in animals fed the HF diet. In contrast, receptor mRNA expression of AdipoR1 and AdipoR2 increased by 25% and 30%, respectively, in muscle tissue. No effect was found on hepatic adenosine monophosphate‐activated protein kinase expression; however, a significant reduction of phosphoadenosine monophosphate kinase levels in muscles was observed. Hepatic acetyl‐coenzyme A carboxylase was similar between groups, but in muscles, the inactive form phosphoacetyl‐coenzyme A carboxylase was significantly reduced (p < 0.05). Discussion: The HF diet led to decreased insulin sensitivity accompanied by impaired activity of adiponectin‐related enzymes in skeletal muscles but not in the liver. These results suggest that the HF diet has a tissue‐specific effect on adiponectin and associated enzyme expression.     

Effects of Metformin and Weight Loss on Serum Alanine Aminotransferase Activity in the Diabetes Prevention Program

Nonalcoholic fatty liver disease (NAFLD) is associated with obesity, insulin resistance, and impaired glucose tolerance. We investigated whether metformin or changes in metabolic measurements (weight, fasting plasma glucose (FPG), or fasting insulin (FI)) improved serum alanine aminotransferase (ALT) activity, as a marker for NAFLD, in the Diabetes Prevention Program (DPP). From 1996 to 1999, 2,153 participants without marked elevations of serum ALT at baseline were randomized (1,081 to placebo, 1,072 to metformin) and treated for an average of 3.2 years. ALT increased during the first 2 years of the study, and was slightly but significantly lower in the participants randomized to metformin. In regression models adjusted for sex, baseline age, FPG, and FI, these differences remained significant, but disappeared after adjustment for weight, FPG, and FI changes at each examination. The 3‐year cumulative incidence for development of abnormal ALT concentrations was not significantly different ((mean ± s.e.) 21.4 ± 1.4% and 24.6 ± 1.4%, P = 0.11) in the metformin vs. placebo groups but was lower in individuals in both groups that lost more weight by the end of year 1 (metformin: 19.4 ± 2.4% vs. 27.5 ± 3.7%, for highest vs. lowest quartile of weight loss; placebo: 18.7 ± 3.4% vs. 28.8 ± 2.6%). Over 3 years of follow‐up in persons at high risk for development of diabetes, serum ALT was consistently lower in those treated with metformin compared with placebo. This effect was mediated by weight loss, indicating that the effects of metformin therapy on ALT is via its effects on weight.     

Leptin, superoxide dismutase, and weight loss: initial leptin predicts weight loss

Objective: Our goal was to study how plasma leptin concentration, superoxide dismutase (SOD) activity, and weight loss are related in obese adults. Research Methods and Procedures: Serum leptin concentration, SOD activities, general biochemical data, and body composition measurements were obtained for 62 overweight and obese subjects before and after an 8‐week body weight reduction (BWR) regimen. The subjects were on dietary control, performed moderate aerobic and strength training exercises, and attended educational lectures. Results: The measurement results indicated that the following criteria were significantly reduced: body weight [84.4 ± 17.0 vs. 79.3 ± 16.1 (standard error) kg, p < 0.001]; BMI (31.5 ± 4.3 vs. 29.4 ± 4.2 kg/m², p < 0.001), and fat mass (33.3 ± 10.0 vs. 29.8 ± 10.4 kg, p < 0.001). Plasma leptin levels also significantly decreased from 31.5 ± 17.6 to 26.5 ± 17.2 ng/mL (p < 0.001). Additionally, SOD activity was significantly increased from 261.4 ± 66.0 to 302.7 ± 30.9 U/mL (p < 0.001). Based on linear regression analysis results, a 3.78‐ to 8.13‐kg reduction in weight can be expected after the 8‐week BWR regimen when initial leptin concentration was 5 to 30 ng/mL. Discussion: We found that an 8‐week exercise and diet program was effective in reducing weight and fat mass and, notably, had further beneficial effects on leptin resistance and SOD activity. Additionally, this study demonstrated that initial plasma leptin concentration may be used as a predictor for weight loss outcome.