The general US population should increase their daily physical activity levels to decrease the rising prevalence of obesity.

Background: Obese persons generally regain lost weight, suggesting that adaptive metabolic changes favor return to a preset weight. Objective: Our objective was to determine whether adaptive changes in resting metabolic rate (RMR) and thyroid hormones occur in weight-reduced persons, predisposing them to longterm weight gain. Design: Twenty-four overweight, postmenopausal women were studied at a clinical research center in four 10-d study phases: the overweight state (phase 1, energy balance; phase 2, 3350 kJ/d) and after reduction to a normal-weight state (phase 3, 3350 kJ/d; phase 4, energy balance). Weight-reduced women were matched with 24 never-overweight control subjects. After each study phase, assessments included RMR (by indirect calorimetry), body composition (by hydrostatic weighing), serum triiodothyronine (T 3 ), and reverse T 3 (rT 3 ). Body weight was measured 4 y later, without intervention. Results: Body composition-adjusted RMR and T 3 :rT 3 fell during acute (phase 2) and chronic (phase 3) energy restriction (P < 0.01), but returned to baseline in the normal-weight, energybalanced state (phase 4; mean weight loss: 12.9 ± 2.0 kg). RMR among weight-reduced women (4771 ± 414 kJ/d) was not significantly different from that in control subjects (4955 ± 414 kJ/d; P = 0.14), and lower RMR did not predict greater 4-y weight regain (r = 0.27, NS). Conclusions: Energy restriction produces a transient hypothyroid-hypometabolic state that normalizes on return to energybalanced conditions. Failure to establish energy balance after weight loss gives the misleading impression that weight-reduced persons are energy conservative and predisposed to weight regain. Our findings do not provide evidence in support of adaptive metabolic changes as an explanation for the tendency of weight-reduced persons to regain weight.Am J Clin Nutr 2000;72:1088-94.

Since virtually no information is available concerning the myo-inositol content of dietary constituents, we have measured the amount of this material present in 487 foods by gas-liquid chromatography. We observed that the greatest amounts of myo-inositol were present in fruits, beans, grains, and nuts. Fresh vegetables and fruits were found to contain more myo-inositol than did frozen, canned, or salt-free products. The data provided in this report were used to develop diets that contained varying, but known amounts of myo-inositol. The myo-inositol intake that could be provided by such diets ranged from 225 to 1500 mg/day per 1800 kcal and within this range the agreement between the calculated and measured amounts of this material was excellent (r = 0.98). Since abnormalities in the metabolism of myo-inositol have been speculated to play a role in the pathogenesis of the polyneuropathies associated with diabetes mellitus and chronic renal failure, it is possible that the natural history of these neuropahties can be altered by modifying the amount of dietary myo-inositol that is ingested by patients with these diseases.

objective:To determine what effect diet-induced ~12 kg weight loss in combination with exercise training has on body composition and resting energy expenditure (REE) in premenopausal African-American (AA) and European-American (EA) women. Methods and Procedures: This study was a longitudinal, randomized weight loss clinical intervention, with either aerobic (AT), resistance (RT), or no exercise training (NT). Forty-eight AA and forty-six EA premenopausal overweight (BMI between 27 and 30) women underwent weight loss to a BMI <25. Body composition (densitometry), REE (indirect calorimetry), maximal oxygen uptake (VO 2 max), and muscular strength (isometric elbow flexion) were evaluated when subjects were in energy balance. Results: AA women lost less fat-free mass (FFM, P ≤ 0.05) (47.0 ± 4.6 to 46.9 ± 5.0 kg) than EA women (46.4 ± 4.9 to 45.2 ± 4.6 kg). Regardless of race, RT maintained FFM (P ≤ 0.05) following weight loss (46.9 ± 5.2 to 47.2 ± 5.0 kg) whereas AT (45.4 ± 4.2 to 44.4 ± 4.1 kg) and NT (47.9 ± 4.7 to 46.4 ± 5.1 kg) decreased FFM (P ≤ 0.05). Both AT and NT decreased in REE with weight loss but RT did not. Significant time by group interactions (all P ≤ 0.05) for strength indicated that RT maintained strength and AT did not. Discussion: AA women lost less FFM than EA women during equivalent weight losses. However, following weight loss in both AA and EA, RT conserved FFM, REE, and strength fitness when compared to women who AT or did not train.

No abstract

This prospective study was designed to identify abnormalities of energy expenditure and fuel utilization which distinguish post-obese women from never-obese controls. 24 moderately obese, postmenopausal, nondiabetic women with a familial predisposition to obesity underwent assessments of body composition, fasting and postprandial energy expenditure, and fuel utilization in the obese state and after weight loss (mean 12.9 kg) to a post-obese, normal-weight state. The post-obese women were compared with 24 never-obese women of comparable age and body composition. Four years later, without intervention, body weight was reassessed in both groups. Results indicated that all parameters measured in the post-obese women were similar to the never-obese controls: mean resting energy expenditure, thermic effect of food, and fasting and postprandial substrate oxidation and insulinglucose patterns. Four years later, post-obese women regained a mean of 10.9 kg while control subjects remained lean (mean gain 1.7 kg) (P < 0.001 between groups). Neither energy expenditure nor fuel oxidation correlated with 4-yr weight changes, whereas self-reported physical inactivity was associated with greater weight regain.The data suggest that weight gain in obesity-prone women may be due to maladaptive responses to the environment, such as physical inactivity or excess energy intake, rather than to reduced energy requirements. (J. Clin. Invest. 1995. 95:980-985.)

Objective-To determine whether eucaloric diets either enriched with monounsaturated fatty acids (MUFA; 17% energy) or low in carbohydrates (Low CHO; 43% energy) would increase insulin sensitivity (Si) and decrease circulating insulin concentrations, relative to a standard diet (STD; 56% CHO, 31% fat, 16% protein), among women with polycystic ovary syndrome (PCOS). Design-Crossover.Setting-Academic research environment. Patient(s)-Healthy women with PCOS not on hormonal or insulin-sensitizing therapy.Intervention(s)-Subjects consumed three, 16-day, eucaloric diets, each separated by a 3-week washout period. A frequently sampled, intravenous, glucose tolerance test was administered at baseline and following each diet.Main Outcome Measure(s)-Fasting glucose, insulin, the acute insulin response to glucose (AIRg), Si, sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEAS), total testosterone (T), free T, A4, total cholesterol, high-density lipoprotein cholesterol (HDL-C), tryglycerides (TG), and free fatty acids (FFA).Result(s)-Fasting insulin was lower following the Low CHO diet relative to the STD diet; AIRg was lower following the Low CHO diet relative to the MUFA diet. Fasting glucose, Si, and the circulating concentrations of reproductive hormones were not significantly affected by the intervention. Polycystic ovary syndrome (PCOS) is an endocrine disorder found in approximately 6.5% of reproductive-age women (1), and is commonly associated with obesity, menstrual irregularity, infertility, insulin resistance (IR), and clinical hyperandrogenism and/or hyperandrogenemia. Although the pathogenesis of PCOS remains unclear, evidence points to the role of IR and the associated hyperinsulinemia as possible contributing factors. Insulin inhibits the hepatic production of sex hormone-binding globulin (SHBG) (2-4) and insulinlike growth factor binding protein-I (IGFBP-I) (5), and stimulates ovarian P450c17α activity and androgen production (6, 7). Insulin resistance has been identified in the majority of lean and obese PCOS subjects, although obesity appears to exacerbate both IR and hyperinsulinemia. Conclusion(s)- NIH Public AccessTreatment for PCOS subjects typically includes insulin-lowering drugs, anti-androgen therapy, oral contraceptives, and the implementation of lifestyle changes, including weight loss if necessary. Weight loss, accompanied by an increase in insulin sensitivity (Si), has proven to be a successful treatment for the metabolic and hormonal abnormalities characteristic of the PCOS population (8-10). Weight loss has also proven to be an effective treatment for type 2 diabetes mellitus (T2DM; 11-13), a disease that shares similar clinical and metabolic features with PCOS, including generalized and abdominal obesity, IR, hyperinsulinemia, dyslipidemia, and an increased risk for the development of cardiovascular disease.Current dietary recommendations for subjects with T2DM reflect earlier observations regarding the beneficial effects of high monounsaturated fatty acid (MUF...

African American women had lower aerobic fitness than did white women, independent of differences in lean tissue or AEE. Diminished racial differences in SEE, REE, and TEE after adjustment for trunk lean tissue suggest that low EE in African American women is mediated by low volumes of metabolically active organ mass.