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Objective Little is known about long-term metabolic (energy expenditure) adaptation after bariatric surgery. Methods Resting metabolic rate under basal conditions (RMR), total daily energy expenditure (TDEE), and body composition were measured in 25 participants in the Longitudinal Assessment of Bariatric Surgery-2. Results Six months after surgery, BMI (±SD) decreased (47 ± 6 kg/m2 to 37 ± 5 kg/m2 ), body fat went from 48% ± 6% to 40% ± 6% fat, and fat-free mass went from 67 ± 9 kg to 60 ± 9 kg. In absolute terms, RMR and TDEE both decreased significantly (1,730 ± 278 kcal/d vs. 1,430 ± 200 kcal/d and 2,879 ± 544 kcal/d vs. 2,369 ± 304 kcal/d), and the achieved energy balance was -1,293 ± 355 kcal/d. Sixteen of these participants underwent repeated measures at ∼24 months; TDEE decreased 6 months postoperatively (2,957 ± 540 kcal/d to 2,423 ± 324 kcal/d; P = 0.0003), but at ∼24 months, TDEE (2,602 ± 471 kcal/d) was not significantly different compared with month 6. The average negative energy balance from baseline to month 24 was -379 ± 131 kcal/d. Conclusions RMR and TDEE fall precipitously in the first 6 months after bariatric surgery, but these adaptive changes were no longer significant after 2 years.

Donor lymphocyte infusion (DLI) is often given to induce a graft-versus-leukemia (GVL) effect after allogeneic hematopoietic stem cell transplantation (HSCT). However, efficacy of DLI is limited in most hematologic cancers. As antigen presenting cells, dendritic cells (DC) bolster immune responses. We conducted a Phase I trial testing the coinfusion of DC followed by DLI. DC were generated by culturing peripheral blood mononuclear cells from HLA matched-related donors in GM-CSF and IL-4 for 7 days, followed by TNF-α for 3 days. DC were administered intravenously on 3 dose levels (5 × 106; 1 × 107; 5 × 107 cells). DLI (3 × 107 CD3+ cells/kg) was administered intravenously 1 day after the DC. Sixteen patients with hematologic cancers relapsed after HSCT were treated. A maximum tolerated dose for DC was not reached. Two of 16 patients met criteria for DLT within 10 weeks of the infusion: 1 idiopathic respiratory failure, 1 ventricular cardiac arrest. None developed grade III/IV GVHD. One patient developed grade II acute intestinal graft-vs.-host disease (GVHD) and 1 chronic GVHD within 6 months of the infusion. Both resolved with corticosteroids. Four of 14 patients evaluable for disease response achieved durable remissions and are alive and cancer free 6.7, 8.4, 8.8, and 10.1 years from infusion. Sequential infusion of donor-derived DC with DLI is feasible in patients with relapsed hematologic cancers after allogeneic HSCT. Future studies may consider donor DC preloaded with tumor antigens to investigate whether DC infusion could augment the GVL effect. Am. J. Hematol. 89:1092–1096, 2014. © 2014 Wiley Periodicals, Inc.

The purpose of this study was to determine whether there are differences in energy intake or energy expenditure that distinguish overweight/obese women with and without binge eating disorder (BED). Seventeen overweight/obese women with BED and 17 overweight/obese controls completed random 24-h dietary recall interviews, and had total daily energy expenditure (TDEE) assessed by the doubly labeled water (DLW) technique with concurrent food log data collection. Participants received two baseline dual-energy X-ray absorptiometry (DXA) scans and had basal metabolic rate (BMR) and thermic effect of food (TEF) measured using indirect calorimetry. Results indicated no between group differences in TDEE, BMR, and TEF. As in our previous work, according to dietary recall data, the BED group had significantly higher caloric intake on days when they had binge eating episodes than on days when they did not (3,255 vs. 2,343 kcal). There was no difference between BED nonbinge day intake and control group intake (2,233 vs. 2,140 kcal). Similar results were found for food log data. Dietary recall data indicated a trend toward higher average daily intake in the BED group (2,587 vs. 2,140 kcal). Furthermore, when comparing TDEE to dietary recall and food log data, both groups displayed significant under-reporting of caloric intake of similar magnitudes ranging from 20 to 33%. Predicted energy requirements estimated via the Harris—Benedict equation (HBE) underestimated measured TDEE by 23–24%. Our data suggest that increased energy intake reported by BED individuals is due to increased food consumption and not metabolic or under-reporting differences.

We evaluated the EchoMRI-900 combination rat and mouse quantitative magnetic resonance (QMR) body composition method in comparison to traditional whole-body chemical carcass composition analysis (CCA) for measurements of fat and fat-free mass in rodents. Live and postmortem (PM) QMR fat and lean mass measurements were obtained for lean, obese and outbred strains of rats and mice, and compared with measurements obtained using CCA. A second group of rats was measured before and after 18 h food or water deprivation. Significant positive correlations between QMR and CCA fat and lean mass measurements were shown for rats and mice. Although all live QMR fat and lean measurements were more precise than CCA for rats, values obtained for mice significantly differed from CCA for lean mass only. QMR performed PM slightly overestimated fat and lean values relative to live QMR but did not show lower precision than live QMR. Food deprivation reduced values for both fat and lean mass; water deprivation reduced estimates of lean mass only. In summary, all measurements using this QMR system were comparable to those obtained by CCA, but with higher overall precision, similar to previous reports for the murine QMR system. However, PM QMR measurements slightly overestimated live QMR values, and lean and fat mass measurements in this QMR system are influenced by hydration status and animal size, respectively. Despite these caveats, we conclude that the EchoMRI QMR system offers a fast in vivo method of body composition analysis, well correlated to but with greater overall precision than CCA.

The rise in obesity is associated with a decline in the amount of physical activity in which people engage. The energy expended through everyday non-exercise activity, called non-exercise activity thermogenesis (NEAT), has a considerable potential impact on energy balance and weight gain. Comparatively little attention has been paid to the central mechanisms of energy expenditure and how decreases in NEAT might contribute to obesity. In this review, we first examine the sensory and endocrine mechanisms through which energy availability and energy balance are detected that may influence NEAT. Second, we describe the neural pathways that integrate these signals. Lastly, we consider the effector mechanisms that modulate NEAT through the alteration of activity levels as well as through changes in the energy efficiency of movement. Systems that regulate NEAT according to energy balance may be linked to neural circuits that modulate sleep, addiction and the stress response. The neural and endocrine systems that control NEAT are potential targets for the treatment of obesity.

Background: Sedentary time has been shown to have deleterious effects on health. Today's workforce spends most of the day sitting. The objective of this study was to evaluate the effect of workplac...

Brain neuromedin U (NMU) has been associated with the regulation of both energy intake and expenditure. We hypothesized that NMU induces changes in spontaneous physical activity and nonexercise activity thermogenesis (NEAT) through its actions on hypothalamic nuclei. We applied increasing doses of NMU directly to the paraventricular (PVN) and arcuate hypothalamic nuclei using chronic unilateral guide cannulae. In both nuclei, NMU significantly and dose-dependently increased physical activity and NEAT. Moreover, NMU increased physical activity and NEAT during the first hour of the dark phase, indicating that the reduction of sleep is unlikely to account for the increased physical activity seen with NMU treatment. As a positive control, we demonstrated that paraventricular NMU also significantly decreased food intake, as well as body weight. These data demonstrate that NMU is positively associated with NEAT through its actions in the PVN and arcuate nucleus. In co-ordination with its suppressive effects on feeding, the NEAT-activating effects of NMU make it a potential candidate in the combat of obesity.

Objective: The contribution of basal metabolic rate (BMR) to weight gain susceptibility has long been debated. We wanted to examine whether BMR changes in a linear fashion with overfeeding. Our hypothesis was that BMR does not increase linearly with 1000-kcal/d overfeeding in lean healthy subjects over 8 weeks. The null hypothesis states that BMR increases linearly with 1000-kcal/d overfeeding in lean healthy subjects. Research Methods and Procedures: Initially, 16 lean healthy sedentary subjects completed 2 weeks of weight maintenance feeding at the General Clinical Research Center. The subjects were then overfed by 1000 kcal/d over 8 weeks. BMR was measured under standard conditions each week using indirect calorimetry. Results: Baseline BMR was 1693 ± 154.5 kcal/d. BMR increased from 1711 ± 201.3 kcal/d at week 1 of overfeeding to 1781 ± 171.65 kcal/d at the second week of overfeeding (p = 0.05). BMR fell during the third week of overfeeding to 1729 ± 179.5 kcal/d (p = 0.05). After 5 weeks of overfeeding, BMR reached a plateau. Thereafter, there was no further change. Comparison of BMR with weeks of overfeeding was significantly different compared with the linear model (p < 0.05). Discussion: Increases in BMR in lean sedentary healthy subjects with 1000-kcal/d overfeeding are not linear over 8 weeks. There seems to be a short-term increase in BMR in the first 2 weeks of overfeeding that is not representative of longer-term changes.

Obesity is associated with devastating health and fiscal consequences in countries where it is epidemic. It is beholden on us all to try to prevent obesity emerging in countries where its prevalence is starting to increase. There are many countries in Asia where this is so. Obesity prevention necessitates attention to both increasing physical activity and improving nutrition. In this paper we discuss a strategic approach for increasing physical activity. First, we need to better understand physical activity levels and the factors that impact it. Next, we need to design specific and targeted governmentally supported strategies to promote physical activity. Finally we need to critically and objectively evaluate these strategies and then promote those that are successful, and channel limited resources away from those that are not. These goals are achievable through collaborating and sharing technologies. We hope to prevent obesity from engulfing Asia.

KIM, DOE-YOUNG, MICHAEL CAMILLERI, JOSEPH A. MURRAY, DEBRA A. STEPHENS, JAMES A. LEVINE, AND DUANE D. BURTON. Is there a role for gastric accommodation and satiety in asymptomatic obese people? Obes Res. 2001;9:655-661. Objective: The relationships of gastric accommodation and satiety in moderately obese individuals are unclear. We hypothesized that obese people had increased gastric accommodation and reduced postprandial satiety. The objective of this study was to compare gastric accommodation and satiety between obese and non-obese asymptomatic subjects. Research Methods and Procedures: In 13 obese (body mass index [BMI] $ 30 kg/m 2 ; mean BMI, 37.0 6 4.9 kg/m 2 ) and 19 non-obese control subjects (BMI , 30 kg/ m 2 ; mean BMI, 26.2 6 2.9 kg/m 2 ), we used single photon emission computed tomography to measure fasting and postprandial gastric volumes and expressed the accommodation response as the ratio of postprandial/fasting volumes. The satiety test measured maximum tolerable volume of ingestion of liquid nutrient meal (Ensure) and symptoms 30 minutes after cessation of ingestion. Results: Total fasting and postprandial gastric volumes and the ratio of postprandial/fasting gastric volume were not different between asymptomatic obese and control subjects. However, the fasting volume of the distal stomach was greater in obese than in control subjects. Maximum tolerable volume of ingested Ensure and aggregate symptom score 30 minutes later were also not different between obese and control subjects. Discussion: Asymptomatic obese individuals (within the BMI range of 32.6 to 48 kg/m 2 ) did not show either increased postprandial gastric accommodation or reduced satiety. These data suggest that gastric accommodation is unlikely to provide an important contribution to development of moderate obesity.

Background In healthy subjects, alcohol decreases lipid oxidation favouring fat deposition. However, individuals who chronically abuse alcohol are not obese. To investigate this paradox, we measured energy expenditure (EE) and fuel utilization in chronic alcohol abusers in relation to their drinking behaviour. Methods Resting and postprandial EE and nonprotein respiratory quotient (NPRQ) were measured using indirect calorimetry, in 36 alcohol abusers [mean (± SE) age 42 ± 2 years; weight 67 ± 2 kg; 21 with steatosis, eight with hepatitis; seven with cirrhosis] and in 36 gender-, age- and weight-matched healthy controls. Alcoholic patients were re-evaluated either after 14 days (n = 14) or on days 2, 4, 6, 8, 14 and 42 (n = 6) after abstinence. Results When alcoholics were compared to healthy controls, mean energy intake was greater, 15 ± 1 MJ day−1 (38 ± 2% from alcohol) cf. 9 ± 1 MJ day−1 (P

BackgroundPhysical activity is important in obesity, metabolic and cardiovascular diseases and cancer prevention. Several cell phone platforms integrate an accelerometer onto the motherboard. We wr...

Splinter hemorrhages can be a feature of the antiphospholipid syndrome. We describe a patient in whom splinter hemorrhages developed following radial artery puncture. The implications of this findings in patients with the antiphospholipid syndrome are discussed.

A critique is offered of’ the methodology of the criminal victimization survey and several sources of error that may result in artificially inflated crime rates based on such data are identified. It is argued that much information about crimes given by respondents may be incorrect due to misunderstandings about what transpired, ignorance about legal definitions, memory failures about when crimes occurred, and outright prefabrication. Organizational imperatives that may cause interviewers and coders to skew the data toward a showing of greater criminality are analyzed. Some ideas for measuring response error more precisely are presented.