Abstract: Objective To examine the relationship between local food environments and obesity and assess the quality of studies reviewed. Methods Systematic keyword searches identified studies from US and Canada that assessed the relationship of obesity to local food environments. We applied a quality metric based on design, exposure and outcome measurement, and analysis. Results We identified 71 studies representing 65 cohorts. Overall, study quality was low; 60 studies were cross-sectional. Associations between food outlet availability and obesity were predominantly null. Among non-null associations, we saw a trend toward inverse associations between supermarket availability and obesity (22 negative, 4 positive, 67 null) and direct associations between fast food and obesity (29 positive, 6 negative, 71 null) in adults. We saw direct associations between fast food availability and obesity in lower income children (12 positive, 7 null). Indices including multiple food outlets were most consistently associated with obesity in adults (18 expected, 1 not expected, 17 null). Limiting to higher quality studies did not affect results. Conclusions Despite the large number of studies, we found limited evidence for associations between local food environments and obesity. The predominantly null associations should be interpreted cautiously due to the low quality of available studies.

Abstract: Objective This review will focus on the immunological aspects of adipose tissue and its potential role in development of chronic inflammation that instigates obesity-associated co-morbidities.

Abstract: Objective The concept of “breaks” in sedentary behavior has emerged as a potential modifier of detrimental effects on adiposity caused by sedentary behavior. The existing research investigating the relationship between breaks in sedentary behavior with adiposity and cardiometabolic health in adults was systematically reviewed and quantitatively synthesized by this study. Methods Observational and experimental studies that examined the relationships between the frequency of interruptions of sedentary behavior and markers of adiposity and cardiometabolic health in adults were identified by a systematic search of the literature. A meta-analysis was conducted by using the inverse variance method for experimental trials and a Bayesian posterior probability of existence of an association between breaks with adiposity and cardiometabolic markers for observational studies. Results: It was revealed by the pooled results from nine experimental studies that breaks in sedentary periods of at least light intensity may have a positive effect on glycemia but not on lipidemia for adults. It is unclear whether this effect is independent of total sitting time. However, the 10 identified observational studies showed an association with breaks, which was independent of total sedentary time, but only for obesity metrics. Conclusions The theory that interrupting bouts of sedentary behavior with light-intensity activity might help control adiposity and postprandial glycemia was supported by the evidence. Further investigations with better methods of measuring sedentary behavior patterns and improved study designs are necessary to confirm this preliminary evidence.

Abstract: The idea of quantitative measurement came to obesity in stages. Quetelet (1) introduced the body mass index (BMI) which was applied nearly a century later to the evaluation of degree of overweight in studies of familial inheritance of obesity. Publication of average weight tables in the 1850s was expanded to “ideal” weight tables by the life insurance industry in the mid-20th century. The relation of increasing weight to risk for many diseases was extended by the Framingham Study from which Gordon and Kannel (2) concluded that if everyone were at optimal weight, the incidence of coronary heart disease would be reduced by 25% and congestive failure and brain infarctions would be reduced by 35%. By 1975 there had been many observations about the association of obesity and a variety of health problems. Yet at this time, there were no generally agreed upon metrics for evaluating health effects of weight loss. In 1973, Dr. Thaddeus Prout (3) authored a final report to the Food and Drug Administration (FDA) Director of Anorectic Drugs which interpreted the statistically significant differences between placebo and anorectic drugs in the short-term clinical trials reviewed by the FDA as being “clinically trivial” (p 501). Bray (4) at the 1973 Fogarty International Center Conference noted: “Little uniformity exists in the criteria which are used for evaluating weight loss or in the uniformity of follow-up between various clinical trials” (p 60). The Fogarty Conference report suggests several criteria, including percent achieving 20and 40-pound weight loss and a weight reduction index. Clearly, in the mid-1970s the obvious question was “What defines clinically significant weight loss?” Up to this point in the story, few, if any, had suggested that modest weight losses might have important health benefits.

Abstract: Objective While evidence regarding associations between weight stigma and biopsychosocial outcomes is accumulating, outcomes are considered in isolation. Thus, little is known about their complex relationships. This article extends existing work by systematically reviewing the biopsychosocial consequences of stigma in adults with overweight/obesity. Methods Articles were identified through Medline, CINAHL, PsycINFO, Embase, Web of Science, and Cochrane databases. Independent extraction of articles was conducted using predefined data fields, including data on biopsychosocial correlates in each study. Results Twenty-three studies published from 2001 and addressing correlates of stigma in adults with overweight/obesity (body mass index ≥25 kg m−2; 18-65 years) were identified. Numerous biopsychosocial correlates of weight stigma were studied, particularly in treatment-seeking individuals. Available research shows that weight stigma is consistently associated with medication non-adherence, mental health, anxiety, perceived stress, antisocial behavior, substance use, coping strategies, and social support. Biopsychosocial correlates were not considered in combination in research. Psychological correlates were well documented in comparison to biological and social correlates for each weight stigma type. There were some indications that associations are stronger once stigma is internalized. Conclusions While there is evidence for biopsychosocial correlates of weight stigma, these are not considered in combination in research; thus their inter-relationships are unknown. Conclusions from the review are limited by this and the small number of studies, types of designs, and variables considered.

Abstract: Objective This study characterized the kynurenine pathway (KP) in human obesity by evaluating circulating levels of kynurenines and the expression of KP enzymes in adipose tissue. Methods Tryptophan and KP metabolite levels were measured in serum of individuals from the D.E.S.I.R. cohort (case-cohort study: 212 diabetic, 836 randomly sampled) and in women with obesity, diabetic or normoglycemic, from the ABOS cohort (n = 100). KP enzyme gene expressions were analyzed in omental and subcutaneous adipose tissue of women from the ABOS cohort, in human primary adipocytes and in monocyte-derived macrophages. Results In the D.E.S.I.R. cohort, kynurenine levels were positively associated with body mass index (BMI) (P = 4.68 × 10) and with a higher HOMA2-IR insulin resistance index (P = 6.23 × 10). The levels of kynurenine, kynurenic acid, and quinolinic acid were associated with higher BMI (P < 0.05). The expression of several KP enzyme genes (indoleamine 2,3-dioxygenase 1 [IDO1], kynureninase [KYNU], kynurenine 3-monooxygenase [KMO], and kynurenine aminotransferase III [CCBL2]) was increased in the omental adipose tissue of women with obesity compared to lean (P < 0.05), and their expression was induced by proinflammatory cytokines in human primary adipocytes (P < 0.05), except for KMO that is not expressed in these cells. The expressions of IDO1, KYNU, KMO, and CCBL2 were higher in proinflammatory than in anti-inflammatory macrophages (P < 0.05). Conclusions In the context of obesity, the presence of macrophages in adipose tissue may contribute to diverting KP toward KMO activation.

Abstract: Objectives In men, androgen deprivation contributes to the development of metabolic syndrome and type 2 diabetes (T2D). In women, androgen excess predisposes to insulin resistance and T2D. There is a bidirectional modulation of glucose homeostasis by androgen in males and females that we analyze in this review.

Abstract: Objective Regular self-weighing, which in this article is defined as weighing oneself regularly over a period of time (e.g., daily, weekly), is recommended as a weight loss strategy. However, the published literature lacks a review of the recent evidence provided by prospective, longitudinal studies. Moreover, no paper has reviewed the psychological effects of self-weighing. Therefore, the objective is to review the literature related to longitudinal associations between self-weighing and weight change as well as the psychological outcomes. Methods Electronic literature searches in PubMed, Ovid PsycINFO, and Ebscohost CINAHL were conducted. Keywords included overweight, obesity, self-weighing, etc. Inclusion criteria included trials that were published in the past 25 years in English; participants were adults seeking weight loss treatment; results were based on longitudinal data. Results The results (N = 17 studies) revealed that regular self-weighing was associated with more weight loss and not with adverse psychological outcomes (e.g., depression, anxiety). Findings demonstrated that the effect sizes of association between self-weighing and weight change varied across studies and also that the reported frequency of self-weighing varied across studies. Conclusions The findings from prospective, longitudinal studies provide evidence that regular self-weighing has been associated with weight loss and not with negative psychological outcomes.

Abstract: Objective The main objective of this systematic review is to assess the effects of obesity on telomere length. Methods The following databases were searched: MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library), LILACS, SPORTdiscus, and Web of Science from inception to August 2014. The search was performed using the following combinations of terms: telomere AND “overweight” OR “obesity” OR “adiposity,” without language restriction. Results Sixty-three original studies were included in this systematic review, comprising 119,439 subjects. Thirty-nine studies showed either weak or moderate correlation between obesity and telomere length; however, they showed an important heterogeneity. Conclusions There is a tendency toward demonstrating negative correlation between obesity and telomere length. The selected studies showed weak to moderate correlation for the main search, and there was an important heterogeneity. For this reason, the causal relationship of obesity and telomere length remains open. Additional controlled longitudinal studies are needed to investigate this issue.

Abstract: Objective To investigate ethnic difference in the associations of BMI with comorbidity, mortality, and body composition between mainland Chinese and U.S. whites. Methods Ethnic-comparison study using data from China Health and Nutrition Survey, U.S. National Health and Nutrition Examination Survey, and data from Zhejiang University (China) and Columbia University (U.S.). Results Chinese people experienced greater odds of comorbidities than whites for a given BMI after standardizing for age and sex: 43% for diabetes, 30% for dyslipidemia, 28% for hypertension, 38% for metabolic syndrome, and 48% for hyperuricemia. Comparisons of BMI-mortality associations found that the U-shaped BMI-mortality curve shifted 1-2 kg m(-2) to the left in Chinese compared to whites. Compared to whites at BMIs of 25 and 30 kg m(-2), corresponding cutoffs in Chinese were 22.5 and 25.9 kg m(-2) in men, and 22.8 and 26.6 kg m(-2) in women after both fat and fat distribution were taken into account. Conclusions Comorbidity, mortality, and body composition data consistently support the use of lower BMI cutoffs in Chinese than those in whites.

Abstract: Objective To distinguish the effects of dietary fat profile on gut parameters and their relationships with metabolic changes and to determine the capacity of n-3 fatty acids to modify gut variables in the context of diet-induced metabolic dysfunctions. Methods Mice received control or high-fat diets emphasizing saturated (HFD-sat), n-6 (HFD-n6), or n-3 (HFD-n3) fatty acids for 8 weeks. In another cohort, mice that were maintained on HFD-sat received n-3-rich fish oil or resolvin D1 supplementation. Results HFD-sat and HFD-n6 induced similar weight gain, but only HFD-sat increased index of insulin resistance (HOMA-IR), colonic permeability, and mesenteric fat inflammation. Hydrogen sulfide-producing bacteria were one of the major groups driving the diet-specific changes in gut microbiome, with the overall microbial profile being associated with changes in body weight, HOMA-IR, and gut permeability. In mice maintained on HFD-sat, fish oil and resolvin D1 restored barrier function and reduced inflammation in the colon but were unable to normalize HOMA-IR. Conclusions Different dietary fat profiles led to distinct intestinal and metabolic outcomes that are independent of obesity. Interventions targeting inflammation successfully restored gut health but did not reverse systemic aspects of diet-induced metabolic dysfunction, implicating separation between gut dysfunctions and disease-initiating and/or -maintaining processes.

Abstract: Objective Preclinical studies indicate that oxytocin is anorexigenic and has beneficial metabolic effects. Oxytocin effects on nutrition and metabolism in humans are not well defined. It was hypothesized that oxytocin would reduce caloric intake and appetite and alter levels of appetite-regulating hormones. Metabolic effects of oxytocin were also explored. Methods A randomized, placebo-controlled crossover study of single-dose intranasal oxytocin (24 IU) in 25 fasting healthy men was performed. After oxytocin/placebo, subjects selected breakfast from a menu and were given double portions. Caloric content of food consumed was measured. Visual analog scales were used to assess appetite, and blood was drawn for appetite-regulating hormones, insulin, and glucose before and after oxytocin/placebo. Indirect calorimetry assessed resting energy expenditure (REE) and substrate utilization. Results Oxytocin reduced caloric intake with a preferential effect on fat intake and increased levels of the anorexigenic hormone cholecystokinin without affecting appetite or other appetite-regulating hormones. There was no effect of oxytocin on REE. Oxytocin resulted in a shift from carbohydrate to fat utilization and improved insulin sensitivity. Conclusions Intranasal oxytocin reduces caloric intake and has beneficial metabolic effects in men without concerning side effects. The efficacy and safety of sustained oxytocin administration in the treatment of obesity warrants investigation.

Abstract: Objective Endogenous acetone production is a by-product of the fat metabolism process. Because of its small size, acetone appears in exhaled breath. Historically, endogenous acetone has been measured in exhaled breath to monitor ketosis in healthy and diabetic subjects. Recently, breath acetone concentration (BrAce) has been shown to correlate with the rate of fat loss in healthy individuals. In this review, the measurement of breath acetone in healthy subjects is evaluated for its utility in predicting fat loss and its sensitivity to changes in physiologic parameters. Results BrAce can range from 1 ppm in healthy non-dieting subjects to 1,250 ppm in diabetic ketoacidosis. A strong correlation exists between increased BrAce and the rate of fat loss. Multiple metabolic and respiratory factors affect the measurement of BrAce. BrAce is most affected by changes in the following factors (in descending order): dietary macronutrient composition, caloric restriction, exercise, pulmonary factors, and other assorted factors that increase fat metabolism or inhibit acetone metabolism. Pulmonary factors affecting acetone exchange in the lung should be controlled to optimize the breath sample for measurement. Conclusions When biologic factors are controlled, BrAce measurement provides a non-invasive tool for monitoring the rate of fat loss in healthy subjects.

Abstract: Objective The aim was to assess associations between lifestyle behaviors and obesity in a multinational study of children from 12 countries representing a wide range of human development. Methods The sample included 6,025 children 9–11 years of age. Behavioral risk factors included nocturnal sleep duration, moderate to vigorous physical activity (MVPA), television viewing (TV time), and healthy and unhealthy diet pattern scores. Multilevel analyses were used to obtain odds ratios for obesity expressed per standard deviation of each behavioral risk factor. Results The odds ratios (95% confidence intervals) for obesity from multilevel, multivariable models were 0.79 (0.71–0.90) for nocturnal sleep duration, 0.52 (0.45–0.60) for MVPA, 1.15 (1.05–1.27) for TV time, 1.08 (0.96–1.20) for healthy diet score, and 0.93 (0.83–1.04) for unhealthy diet score in boys and 0.71 (0.63–0.80) for nocturnal sleep duration, 0.43 (0.35–0.53) for MVPA, 1.07 (0.96–1.19) for TV time, 1.05 (0.93–1.19) for healthy diet score, and 0.96 (0.82–1.11) for unhealthy diet score in girls. Conclusions Behavioral risk factors are important correlates of obesity in children, particularly low MVPA, short sleep duration, and high TV viewing.

Abstract: Objective Diet-induced thermogenesis (DIT) is lower in the evening and at night than in the morning. This may help explain why meal timing affects body weight regulation and why shift work is a risk factor for obesity. The separate effects of the endogenous circadian system—independent of behavioral cycles—and of circadian misalignment on DIT are unknown. Methods Thirteen healthy adults undertook a randomized crossover study with two 8-day laboratory visits: three baseline days followed either by repeated simulated night shifts including 12-h inverted behavioral cycles (circadian misalignment) or by recurring simulated day shifts (circadian alignment). DIT was determined for up to 114 min (hereafter referred to as “early DIT”) following identical meals given at 8AM and 8PM in both protocols. Results During baseline days, early DIT was 44% lower in the evening than morning. This was primarily explained by a circadian influence rather than any behavioral cycle effect; early DIT was 50% lower in the biological evening than biological morning, independent of behavioral cycle influences. Circadian misalignment had no overall effect on early DIT. Conclusions The circadian system plays a dominating role in the morning/evening difference in early DIT and may contribute to the effects of meal timing on body weight regulation.

Abstract: Objective To review recent advances in understanding the cellular mechanisms that regulate fat distribution.

Abstract: Objective Examine the relationship between 1- and 2-month weight loss (WL) and 8-year WL among participants enrolled in a lifestyle intervention.

Abstract: Author(s): Himmelstein, Mary S; Incollingo Belsky, Angela C; Tomiyama, A Janet | Abstract: ObjectiveRates of weight-based stigmatization have steadily increased over the past decade. The psychological and physiological consequences of weight stigma remain understudied.MethodsThis study examined the effects of experimentally manipulated weight stigma on the stress-responsive hypothalamic-pituitary-adrenal axis (HPA) in 110 female undergraduate participants (BMI: M=19.30, SD=1.55). Objective BMI and self-perceived body weight were examined as moderators of the relationship between stigma and HPA reactivity.ResultsResults indicated participants' perceptions of their own body weight (but not objective BMI) moderated the effect of weight stigma on cortisol reactivity: F(1,102)=13.48, Pl0.001, η(2) p =0.12 (interaction 95% CI range [-2.06 to -1.44, -1.31 to -0.99]). Specifically, participants who perceived themselves as heavy exhibited sustained cortisol elevation post-manipulation compared with individuals who did not experience the weight-related stigma. Cortisol change did not vary by condition for participants who perceived themselves as average weight.ConclusionsIn the first study to examine physiological consequences of active interpersonal exposure to weight stigma, experiencing weight stigma was stressful for participants who perceived themselves as heavy, regardless of their BMI. These results are important because stress and cortisol are linked to deleterious health outcomes, stimulate eating, and contribute to abdominal adiposity.

Abstract: Objective To determine the prevalence of and risk factors for postprandial hypoglycemic symptoms among bariatric surgery patients.

Abstract: Objective To use quantitative magnetic resonance imaging (MRI) to test whether mediobasal hypothalamic (MBH) gliosis is associated with obesity and insulin resistance in humans. Methods Sixty-seven participants underwent a fasting blood draw and MRI. Cases with radiologic evidence of MBH gliosis (N = 22) were identified as the upper tertile of left MBH T2 relaxation time and were compared to controls (N = 23) from the lowest tertile. In a separate postmortem study, brain slices (N = 10) through the MBH were imaged by MRI and stained for glial fibrillary acidic protein (GFAP). Results In all participants, longer T2 relaxation time in the left MBH was associated with higher BMI (P = 0.01). Compared with controls, cases had longer T2 relaxation times in the right MBH (P < 0.05), as well as higher BMI (P < 0.05), fasting insulin concentrations (P < 0.01), and HOMA-IR values (P < 0.01), adjusted for sex and age. Elevations in insulin and HOMA-IR were also independent of BMI. In the postmortem study, GFAP staining intensity was positively associated with MBH T2 relaxation time (P < 0.05), validating an MRI-based method for the detection of MBH gliosis in humans. Conclusions These findings link hypothalamic gliosis to insulin resistance in humans and suggest that the link is independent of the level of adiposity.

Abstract: Obesity Original Article EPIDEMIOLOGY/GENETICS Relationship Between Sleep Duration and Body Mass Index Depends on Age Michael A. Grandner 1,2 , Elizabeth A. Schopfer 2 , Megan Sands-Lincoln 3 , Nicholas Jackson 4 , and Atul Malhotra 5 Objective: Sleep duration is associated with obesity and cardiometabolic disease. It is unclear, though, how these relationship differs across age groups. Methods: Data from 2007 to 2008 National Health and Nutrition Examination Survey (NHANES) were used, including respondents aged 161 with complete data (N 5 5,607). Sleep duration and age were evaluated by self-report, and body mass index (BMI) was assessed objectively. Sleep duration was eval- uated continuously and categorically [very short (4 h), short (5-6 h), and long (9 h) versus average (7-8 h)]. Age was also evaluated continuously and categorically [adolescent (16-17 years), young adult (18-29 years), early middle age (30-49 years), late middle age (50-64 years), and older adult (65 years)]. Results: There was a significant interaction with age for both continuous (P interaction 5 0.014) and categor- ical (P interaction 5 0.035) sleep duration. A pseudo-linear relationship was seen among the youngest respondents, with the highest BMI associated with the shortest sleepers and the lowest BMI associated with the longest sleepers. This relationship became U-shaped in middle-age, and less of a relationship was seen among the oldest respondents. Conclusions: These findings may provide insights for clinical recommendations and could help to guide mechanistic research regarding the sleep-obesity relationship. Obesity (2015) 00, 00–00. doi:10.1002/oby.21247 Introduction Obesity is a major global health problem, and in the US the preva- lence has increased at an alarming rate. Obesity is a major risk fac- tor for cardiometabolic disease and other adverse health outcomes, many of which are linked to the leading causes of death in the popu- lation. Substantial research has clarified the role of behavioral fac- tors in the etiology of obesity—particularly diet and exercise. How- ever, it is recognized that other health behaviors are also important (1). More recently, sleep has been identified as a health behavior that may play a role in obesity as well (2). Associations between sleep duration and obesity are well-characterized (3). Empirical evidence suggests a strong association between habitual sleep duration and obesity. Proposed mechanisms for this relationship include insulin and glucose dysregulation (4), an orexigenic pattern due to decreased leptin and/or increased ghrelin (5), increased caloric con- sumption or other dietary changes (6), increased systemic inflammation (7), or decreased physical activity, perhaps due to increased daytime sleepiness (8). These and other pathways may explain the mechanisms underlying why short sleep may cause increased body weight. Despite the general agreement across studies that there is an associa- tion between sleep duration and obesity (3), there is some notable inconsistency regarding the nature of this relationship. Some studies tend to show a relatively linear negative association between sleep duration and adiposity/obesity (9,10); however, others show a U-shaped association that implicates both short and long sleep dura- tion (11), similar in pattern to the frequently observed relationship between sleep duration and mortality (12). These inconsistencies across studies may be due to differences in measurement approaches for both sleep and obesity/adiposity, differences in adjustment for potential confounders, and differences in the characteristics of study populations, particularly among observational studies. Since body mass, and associated chronic disease, generally reflects years of accumulated morbidity, it is possible that the relationship Department of Psychiatry, University of Arizona College of Medicine, Tucson, Arizona, USA. Correspondence: Michael A. Grandner (grandner@email. arizona.edu) 2 Behavioral Sleep Medicine Program, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA 3 Center for Evidence-Based Medicine, Elsevier, Inc., Philadelphia, Pennsylvania, USA 4 Department of Psychology, University of Southern California, Los Angeles, California, USA 5 Division of Pulmonary, Critical Care, and Sleep Medicine, University of California, San Diego, La Jolla, California, USA. Funding agencies: This work was supported by 12SDG9180007 (AHA), K23HL110216 (NHLBI), R21ES022931 (NIEHS), and the University of Pennsylvania CTSA (UL1RR024134). Disclosure: The authors declared no conflict of interest. Additional Supporting Information may be found in the online version of this article. Received: 21 January 2015; Accepted: 28 April 2015; Published online 00 Month 2015. doi:10.1002/oby.21247 www.obesityjournal.org Obesity | VOLUME 00 | NUMBER 00 | MONTH 2015

Abstract: Objective To investigate the influence of food insecurity on women's stress, disordered eating, dietary fat intake, and weight during the postpartum period. Methods The association between marginal food security and food insecurity—measured during pregnancy and postpartum—and stress, disordered eating, dietary fat intake, and weight at 3 and 12 months postpartum was estimated using multivariate linear regression, controlling for demographic and socioeconomic characteristics and health behaviors. Effect modification between level of food insecurity and prepregnancy weight status was assessed, hypothesizing a stronger association would be found among women who started pregnancy with overweight or obesity. Results Food insecurity status during pregnancy was strongly associated with higher levels of stress, disordered eating, and dietary fat intake at 3 and 12 months postpartum; during the postpartum period, food insecurity was associated with these measures at 12 months postpartum. A significant interaction was found between level of food insecurity and prepregnancy weight status; food insecurity was associated with greater weight and BMI at 12 months only among women with overweight or obesity. Conclusions In order to return to one's prepregnancy weight, women with overweight and obesity who face household food insecurity may need multipronged assistance that not only addresses having enough high-quality food, but also include stress reduction and eating behavior interventions.

Abstract: Objective To identify possible mechanisms linking obesity in pregnancy to increased fetal adiposity and growth, a unique mouse model of maternal obesity associated with fetal overgrowth was developed, and the hypothesis that maternal obesity causes up-regulation of placental nutrient transporter expression and activity was tested. Methods C57BL/6J female mice were fed a control (C) or a high-fat/high-sugar (HF/HS) pelleted diet supplemented by ad libitum access to sucrose (20%) solution, mated, and studied at embryonic day 18.5. Results HF/HS diet increased maternal fat mass by 2.2-fold (P < 0.01) and resulted in glucose intolerance with normal fasting glucose. Maternal circulating insulin, leptin, and cholesterol were increased (P < 0.05) whereas total and high-molecular-weight adiponectin was decreased (P < 0.05). HF/HS diet increased fetal weight (+18%, P = 0.0005). In trophoblast plasma membranes (TPM) isolated from placentas of HF/HS-fed animals, protein expression of glucose transporter (GLUT) 1 and 3, sodium-coupled neutral amino acid transporter (SNAT) 2, and large neutral amino acid transporter 1 (LAT1) was increased. TPM System A and L amino acid transporter activity was increased in the HF/HS group. Conclusions Up-regulation of specific placental nutrient transporter isoforms may constitute a mechanism underlying fetal overgrowth in maternal obesity.

Abstract: Objective The objective of this study was to test the hypothesis that the multi-strain probiotic VSL#3 would attenuate the increase in fasting plasma concentrations of trimethylamine-N-oxide (TMAO) following a high-fat diet. Methods Nineteen healthy, non-obese males (18-30 years) participated in the present study. Following a 2-week eucaloric control diet, subjects were randomized to either VSL#3 (900 billion live bacteria) or placebo (cornstarch) during the consumption of a hypercaloric (+1,000 kcal day−1), high-fat diet (55% fat) for 4 weeks. Plasma TMAO, L-carnitine, choline, and betaine (UPLC-MS/MS) were measured at baseline and following a high-fat diet. Results Plasma TMAO significantly increased 89% ± 66% vs. 115% ± 61% in both the VSL#3 and placebo groups, respectively; however, the magnitude of change in plasma TMAO was not different (P > 0.05) between them. Plasma L-carnitine, choline, and betaine concentrations did not increase following the high-fat diet in either group. Conclusions A high-fat diet increases plasma TMAO in healthy, normal-weight, young males. However, VSL#3 treatment does not appear to influence plasma TMAO concentrations following a high-fat diet. Future studies are needed to determine whether other therapeutic strategies can attenuate the production of TMAO.

Abstract: Objective To test whether enhancing the capability of adipose tissue to store lipids using antioxidant supplementation may prevent the lipotoxic effects and improve the metabolic profile of long-term obesity. Methods C57BL/6J mice were randomized into three experimental groups for 28 weeks: control group (n = 10) fed chow diet (10% kcal from fat), obese group (O, n = 12) fed high-fat (HF) diet (45% kcal from fat), and obese group fed HF diet and supplemented twice a week with 150 mg of α-tocopherol (vitamin E) by oral gavage (OE, n = 12). Results HF diet resulted in an obese phenotype with a marked insulin resistance, hypertriglyceridemia, and hepatic steatosis in O mice. Histological analysis of obese visceral adipose tissue (VAT) revealed smaller adipocytes surrounded by a fibrotic extracellular matrix and an increased macrophage infiltration, with the consequent release of proinflammatory cytokines. Vitamin E supplementation decreased oxidative stress and reduced collagen deposition in the VAT of OE mice, allowing a further expansion of the adipocytes and increasing the storage capability. As a result, circulating cytokines were reduced and hepatic steasosis, hypertriglyceridemia, and insulin sensitivity were improved. Conclusions Our results suggest that oxidative stress is implicated in extracellular matrix remodeling and may play an important role in metabolic regulation.

Abstract: Objective To explore the transcriptome of epicardial adipose tissue (EAT) as compared to subcutaneous adipose tissue (SAT) and its modifications in a small number of patients with coronary artery disease (CAD) versus valvulopathy Methods SAT and EAT samples were obtained during elective cardiothoracic surgeries The transcriptome of EAT was evaluated, as compared to SAT, using an unbiased, whole-genome approach in subjects with CAD (n = 6) and without CAD (n = 5), where the patients without CAD had cardiac valvulopathy Results Relative to SAT, EAT is a highly inflammatory tissue enriched with genes involved in endothelial function, coagulation, immune signaling, potassium transport, and apoptosis EAT is lacking in expression of genes involved in protein metabolism, tranforming growth factor-beta (TGF-beta) signaling, and oxidative stress Although underpowered, in subjects with severe CAD, there is an expression trend suggesting widespread downregulation of EAT encompassing a diverse group of gene sets related to intracellular trafficking, proliferation/transcription regulation, protein catabolism, innate immunity/lectin pathway, and ER stress Conclusions The EAT transcriptome is unique when compared to SAT In the setting of CAD versus valvulopathy, there is possible alteration of the EAT transcriptome with gene suppression This pilot study explores the transcriptome of EAT in CAD and valvulopathy, providing new insight into its physiologic and pathophysiologic roles

Abstract: Objective Mice are typically housed at environmental temperatures below thermoneutrality, whereas humans live near thermoneutrality. This difference affects energy physiology and, potentially, anti-obesity drug efficacy. Here we compare β3-adrenergic agonist treatment at thermoneutrality (30°C) versus room temperature (22°C).

Abstract: Objective Research consistently shows a negative view of individuals with obesity in the general public and in various other settings. Stigma and discrimination can be considered chronic stressors, as these factors have a profound impact on the psychological well-being of the affected individuals. This article proposes a framework that entails a mediation of the adverse effects of discrimination and stigmatization on mental well-being through elevated psychological risk factors that are not unique to weight but that could affect overweight and normal-weight individuals alike. Methods A systematic review was conducted to assess the prevalence of psychological risk factors, such as self-esteem and coping, in individuals with obesity. Results Forty-six articles were assessed and included for detailed analysis. The number of studies on these topics is limited to certain dimensions of psychological processes. The best evaluated association of obesity and psychosocial aspects is seen for self-esteem. Most studies establish a negative association of weight and self-esteem in children and adults. All studies with mediation analysis find a positive mediation through psychological risk factors on mental health outcomes. Conclusions This review shows that elevated psychological risk factors are existent in individuals with obesity and that they may be a mediator between weight discrimination and pathopsychological outcomes.