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Objective: Obesity is a major public health challenge, and the US military veteran population is disproportionately affected. Using deidentified records from a local weight management clinic and a national clinical data repository, obesity pharmacotherapy use and effectiveness for weight loss and obesity comorbidities in this vulnerable population were assessed.Methods: During the initial year of the local clinic, 43 records with monthly follow-up of MOVE! lifestyle intervention augmented by obesity pharmacotherapy were found. Nationally, more than 2 million records of prescribed obesity pharmacotherapy compared with metformin as control were identified. Records with detailed documentation of weight trends from 1 year before to 1 year after the prescription date for further analysis were selected for review.Results: The most commonly prescribed medications in the local clinic were metformin, liraglutide, and combination phentermine/topiramate. On average, weight loss of -4.0 ± 2.1 kg over the initial 6-month intervention was observed. In the national cohort, 577,491 records with an obesity or control metformin prescription and adequate weight documentation were identified. The most effective pharmacotherapy in the national cohort was phentermine/topiramate (-0.0931 ± 0.0198 kg/wk difference), followed by liraglutide, lorcaserin, and orlistat.Conclusions: Obesity pharmacotherapy is effective in achieving clinically meaningful weight loss in veterans as part of an integrated care approach. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to determine the effects of empagliflozin on glycerol-derived hepatic gluconeogenesis in adults with obesity without type 2 diabetes mellitus (T2DM) using oral carbon 13 (13 C)-labeled glycerol.Methods: A randomized, double-blind, placebo-controlled trial was performed in participants with magnetic resonance imaging assessment of body fat and measurement of glycerol-derived 13 C enrichment in plasma glucose by nuclear magnetic resonance spectroscopy following ingestion of [U-13 C3 ]glycerol. Participants were randomized to oral empagliflozin 10 mg once daily or placebo for 3 months. Glycerol-derived 13 C enrichment studies were repeated, and treatment differences in the mean percentage of 13 C glycerol enrichment in glucose were compared using mixed linear models.Results: Thirty-five participants completed the study. Empagliflozin increased glycerol-derived 13 C enrichment between baseline and follow-up by 6.5% (P = 0.005), consistent with less glycerol from visceral adipose tissue (VAT). No difference was found with placebo. Glycerol-derived 13 C enrichment was lower in participants with high VAT compared with low VAT by 12.6% (P = 0.04), but there was no heterogeneity of the treatment effect by baseline VAT. Glycerol-derived 13 C enrichment was inversely correlated with VAT but was not correlated with weight loss.Conclusions: VAT is associated with endogenous glycerol-derived hepatic gluconeogenesis, and empagliflozin reduces endogenous glycerol gluconeogenesis in adults with obesity without T2DM. These findings suggest a mechanism by which sodium-glucose cotransporter 2 inhibitors may prevent T2DM in obesity. [ABSTRACT FROM AUTHOR]

Objective: A minipig model was employed to explore the changes in endogenous leptin transport into the central nervous system and in hypothalamic sensitivity to exogenous leptin when individuals are placed on high-fat diet (HFD) compared with standard diet.Methods: Serum and cerebrospinal fluid (CSF) leptin concentrations during 10 weeks of HFD versus standard diet and exogenous leptin-induced STAT3 phosphorylation in the hypothalamus of minipigs were assessed, and the hypothalamic leptin-sensitive cells were characterized by immunofluorescence.Results: The efficiency of the passage of endogenous blood-borne leptin into the CSF (measured as the log [CSF:serum leptin ratio]) decreased over time in minipigs fed a HFD (β = -0.04 ± 0.005 per kilogram of weight gain in HFD; P < 0.0001), while it remained stable in minipigs fed a standard diet. However, the ability of peripherally administered leptin to activate its receptor in hypothalamic neurons was preserved in obese minipigs at 10 weeks of HFD.Conclusions: Together, these data are consistent with the existence of an early-onset tranport deficiency for endogenous circulating leptin into the brain in individuals developing obesity, preceding the acquisition of hypothalamic leptin resistance. Although additional studies are required to identify the underlying mechanisms, our study paves the way for the development of new preclinical pharmacological models targeting the restoration of the shuttling of peripheral leptin into the central nervous system to manage obesity. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to examine the associations of BMI and waist circumference with all-cause mortality in a general adult population from the China Health and Nutrition Survey.Methods: Based on the World Health Organization recommendations, the general adult population was divided into underweight (BMI < 18.5 kg/m2 ), normal weight (18.5 kg/m2  ≤ BMI < 23.0 kg/m2 ), overweight (23 kg/m2  ≤ BMI < 27.5 kg/m2 ), and obesity (BMI ≥ 27.5 kg/m2 ), as well as abdominal obesity (waist circumference value ≥ 90 cm for males and ≥ 80 cm for females).Results: Overweight was associated with lower all-cause mortality in the 18- to 29-year-old and 30- to 39-year-old subgroups in males (P = 0.0490 and 0.0234; hazard ratio: 0.136 and 0.462, respectively), and underweight had the opposite association in the 50- to 59-year-old and ≥ 60-year-old subgroups in males (P = 0.0074 and 0.0398, respectively) and in all subgroups in females except the 30- to 39-year-old and 50- to 59-year-old groups (P = 0.0786 and 0.0538, respectively). Abdominal obesity was associated with lower all-cause mortality in ≥ 60-year-old females (P = 0.0071).Conclusions: Overweight was associated with lower all-cause mortality in young males and middle-aged females, but underweight demonstrated the opposite association in all elderly participants. Abdominal obesity could decrease all-cause mortality in elderly females. [ABSTRACT FROM AUTHOR]

Objective: Atrial fibrillation (AF) is the most common arrhythmia and has been described as a global epidemic. Although AF is associated with both obesity and its metabolic consequences, little is known about the association between metabolically healthy obesity and AF.Methods: In a population-based study, 47,870 adults were followed for incident AF from 2006 to 2008 until 2015. Participants were classified according to BMI and metabolic status (using waist circumference, triglycerides, high-density lipoprotein cholesterol, blood pressure, and glucose) at baseline.Results: During a median follow-up of 8.1 years, 1,758 participants developed AF. Compared with metabolically healthy individuals with BMI < 25 kg/m2 , the multivariable-adjusted hazard ratios for metabolically healthy and unhealthy obesity were 1.6 (95% CI: 1.2 to 2.1) and 1.6 (95% CI: 1.3 to 1.9), respectively. AF risk increased according to the severity of obesity.Conclusions: Metabolically healthy and unhealthy obesity increased AF risk to a similar extent. Severity of obesity was positively associated with AF risk regardless of metabolic status. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to examine the association between BMI categories, stratified by metabolic health status, and the risk of kidney function decline (KFD). Methods: In this study, 42,128 adult patients with a stable BMI were classified over a 3‐year baseline window by BMI and metabolic health status (assessed by Adult Treatment Panel‐III criteria). KFD was defined as an estimated glomerular filtration rate (eGFR) decline ≥ 30%, eGFR < 15 mL/min/1.73 m2, or receipt of dialysis and/or transplant. Results: Over a median of 5.1 years (interquartile range 2.1‐8.9), 6,533 (15.5%) individuals developed KFD. Compared with the normal weight, metabolically healthy category, metabolically healthy obesity was associated with a higher risk of KFD (adjusted hazard ratio [aHR] 1.52; 95% CI: 1.22‐1.89). aHRs for KFD were 1.17 (95% CI: 0.89‐1.53), 2.21 (95% CI: 1.59‐3.08), and 2.20 (95% CI: 1.55‐3.11) for metabolically healthy obesity with BMI 30 to 34.9, BMI 35 to 39.9, and BMI ≥ 40 kg/m2. These associations were consistent among men and women, patients with eGFR ≥ or < 90 mL/min/1.73 m2, and age ≥ or < 55 years. The risk of KFD was highest among metabolically unhealthy individuals with BMI ≥ 40 (aHR 4.02; 95% CI: 3.40‐4.75 vs. metabolically healthy individuals with normal weight). Conclusions: Obesity, whether in the presence or absence of metabolic health, is a risk factor for KFD. [ABSTRACT FROM AUTHOR]

Objective: This study examined whether metabolic health status is associated with risk of cancer mortality and whether this varies by body mass index (BMI) category.Methods: A prospective study of 22,514 participants from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort was performed. Metabolically unhealthy status was defined as having three or more of the following: (1) elevated fasting glucose, (2) high triglycerides, (3) dyslipidemia, (4) hypertension, and (5) elevated waist circumference. Participants were categorized into normal weight (BMI 18.5-24.9 kg/m2 ), overweight (BMI 25.0-29.9 kg/m2 ), and obesity (BMI ≥ 30 kg/m2 ) groups. Cox proportional hazards regression was performed to estimate hazards ratios (HRs) and 95% confidence intervals (CIs) for cancer mortality during follow-up.Results: Among participants with normal weight, participants who were metabolically unhealthy had an increased risk of cancer mortality (HR: 1.65; 95% CI: 1.20-2.26) compared with metabolically healthy participants. The overall mortality risk for participants who were metabolically unhealthy and had normal weight was stronger for obesity-related cancers (HR: 2.40; 95% CI: 1.17-4.91). Compared with participants with normal weight, those who were metabolically healthy and overweight were at a reduced risk of any cancer mortality (adjusted HR: 0.79; 95% CI: 0.63-0.99).Conclusions: There was an increased risk of overall and obesity-related cancer mortality among metabolically unhealthy participants with normal weight. [ABSTRACT FROM AUTHOR]

Objective: To assess the association between midlife body mass index (BMI) and healthy aging (HA) in the French SU.VI.MAX cohort.Methods: HA was assessed in 2007 to 2009 among 2,733 individuals, aged 45 to 60 years and free of diabetes, cardiovascular disease and cancer at baseline (1994-1995). HA was defined as not developing any major chronic disease, good physical and cognitive functioning, no limitations in instrumental activities of daily living, no depressive symptoms, no health-related limitations in social life, good overall self-perceived health, and no function-limiting pain. Associations between anthropometric indicators (measured in 1995-1996) and HA were assessed using robust-error-variance Poisson regression.Results: After adjustment for potential confounders, BMI (continuous) was negatively associated with HA: relative risk (RR) = 0.97 (95% confidence interval = 0.96-0.99). Moreover, the detrimental role of obesity (RRobesity vs. normal weight  = 0.67 [0.51-0.88]) was substantially stronger than that of overweight (RRoverweight vs. normal weight  = 0.91 [0.81-1.01]). Furthermore, while metabolically healthy individuals with overweight had a similar HA probability as metabolically healthy individuals with normal weight, metabolically unhealthy overweight individuals had a substantially lowered HA probability.Conclusions: This study provides novel evidence that an elevated BMI at midlife may jeopardize the preservation of health during aging. Our results also highlight the importance of maintaining a healthy metabolic profile during midlife. [ABSTRACT FROM AUTHOR]

Objective: To investigate the association between the metabolically healthy obesity (MHO) phenotype and incident chronic kidney disease (CKD) in a Chinese population and whether systemic inflammation affects this association.Methods: A cohort study was performed with 2,491 Chinese adults. Body mass index ≥ 25.0 kg/m2 was defined as obesity. CKD was defined as estimated glomerular filtration rate < 60 mL/min per 1.73 m2 or urinary albumin-to-creatinine ratio ≥ 30 mg/g. High-sensitivity C-reactive protein (hsCRP) was used as a surrogate marker of systemic inflammation.Results: Over a median follow-up period of 3.9 years, 243 of 2,491 participants developed incident CKD (9.8%). Compared with metabolically healthy nonobesity (MHNO), MHO was associated with incident CKD (odds ratio [OR] = 1.65, 95% confidence interval [CI] 1.01-2.69), but not after adjustment for hsCRP. The MHO/hsCRP ≥ 0.20 mg/L group, but not the MHO/hsCRP < 0.20 mg/L group, had an increased OR for incident CKD (OR = 2.66, 95% CI 1.37-5.14), with the MHNO/hsCRP < 0.20 mg/L group as the reference.Conclusions: MHO was significantly associated with incident CKD, and the level of systemic inflammation partially explained this association. [ABSTRACT FROM AUTHOR]

Objective: To characterize the adoption of antiobesity pharmacotherapies, as compared with that of the newest antidiabetes pharmacotherapy, subtype 2 sodium-glucose transport protein inhibitors (SGLT2s), among prescribers in the United States.Methods: A retrospective analysis of 2012 to 2015 data extracted from the IMS Health National Prescription Audit™ and Xponent™ assessed adoption rates of antiobesity pharmacotherapies and SGLT2s.Results: The number of dispensed antidiabetes prescriptions was 15 times the number of dispensed antiobesity prescriptions. The antiobesity market share was: 74.0% phentermine, 18.6% new antiobesity pharmacotherapies. The mean increase in prescriptions/month were: 25,259 for SGLT2s, 5,154 for new antiobesity pharmacotherapies, and 2,718 for phentermine. Medical specialties prescribing the majority of the analysis medications were Family Medicine/General Practice and Internal Medicine. Endocrinology had the highest prevalence of prescribers of any subspecialty.Conclusions: The adoption rate of SGLT2s was nearly exponential, while the adoption rate of new antiobesity pharmacotherapies was linear. Considering the relative prevalence of obesity to diabetes and that obesity is a major cause of diabetes, these results are paradoxical and suggest systematic barriers against the prescribing of antiobesity pharmacotherapies. The under-prescribing of antiobesity pharmacotherapies is widely acknowledged, but this is the first prescription data of these new medications to demonstrate its extent in the United States. [ABSTRACT FROM AUTHOR]

Objective: This study examined whether the metabolically healthy obesity (MHO) phenotype was associated with an increased risk of diabetes in a large cohort of metabolically healthy individuals and whether that association differed by presence of nonalcoholic fatty liver disease (NAFLD).Methods: The cohort consisted of 74,509 Korean adults who were metabolically healthy at baseline, defined as not having any metabolic syndrome component except large waist circumference and having homeostasis model assessment of insulin resistance <2.5. NAFLD was defined as hepatic steatosis on ultrasonography in the absence of excessive alcohol use or any other identifiable cause.Results: Over 304,852.6 person-years of follow-up, 472 participants developed diabetes (incidence density, 1.5 per 1,000 person-years). The multivariable-adjusted hazard ratios (95% confidence intervals) for incident diabetes in subjects with overweight and obesity compared with subjects with normal weight were 1.29 (1.00-2.16) and 1.57 (1.14-2.16), respectively, for subjects without NAFLD and 1.90 (0.95-3.80) and 2.57 (1.32-5.02), respectively, for those with NAFLD (P for interaction =0.57).Conclusions: In this metabolically healthy population, individuals with overweight and obesity exhibited an increased incidence of diabetes, regardless of the presence of NAFLD. This finding suggests that the obese phenotype per se, independent of the presence of NAFLD, can increase the development of diabetes. [ABSTRACT FROM AUTHOR]

Objective: This narrative review examines six important non-nutritive substances in breast milk, many of which were thought to have little to no biological significance. The overall objective is to provide background on key bioactive factors in breast milk believed to have an effect on infant outcomes (growth and body composition).Methods: The evidence for the effects of the following six bioactive compounds in breast milk on infant growth outcomes are reviewed: insulin, leptin, adiponectin, ghrelin, interleukin-6, and tumor necrosis factor-α.Results: The existing literature on the effects of breast milk insulin, ghrelin, interleukin-6, and tumor necrosis factor-α and their associations with infant growth and adiposity is sparse. Of the bioactive compounds reviewed, leptin and adiponectin are the most researched. Data reveal that breast milk adiponectin has negative associations with growth in infancy.Conclusions: There is a need for innovative, well-designed studies to improve causal inference and advance our understanding in the effects of breast milk and its components on offspring growth and body composition. The recommendations provided, along with careful consideration of both known and unknown factors that affect breast milk composition, will help improve, standardize, and ultimately advance this emergent field. [ABSTRACT FROM AUTHOR]

Objective: The metabolically healthy obesity (MHO) phenotype is an important obesity subtype in which obesity is not accompanied by any metabolic comorbidity. However, the underlying molecular mechanisms remain elusive. In this study, a shotgun proteomics approach to identify circulating biomolecules and pathways associated with MHO was used.Methods: The subjects were 20 African-American women: 10 MHO cases and 10 metabolically abnormal individuals with obesity (MAO) controls. Serum proteins were detected and quantified using label-free proteomics. Differential expression of proteins between the two groups was analyzed, and the list of differentially expressed proteins was analyzed to determine enriched biological pathways.Results: Twenty proteins were differentially expressed between MHO and controls. These proteins included: hemoglobin subunits (HBA1, P = 6.00 × 10(-18) ), haptoglobin-related protein (HPR, P = 1.2 × 10(-15) ), apolipoproteins (APOB-100, P = 1.50 × 10(-40) ; APOA4, P = 1.1 × 10(-14) ), retinol-binding protein 4 (RBP4, P = 7.1 × 10(-08) ), and CRP (P = 2.0 × 10(-04) ). MHO was associated with lower levels of proinflammatory and higher levels of anti-inflammatory biomarkers when compared with MAO. Pathway analysis showed enrichment of lipids and inflammatory pathways, including LXR/RXR and FXR/RXR activation, and acute phase response signaling.Conclusions: These findings suggested that protection from dysregulated inflammatory and lipid processes were primary molecular hallmarks of MHO. The candidate biomarkers (AHSG, RBP4, and APOA4) identified in this study are potential prognostic markers for MHO. [ABSTRACT FROM AUTHOR]

Objective: Adult obesity is recognized as a chronic disease. According to principles of chronic disease management, healthcare professionals should work collaboratively with patients to determine appropriate therapeutic strategies that address overweight and obesity, specifically considering a patient's disease status in addition to their individual needs, preferences, and attitudes regarding treatment. A central role and responsibility of healthcare professionals in this process is to inform and educate patients about their treatment options. Although current recommendations for the management of adult obesity provide general guidance regarding safe and proper implementation of lifestyle, pharmacological, and surgical interventions, healthcare professionals need awareness of specific evidence-based information that supports individualized clinical application of these therapies. More specifically, healthcare professionals should be up-to-date on approaches that promote successful lifestyle management and be knowledgeable about newer weight loss pharmacotherapies, so they can offer patients with obesity a wide range of options to personalize their treatment. Accordingly, this educational activity has been developed to provide participants with the latest information on treatment recommendations and therapeutic advances in lifestyle intervention and pharmacotherapy for adult obesity management.Design and Methods: This supplement is based on the content presented at a live CME symposium held in conjunction with ObesityWeek 2014.Results: This supplement provides an expert summary of current treatment recommendations and recent advances in nonsurgical therapies for the management of adult obesity. Patient and provider perspectives on obesity management are highlighted in embedded video clips available via QR codes, and new evidence will be applied using clinically relevant case studies.Conclusions: This supplement provides a topical update of obesity management, including clinical practice examples, for healthcare professionals who treat or provide care for adults with obesity. [ABSTRACT FROM AUTHOR]

Objective The degree of subclinical coronary atherosclerosis detected by coronary multidetector computed tomography (MDCT) in four groups defined by the state of metabolic health and obesity in an asymptomatic Korean population was compared. Methods The data of 4009 asymptomatic subjects who participated in a routine health screening examination were collected. Significant coronary artery stenosis defined as >50% stenosis, plaque, and coronary artery calcium scores (CACS) were assessed by MDCT. Participants were stratified by BMI (cut-off value, 25 kg/m2) and metabolically healthy state, which was defined by Wildman criteria. Results Metabolically healthy obese (MHO) subjects had a significantly higher prevalence of significant subclinical coronary atherosclerotic burden compared with metabolically healthy nonobese (MHNO) subjects. The adjusted odds ratios of the MHO group for various coronary MDCT findings (MHNO group as the reference), such as coronary artery stenosis, any plaque, calcified plaque, mixed plaque, CACS > 0, and CACS > 100, were 1.87 (95% CI 1.15-3.03), 1.31 (1.01-1.71), 1.40 (1.05-1.86), 1.57 (1.01-2.48), 1.38 (1.04-1.82), and 1.69 (1.03-2.78), respectively. Conclusions Our data illustrate that MHO subjects have substantial subclinical coronary atherosclerotic burden. Thus, it is important to consider the metabolic health state and obesity in evaluating cardiovascular risk. [ABSTRACT FROM AUTHOR]

Objective The purpose of this study was to examine the relationship between usual sugar-sweetened beverage (SSB) consumption and prevalence of abnormal metabolic health across body mass index (BMI) categories. Methods The metabolic health of 6,842 non-diabetic adults was classified using cross-sectional data from the Framingham Heart Study Offspring (1998-2001) and Third Generation (2002-2005) cohorts. Adults were classified as normal weight, overweight or obese and, within these categories, metabolic health was defined based on five criteria-hypertension, elevated fasting glucose, elevated triglycerides, low HDL cholesterol, and insulin resistance. Individuals without metabolic abnormalities were considered metabolically healthy. Logistic regression was used to examine the associations between categories of SSB consumption and risk of metabolic health after stratification by BMI. Results Comparing the highest category of SSB consumers (median of 7 SSB per week) to the lowest category (non-consumers), odds ratios (95% confidence intervals) for metabolically abnormal phenotypes, compared to the metabolically normal, were 1.9 (1.1-3.4) among the obese, 2.0 (1.4-2.9) among the overweight, and 1.9 (1.4-2.6) among the normal weight individuals. Conclusions In this cross-sectional analysis, it is observed that, irrespective of weight status, consumers of SSB were more likely to display metabolic abnormalities compared to non-consumers in a dose-dependent manner. [ABSTRACT FROM AUTHOR]

In the nonpregnant population, there is extensive evidence of a systemic low-grade inflammatory status in relation to excess adipose tissue. Less is known about the relation during pregnancy. Objective: Our main objective was therefore to explore the effect of pregnancy on adiposity-related systemic inflammation. Design and Methods: This study is a longitudinal cohort study of 240 pregnant women of Scandinavian heritage at Oslo University hospital-Rikshospitalet, Norway from 2002 to 2005. The inflammatory markers (C-reactive protein [CRP], Interleukin-6 [IL-6], monocyte chemoattractant protein 1 [MCP-1], IL1-Ra, tumor necrosis factor receptor II, and IL-10) were measured at four timepoints during pregnancy and analyzed by enzyme immuno-assay. The women were categorized based on BMI at inclusion (BMI <25, 25-30, and >30 kg/m2). Data were analyzed by Friedman-test, Wilcoxon signed rank test, or Kruskal-Wallis test as appropriate. Results: Maternal adiposity was associated with significantly higher circulatory levels of several inflammatory markers (CRP, MCP-1, IL-6, and IL-1Ra). However, this proinflammatory upregulation was not evident toward the end of pregnancy, as levels of CRP, MCP-1, and IL-6 were not any longer significantly different between the BMI categories. Conclusions: Although normal pregnancy exhibits proinflammatory features, this does not seem to have additive or synergistic effects on the inflammation associated with adiposity. On the contrary, we found that the BMI-dependent increase in proinflammatory markers was not evident at the end of pregnancy. [ABSTRACT FROM AUTHOR]

Emerging evidence suggests that fetal environmental exposures impact on future development of obesity. The objectives of this study were to assess the relationships between (i) maternal insulin sensitivity and glucose tolerance status in pregnancy and (ii) early infant weight gain and adiposity in the first year of life. In this prospective cohort study, 301 women underwent oral glucose tolerance testing for assessment of glucose tolerance status and insulin sensitivity (ISOGTT) in pregnancy. Their infants underwent anthropometric assessment at 12 months of age, including determination of weight gain in the first year of life and sum of skinfold thickness (SFT), a measure of infant adiposity. Infant weight gain and sum of SFT at 12 months did not differ according to maternal glucose tolerance status. On univariate analyses, weight gain from 0 to 12 months and sum of SFT were negatively associated with maternal ISOGTT during pregnancy. On multiple linear regression analysis, negative independent predictors of weight gain from 0 to 12 months were maternal ISOGTT during pregnancy (t = −2.73; P = 0.007), infant female gender (t = −3.16; P = 0.002), and parental education (t = −1.98; P = 0.05), whereas white ethnicity was a positive independent predictor (t = 2.68; P = 0.008). Maternal ISOGTT (t = −2.7; P = 0.008) and parental education (t = −2.58; P = 0.01) were independent negative predictors of sum of SFT at 12 months. Independent of maternal glucose tolerance status, maternal insulin resistance during pregnancy is associated with increased infant weight gain and adiposity over the first year of life. Further longitudinal study to evaluate obesity in this group of children will increase our understanding of the contribution of the intrauterine environment to their long-term health. [ABSTRACT FROM AUTHOR]

Visceral adiposity is strongly associated with insulin resistance; however, little evidence directly demonstrates that visceral fat per se impairs insulin action. Here, we examine the effects of the surgical removal of the greater omentum and its occupying visceral fat, an omentectomy (OM), on insulin sensitivity (SI) and β-cell function in nonobese dogs. Thirteen male mongrel dogs were used in this research study; animals were randomly assigned to surgical treatment with either OM (n = 7), or sham-surgery (SHAM) (n = 6). OM failed to generate measurable changes in body weight (+2%; P = 0.1), or subcutaneous adiposity (+3%; P = 0.83) as assessed by magnetic resonance imaging (MRI). The removal of the greater omentum did not significantly reduce total visceral adipose volume (−7.3 ± 6.4%; P = 0.29); although primary analysis showed a trend for OM to increase SI when compared to sham operated animals (P = 0.078), further statistical analysis revealed that this minor reduction in visceral fat alleviated insulin resistance by augmenting SI of the periphery (+67.7 ± 35.2%; P = 0.03), as determined by the euglycemic–hyperinsulinemic clamp. Insulin secretory response during the hyperglycemic step clamp was not directly influenced by omental fat removal (presurgery 6.82 ± 1.4 vs. postsurgery: 6.7 ± 1.2 pmol/l/mg/dl, P = 0.9). These findings provide new evidence for the deleterious role of visceral fat in insulin resistance, and suggest that a greater OM procedure may effectively improve insulin sensitivity.Obesity (2009) 17 4, 674–680. doi:10.1038/oby.2008.642 [ABSTRACT FROM AUTHOR]

Obesity is associated with an increase in chronic, low-grade inflammation which has been implicated in the development of type 2 diabetes mellitus and cardiovascular disease. The purpose of this study was to determine whether obesity was associated with an elevation of whole blood lipopolysaccharide (LPS)-stimulated tumor necrosis factor-α (TNF-α) production. African-American women were recruited from a larger study and assigned to one of five groups based on BMI: normal weight (NORM; BMI 20–25, n = 7), overweight (OVER; BMI 25–30, n = 12), class 1 obese (OB1; BMI 30–35, n = 19), class 2 obese (OB2; BMI 35–40, n = 10), or class 3 obese (OB3; BMI >40, n = 17). Body composition was determined via a whole body dual-energy X-ray absorptiometry (DXA) scan. Venous blood samples were collected following an overnight fast (>8 h), and stimulated with five doses of LPS (Salmonella enteriditis): 80, 40, 20, 10, and 5 µg/ml for 24 h in a 37 °C, 5% CO2 incubator. Following stimulation, TNF-α was measured using enzyme-linked immunosorbent assay. OB3 produced 365% more TNF-α than NORM at an LPS dose of 20 µg/ml (P < 0.05). When maximal TNF-α production was assessed regardless of LPS dose, OB3 produced 230% more than NORM and OVER produced 190% more than NW (P = 0.001). Total and trunk fat mass and BMI were significantly correlated with maximal TNF-α production and LPS = 20 µg/ml. Our findings are consistent with previous reports suggesting a relationship between increased adiposity and inflammatory marker production. This is one of the first studies to focus on African-American women, who have higher rates of obesity.Obesity (2009) 17 3, 447–451. doi:10.1038/oby.2008.552 [ABSTRACT FROM AUTHOR]

The article presents a study on the relationship between metabolic syndrome and high-sensitivity C-reactive protein in Brazilian overweight and obese youth. A total of 407 students classified into two groups were evaluated. The study found that high-sensitivity C-protein is strongly related with metabolic syndrome and its components.

The article discusses a study which examines ethnic differences in obesity and physical activity among Aboriginal and non-Aboriginal Canadians. The results showed that the prevalence of obesity in children and youth was higher among Aboriginals compared to non-Aboriginals. Physical inactivity was said to be a predictor of obesity in both the Aboriginal and non-Aboriginal participants. The study also notes the need for further investigation to delineate the determinants of obesity in the said population.

The article presents research which assessed the effect of adipose tissue interleukin-18 messenger ribonucleic acid (AT IL-18 mRNA) and plasma interleukin-18 on obesity and exercise. Researchers argued that the training-induced lowering of AT IL-18 mRNA content may contribute to the beneficial effects of regular physical activity with improved insulin sensitivity.

The article discusses a study on the impact of central obesity as a prerequisite in diagnosing metabolic syndrome (MS) in Southeast Asians living in Singapore. The study compares the prevalence of MS defined according to the American Heart Association (AHA)/National Heart Lung and Blood Institute (NHLBI) and the International Diabetes Federation (IDF). About 6.7% of subjects show features of MS without central obesity. The AHA/NHLBI and IDF have different definitions of MS.