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This joint expert review by the Obesity Medicine Association (OMA) and National Lipid Association (NLA) provides clinicians an overview of the pathophysiologic and clinical considerations regarding obesity, dyslipidemia, and cardiovascular disease (CVD) risk. This joint expert review is based upon scientific evidence, clinical perspectives of the authors, and peer review by the OMA and NLA leadership. Among individuals with obesity, adipose tissue may store over 50% of the total body free cholesterol. Triglycerides may represent up to 99% of lipid species in adipose tissue. The potential for adipose tissue expansion accounts for the greatest weight variance among most individuals, with percent body fat ranging from less than 5% to over 60%. While population studies suggest a modest increase in blood low-density lipoprotein cholesterol (LDL-C) levels with excess adiposity, the adiposopathic dyslipidemia pattern most often described with an increase in adiposity includes elevated triglycerides, reduced high-density lipoprotein cholesterol (HDL-C), increased non-HDL-C, elevated apolipoprotein B, increased LDL particle concentration, and increased small, dense LDL particles. Obesity increases CVD risk, at least partially due to promotion of an adiposopathic, atherogenic lipid profile. Obesity also worsens other cardiometabolic risk factors. Among patients with obesity, interventions that reduce body weight and improve CVD outcomes are generally associated with improved lipid levels. Given the modest improvement in blood LDL-C with weight reduction in patients with overweight or obesity, early interventions to treat both excess adiposity and elevated atherogenic cholesterol (LDL-C and/or non-HDL-C) levels represent priorities in reducing the risk of CVD. [Display omitted] [ABSTRACT FROM AUTHOR]

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• Obesity could induce alterations in adipose tissue microenvironment. • Several immune cells present functional alteration under obese status. • Vascular structure and function impaired in obese individuals. • Adiposopathy promote cardiovascular risk factors which in turn directly and indirectly promotes cardiovascular disease. • Physical activity restores the size of adipocytes and helps in re-browning of white adipose tissue. Positive calorie balance disrupts the function of visceral adipose tissue, including the cardiac adipose tissue and the perivascular adipose tissue. The inflammatory and hormonal factors, which are released from adipose tissue, play a central role in inter-organ cross talk, affecting the development of obesity. Excess fat in visceral adipocytes impairs endocrine as well as immune response, leading to multiple aberrant status and posing serious risks to the future health of humans. As confirmed in previous studies, up-regulated pro-inflammatory and down-regulated anti-inflammatory cytokines disturb the communication among muscle, liver, and vasculature. In other words, adiposopathy promote cardio-metabolic risk factors, such as atherosclerosis, hypertension, insulin resistance, dyslipidemia, and pro-thrombotic state, which in turn directly and indirectly promote cardio-metabolic disorder diseases. Increasing evidence from human and animal studies has shown that physical activity restores the size of adipocytes and helps in re-browning of white adipose tissue (WAT). This review summarizes the current evidence on the roles of adiposopathy on cardio-metabolic disorder diseases and the importance of physical activity in restoring the function of adipocytes. [ABSTRACT FROM AUTHOR]

Abstract Obesity-related disease complications reduce life quality and expectancy and increase health-care costs. Some studies have suggested that obesity not always entails metabolic abnormalities and increased risk of cardiometabolic complications. Because of the lack of universally accepted criteria to identify metabolically healthy obesity (MHO), its prevalence varies widely among studies. Moreover, the prognostic value of MHO is hotly debated, mainly because it likely shifts gradually towards metabolically unhealthy obesity (MUO). In this review, we outline the differential factors contributing to the metabolic heterogeneity of obesity by discussing the behavioral, genetic, phenotypical, and biological aspects associated with each of the two metabolic phenotypes (MHO and MUO) of obesity and their clinical implications. Particular emphasis will be laid on the role of adipose tissue biology and function, including genetic determinants of body fat distribution, depot-specific fat metabolism, adipose tissue plasticity and, particularly, adipogenesis. Finally, the emerging role of gut microbiota in obesity and adipose tissue dysfunction as well as the search for novel biomarkers for the obesity-related metabolic traits and associated diseases will be briefly presented. A better understanding of the main determinants of a healthy metabolic status in obesity would allow promotion of this favorable condition by targeting the relevant pathways. Highlights • Obesity not always entails metabolic abnormalities. • Metabolically healthy obese have less risk for cardiovascular disease. • Metabolically healthy obesity may be a "honeymoon phase" of obesity. • Both genetic and lifestyle factors contribute to metabolic heterogeneity in obesity. • Adiposopathy may explain metabolic heterogeneity of obese individuals. [ABSTRACT FROM AUTHOR]

Obesity has become an unprecedented epidemic worldwide owing to a prolonged imbalance between energy intake and expenditure. Available therapies primarily suppress energy intake but often fail to produce sustained fat loss, necessitating a more efficacious strategy to combat obesity. In this study, a polyherbal formulation, Divya-WeightGo (DWG) has been investigated for its anti-obesity activity using in-vitro and in-vivo assays. Ultra-high performance liquid chromatography (UHPLC) analysis revealed the presence of phytocompounds including gallic acid, methyl gallate, corilagin, ellagic acid, pentagalloyl glucose, withaferin A and hydroxycitric acid, proven to aid in weight loss. The exposure of 3T3-L1 cells to DWG at cytosafe concentrations inhibited lipid and triglyceride accumulation and downregulated the expression of several adipogenic and lipogenic markers like PPARy, C/EBPα, C/EBPβ, SREBP-1c, FASN and DGAT1. DWG reduced LPS-induced pro-inflammatory cytokine release and NF-κB activity in THP-1 cells. The in-vivo anti-obesity activity of DWG, both alone and in combination with moderate aerobic exercise, was assessed in a high fat diet-induced obese mouse model. DWG mitigated the obesity associated increased body weight gain, feed efficiency ratio, glucose intolerance, diminished insulin sensitivity, dyslipidemia, altered liver function profile, lipid accumulation and adiposopathy in obese mice, alone as well as in combination intervention, with better efficacy in the combination approach. Thus, the findings of this study suggest that DWG could be a promising therapeutic avenue to treat obesity through attenuation of lipid and fat accumulation in liver and adipose tissues and could be utilized as an adjunct with lifestyle interventions to combat obesity and associated complications. [Display omitted] • Divya-WeightGo (DWG) contains phytoconstituents with potential anti-obesity activity. • DWG reduces lipid accumulation, expression of obesogenic genes and inflammation. • DWG along with exercise decreases body weight related parameters in mice fed a high fat diet. • DWG markedly enhances the glucose excursion and insulin sensitivity. • DWG modulates the lipid accumulation, liver function profile and adiposopathy. [ABSTRACT FROM AUTHOR]

Bariatric procedures generally improve dyslipidemia, sometimes substantially so. Bariatric procedures also improve other major cardiovascular risk factors. This 2-part Scientific Statement examines the lipid effects of bariatric procedures and reflects contributions from authors representing the American Society for Metabolic and Bariatric Surgery (ASMBS), the National Lipid Association (NLA), and the Obesity Medicine Association (OMA). Part 1 was published in the Journal of Clinical Lipidology, and reviewed the impact of bariatric procedures upon adipose tissue endocrine and immune factors, adipose tissue lipid metabolism, as well as the lipid effects of bariatric procedures relative to bile acids and intestinal microbiota. This Part 2 reviews: (1) the importance of nutrients (fats, carbohydrates, and proteins) and their absorption on lipid levels; (2) the effects of bariatric procedures on gut hormones and lipid levels; (3) the effects of bariatric procedures on nonlipid cardiovascular disease (CVD) risk factors; (4) the effects of bariatric procedures on lipid levels; (5) effects of bariatric procedures on CVD; and finally, (6) the potential lipid effects of vitamin, mineral, and trace element deficiencies, that may occur after bariatric procedures. [ABSTRACT FROM AUTHOR]

Bariatric procedures often improve lipid levels in patients with obesity. This 2 part scientific statement examines the potential lipid benefits of bariatric procedures and represents the contributions from authors representing the National Lipid Association, American Society for Metabolic and Bariatric Surgery, and the Obesity Medicine Association. The foundation for this scientific statement was based on published data through June 2015. Part 1 of this 2 part scientific statement provides an overview of: (1) adipose tissue, cholesterol metabolism, and lipids; (2) bariatric procedures, cholesterol metabolism, and lipids; (3) endocrine factors relevant to lipid influx, synthesis, metabolism, and efflux; (4) immune factors relevant to lipid influx, synthesis, metabolism, and efflux; (5) bariatric procedures, bile acid metabolism, and lipids; and (6) bariatric procedures, intestinal microbiota, and lipids, with specific emphasis on how the alterations in the microbiome by bariatric procedures influence obesity, bile acids, and inflammation, which in turn, may all affect lipid levels. Included in part 2 of this comprehensive scientific statement will be a review of (1) the importance of nutrients (fats, carbohydrates, and proteins) and their absorption on lipid levels; (2) the effects of bariatric procedures on gut hormones and lipid levels; (3) the effects of bariatric procedures on nonlipid cardiovascular disease (CVD) risk factors; (4) the effects of bariatric procedures on lipid levels; (5) effects of bariatric procedures on CVD; and finally, (6) the potential lipid effects of vitamin, mineral, and trace element deficiencies that may occur after bariatric procedures. This document represents the full report of part 1. [ABSTRACT FROM AUTHOR]

Bariatric procedures often improve lipid levels in patients with obesity. This 2-part scientific statement examines the potential lipid benefits of bariatric procedures and represents contributions from authors representing the National Lipid Association, American Society for Metabolic and Bariatric Surgery, and the Obesity Medicine Association. The foundation for this scientific statement was based on data published through June 2015. Part 1 of this 2-part scientific statement provides an overview of: (1) adipose tissue, cholesterol metabolism, and lipids; (2) bariatric procedures, cholesterol metabolism, and lipids; (3) endocrine factors relevant to lipid influx, synthesis, metabolism, and efflux; (4) immune factors relevant to lipid influx, synthesis, metabolism, and efflux; (5) bariatric procedures, bile acid metabolism, and lipids; and (6) bariatric procedures, intestinal microbiota, and lipids, with specific emphasis on how the alterations in the microbiome by bariatric procedures influence obesity, bile acids, and inflammation, which in turn, may all affect lipid levels. Included in part 2 of this comprehensive scientific statement will be a review of: (1) the importance of nutrients (fats, carbohydrates, and proteins) and their absorption on lipid levels; (2) the effects of bariatric procedures on gut hormones and lipid levels; (3) the effects of bariatric procedures on nonlipid cardiovascular disease risk factors; (4) the effects of bariatric procedures on lipid levels; (5) effects of bariatric procedures on cardiovascular disease; and finally (6) the potential lipid effects of vitamin, mineral, and trace element deficiencies that may occur after bariatric procedures. This document represents the executive summary of part 1. [ABSTRACT FROM AUTHOR]

Abstract: Our topic is the evaluation and treatment of obesity in the practice of medicine. I am joined by Dr. Harold Bays who has carried out many studies of dietary and medical interventions in patients with obesity. I am also honored to have Dr. George Bray who is known for his many years of research into causes of obesity and its therapy. Our goal is bring this clinical and research experience to bear on the office practice of medicine. [Copyright &y& Elsevier]

Abstract: Adipose tissue can be considered as a huge gland producing paracrine and endocrine hormones, the adipo(cyto)kines. There is growing evidence that these adipo(cyto)kines may link obesity to cardiovascular diseases. The excessive adipocyte hypertrophy in obesity induces hypoxia in adipose tissue. This leads to adiposopathy, the process that converts “healthy” adipose tissue to “sick” adipose tissue. This is accompanied by a change in profile of adipo(cyto)kines released, with less production of the “healthy” adipo(cyto)kines such as adiponectin and omentin and more release of the “unhealthy” adipo(cyto)kines, ultimately leading to the development of cardiovascular diseases. The present review provides a concise and general overview of the actual concepts of the role of adipo(cyto)kines in endothelial dysfunction, hypertension, atherosclerosis and heart diseases. The knowledge of these concepts may lead to new tools to improve health in the next generations. [Copyright &y& Elsevier]

Objectives: The aim of this study was to determine the utility of waist/height ratio (WHtR) in the specification of cardiometabolic risk in children already stratified by body mass index (BMI). Background: Reflective of its association with cardiometabolic risk, BMI is a commonly used indirect indicator of adiposity in children. The WHtR, a marker of central adiposity, has been advocated as a possibly superior indicator of cardiometabolic risk. Methods: Cross-sectional analysis of 5 National Health and Nutrition Examination Surveys from 1999 to 2008 (ages 5 to 18 years of age). The BMI percentile categories (normal, overweight, and obese) were further stratified on the basis of WHtR (<0.5, 0.5 to <0.6, ≥0.6). Outcome measures were lipid and glycemic profiles, C-reactive protein, liver transaminases, prevalence of hypertension, and metabolic syndrome. Results: Data were available for 14,493 subjects. Overweight and obese subjects with a WHtR <0.5 had a cardiometabolic risk approaching that of subjects with a normal BMI percentile category. Increasing WHtR was significantly associated with increased cardiometabolic risk in overweight and obese subjects, with the greatest associations observed in the obese population. Of obese subjects with WHtR ≥0.6, 26% had elevated non–high-density lipoprotein levels, 18% had elevated C-reactive protein levels, 69% had an elevated homeostatic model assessment–insulin resistance, and 32% had metabolic syndrome. Conclusions: The WHtR further specifies cardiometabolic risk within classifications stratification on the basis of BMI percentile. A significant proportion of obese children with increased WHtRs have abnormal cardiometabolic risk factor levels. The WHtR should be included in the routine screening and assessment of overweight and obese children, and those with an elevated WHtR should undergo a further cardiometabolic risk assessment. [Copyright &y& Elsevier]

Abstract: The term “fat” may refer to lipids as well as the cells and tissue that store lipid (ie, adipocytes and adipose tissue). “Lipid” is derived from “lipos,” which refers to animal fat or vegetable oil. Adiposity refers to body fat and is derived from “adipo,” referring to fat. Adipocytes and adipose tissue store the greatest amount of body lipids, including triglycerides and free cholesterol. Adipocytes and adipose tissue are active from an endocrine and immune standpoint. Adipocyte hypertrophy and excessive adipose tissue accumulation can promote pathogenic adipocyte and adipose tissue effects (adiposopathy), resulting in abnormal levels of circulating lipids, with dyslipidemia being a major atherosclerotic coronary heart disease risk factor. It is therefore incumbent upon lipidologists to be among the most knowledgeable in the understanding of the relationship between excessive body fat and dyslipidemia. On September 16, 2012, the National Lipid Association held a Consensus Conference with the goal of better defining the effect of adiposity on lipoproteins, how the pathos of excessive body fat (adiposopathy) contributes to dyslipidemia, and how therapies such as appropriate nutrition, increased physical activity, weight-management drugs, and bariatric surgery might be expected to impact dyslipidemia. It is hoped that the information derived from these proceedings will promote a greater appreciation among clinicians of the impact of excess adiposity and its treatment on dyslipidemia and prompt more research on the effects of interventions for improving dyslipidemia and reducing cardiovascular disease risk in overweight and obese patients. [Copyright &y& Elsevier]

Being overweight or obese is a worldwide epidemic. Adiposity can cause fat mass–related cardiovascular disease (CVD). Adiposity may also cause adipocyte and adipose tissue anatomic and functional abnormalities, termed adiposopathy (adipose-opathy) or “sick fat,” that result in endocrine and immune derangements. Adiposopathy may directly contribute to CVD through pericardiac and perivascular effects on the myocardium and blood vessels. Adiposopathy may also indirectly contribute to CVD through promoting or worsening major CVD risk factors such as type 2 diabetes mellitus, high blood pressure, and dyslipidemia. Despite CVD being the most common cause of mortality among overweight individuals, the pathophysiologic relationship between adiposity and CVD is often thought mysterious, as evidenced by “obesity paradoxes.” Underlying this uncertainty are suggestions that excessive body fat does not always increase the risk of CVD and, in some cases, may actually decrease such risks. These paradoxical findings are made less paradoxical when the pathogenic potential of excessive body fat is assessed based on adipose tissue dysfunction rather than simply on increased fat mass alone. This introductory review 1) provides a brief historical perspective of the pathogenic potential of adipose tissue; 2) describes the relationships between adipose tissue (histology, embryology, and adipogenesis) and cardiovascular medicine; 3) outlines the anatomic, functional, endocrine, and immune manifestations of adiposopathy; and 4) describes the importance of cross talk and/or interactions of adipose tissue with other body tissues. Finally, this review describes how “sick fat” helps account for various clinical obesity/cardiovascular paradoxes, supporting adiposopathy as a cardiovascular disease. [ABSTRACT FROM AUTHOR]