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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]

Given rapid advancements in medical science, it is often challenging for the busy clinician to remain up-to-date on the fundamental and multifaceted aspects of preventive cardiology and maintain awareness of the latest guidelines applicable to cardiovascular disease (CVD) risk factors. The "American Society for Preventive Cardiology (ASPC) Top Ten CVD Risk Factors 2021 Update" is a summary document (updated yearly) regarding CVD risk factors. This "ASPC Top Ten CVD Risk Factors 2021 Update" summary document reflects the perspective of the section authors regarding ten things to know about ten sentinel CVD risk factors. It also includes quick access to sentinel references (applicable guidelines and select reviews) for each CVD risk factor section. The ten CVD risk factors include unhealthful nutrition, physical inactivity, dyslipidemia, hyperglycemia, high blood pressure, obesity, considerations of select populations (older age, race/ethnicity, and sex differences), thrombosis/smoking, kidney dysfunction and genetics/familial hypercholesterolemia. For the individual patient, other CVD risk factors may be relevant, beyond the CVD risk factors discussed here. However, it is the intent of the "ASPC Top Ten CVD Risk Factors 2021 Update" to provide a succinct overview of things to know about ten common CVD risk factors applicable to preventive cardiology.

Obesity is a complex disease that relapses frequently and associates with multiple complications that comprise a worldwide health priority because of its rising prevalence and association with numerous complications, including metabolic disorders, mechanic pathologies, and cancer, among others. Noteworthy, excess adiposity is accompanied by chronic inflammation, oxidative stress, insulin resistance, and subsequent organ dysfunction. This dysfunctional adipose tissue is initially stored in the visceral depot, overflowing subsequently to produce lipotoxicity in ectopic depots like liver, heart, muscle, and pancreas, among others. People living with obesity need a diagnostic approach that considers an exhaustive pathophysiology and complications assessment. Thus, it is essential to warrant a holistic diagnosis and management that guarantees an adequate health status, and quality of life. The present review summarizes the different complications associated with obesity, at the same time, we aim to fostering a novel framework that enhances a patient-centered approach to obesity management in the precision medicine era. [ABSTRACT FROM AUTHOR]

Obesity and type 2 diabetes (T2DM) are major public health concerns associated with serious morbidity and increased mortality. Both obesity and T2DM are strongly associated with adiposopathy, a term that describes the pathophysiological changes of the adipose tissue. In this review, we have highlighted adipose tissue dysfunction as a major factor in the etiology of these conditions since it promotes chronic inflammation, dysregulated glucose homeostasis, and impaired adipogenesis, leading to the accumulation of ectopic fat and insulin resistance. This dysfunctional state can be effectively ameliorated by the loss of at least 15% of body weight, that is correlated with better glycemic control, decreased likelihood of cardiometabolic disease, and an improvement in overall quality of life. Weight loss can be achieved through lifestyle modifications (healthy diet, regular physical activity) and pharmacotherapy. In this review, we summarized different effective management strategies to address weight loss, such as bariatric surgery and several classes of drugs, namely metformin, GLP-1 receptor agonists, amylin analogs, and SGLT2 inhibitors. These drugs act by targeting various mechanisms involved in the pathophysiology of obesity and T2DM, and they have been shown to induce significant weight loss and improve glycemic control in obese individuals with T2DM. [ABSTRACT FROM AUTHOR]

ABSTRACT: The American Society for Preventive Cardiology (ASPC) ''Ten things to know about ten cardiovascular disease risk factors – 2022'' is a summary document regarding cardiovascular disease (CVD) risk factors. This 2022 update provides summary tables of ten things to know about 10 CVD risk factors and builds upon the foundation of prior annual versions of ''Ten things to know about ten cardiovascular disease risk factors” published since 2020. This 2022 version provides the perspective of ASPC members and includes updated sentinel references (i.e., applicable guidelines and select reviews) for each CVD risk factor section. The ten CVD risk factors include unhealthful dietary intake, physical inactivity, dyslipidemia, pre-diabetes/diabetes, high blood pressure, obesity, considerations of select populations (older age, race/ethnicity, and sex differences), thrombosis (with smoking as a potential contributor to thrombosis), kidney dysfunction and genetics/familial hypercholesterolemia. Other CVD risk factors may be relevant, beyond the CVD risk factors discussed here. However, it is the intent of the ASPC ''Ten things to know about ten cardiovascular disease risk factors – 2022” to provide a tabular overview of things to know about ten of the most common CVD risk factors applicable to preventive cardiology and provide ready access to applicable guidelines and sentinel reviews.

[Display omitted] [ABSTRACT FROM AUTHOR]

A growing amount of epidemiological data from multiple countries indicate an increased prevalence of obesity, more importantly central obesity, among hospitalized subjects with COVID-19. This suggests that obesity is a major factor contributing to adverse outcome of the disease. As it is a metabolic disorder with dysregulated immune and endocrine function, it is logical that dysfunctional metabolism contributes to the mechanisms behind obesity being a risk factor for adverse outcome in COVID-19. Emerging data suggest that in obese subjects, (a) the molecular mechanisms of viral entry and spread mediated through ACE2 receptor, a multifunctional host cell protein which links to cellular homeostasis mechanisms, are affected. This includes perturbation of the physiological renin-angiotensin system pathway causing pro-inflammatory and pro-thrombotic challenges (b) existent metabolic overload and ER stress-induced UPR pathway make obese subjects vulnerable to severe COVID-19, (c) host cell response is altered involving reprogramming of metabolism and epigenetic mechanisms involving microRNAs in line with changes in obesity, and (d) adiposopathy with altered endocrine, adipokine, and cytokine profile contributes to altered immune cell metabolism, systemic inflammation, and vascular endothelial dysfunction, exacerbating COVID-19 pathology. In this review, we have examined the available literature on the underlying mechanisms contributing to obesity being a risk for adverse outcome in COVID-19. [ABSTRACT FROM AUTHOR]

In physiological conditions, the adipose organ resides in well-defined areas, where it acts providing an energy supply and as an endocrine organ involved in the control of whole-body energy metabolism. Adipose tissue adipokines connect the body's nutritional status to the regulation of energy balance. When it surrounds organs, it provides also for mechanical protection. Adipose tissue has a complex and heterogenous cellular composition that includes adipocytes, adipose tissue-derived stromal and stem cells (ASCs) which are mesenchymal stromal cells, and endothelial and immune cells, which signal to each other and to other tissues to maintain homeostasis. In obesity and in other nutrition related diseases, as well as in age-related diseases, biological and functional changes of adipose tissue give rise to several complications. Obesity triggers alterations of ASCs, impairing adipose tissue remodeling and adipose tissue function, which induces low-grade systemic inflammation, progressive insulin resistance and other metabolic disorders. Adipose tissue grows by hyperplasia recruiting new ASCs and by hypertrophy, up to its expandability limit. To overcome this limitation and to store the excess of nutrients, adipose tissue develops ectopically, involving organs such as muscle, bone marrow and the heart. The origin of ectopic adipose organ is not clearly elucidated, and a possible explanation lies in the stimulation of the adipogenic differentiation of mesenchymal precursor cells which normally differentiate toward a lineage specific for the organ in which they reside. The chronic exposition of these newly-formed adipose depots to the pathological environment, will confer to them all the phenotypic characteristics of a dysfunctional adipose tissue, perpetuating the organ alterations. Visceral fat, but also ectopic fat, either in the liver, muscle or heart, can increase the risk of developing insulin resistance, type 2 diabetes, and cardiovascular diseases. Being able to prevent and to target dysfunctional adipose tissue will avoid the progression towards the complications of obesity and other nutrition-related diseases. The aim of this review is to summarize some of the knowledge regarding the presence of adipose tissue in particular tissues (where it is not usually present), describing the composition of its adipogenic precursors, and the interactions responsible for the development of organ pathologies. [ABSTRACT FROM AUTHOR]

Obesity and type 2 diabetes (T2DM) are major public health concerns associated with serious morbidity and increased mortality. Both obesity and T2DM are strongly associated with adiposopathy, a term that describes the pathophysiological changes of the adipose tissue. In this review, we have highlighted adipose tissue dysfunction as a major factor in the etiology of these conditions since it promotes chronic inflammation, dysregulated glucose homeostasis, and impaired adipogenesis, leading to the accumulation of ectopic fat and insulin resistance. This dysfunctional state can be effectively ameliorated by the loss of at least 15% of body weight, that is correlated with better glycemic control, decreased likelihood of cardiometabolic disease, and an improvement in overall quality of life. Weight loss can be achieved through lifestyle modifications (healthy diet, regular physical activity) and pharmacotherapy. In this review, we summarized different effective management strategies to address weight loss, such as bariatric surgery and several classes of drugs, namely metformin, GLP-1 receptor agonists, amylin analogs, and SGLT2 inhibitors. These drugs act by targeting various mechanisms involved in the pathophysiology of obesity and T2DM, and they have been shown to induce significant weight loss and improve glycemic control in obese individuals with T2DM.

Background: Whether HAIR-AN syndrome and polycystic ovarian syndrome (PCOS) are distinct entities or represent a phenotypic spectrum of the same syndrome is still unclear. HAIR-AN syndrome is characterized by high insulin resistance, obesity, and hyperinsulinemia as compared to PCOS and could represent adipose tissue dysfunction as the primary pathophysiologic trigger. This study was undertaken to study the role of adipose tissue dysfunction in HAIR-AN syndrome and PCOS using adipocytokines as surrogate markers of "adiposopathy." Materials and Methods: A cross-sectional observational study was conducted at a tertiary care hospital over a period of 1 year. Serum adiponectin, leptin, IL-6, and TNF-α levels were measured in 30 women with HAIR-AN syndrome and in 30 women with PCOS. Correlations between adipocytokines, inflammatory markers, serum testosterone, and serum insulin were determined. Data analysis was performed using the SPSS version 23.0 (IBM SPSS Statistics Inc., Chicago, IL, USA) software program. Results: Women with HAIR-AN syndrome had significantly higher hyperandrogenemia, hyperinsulinemia, and insulin resistance as compared to PCOS women. They also had high leptin levels and lower adiponectin levels (p < 0.001). However, the levels of inflammatory markers (TNF-α and IL-6) were similar in both the groups (p > 0.05). Serum adiponectin showed a negative correlation with HOMA-IR and testosterone levels, while leptin showed a positive correlation with both in HAIR-AN patients while no such correlation was found in the PCOS group. Conclusion: The significantly raised adipocytokines in HAIR-AN syndrome patients as compared to PCOS patients indicates the primary role of adipose tissue dysfunction ("adiposopathy") in the pathogenesis of HAIR-AN syndrome while only a minor role, if any, in PCOS. Both these syndromes stand as distinct entities pathogenically with an overlapping phenotype. [ABSTRACT FROM AUTHOR]

This review is devoted to the analysis of data on the effect of inhibitors of 3-hydroxy-3-methylglutaryl coenzymate-reductase on the endocrine function of adipose tissue in obesity. Violation of metabolism of adipose tissue, as well as the amount of fat, are a a key factor in the pathophysiology of obesity and the development of concomitant diseases. Statins are competitive inhibitors of 3-hydroxy-3-methylglutaryl-kofermenta reductase (HMG-COA reductase) that catalyze the initial stage of cholesterol biosynthesis in the liver. Therefore, traditionally, the liver is considered as the main target organ for statins. The results of studies of molecular mechanisms of action of statins on carbohydrate and lipid metabolism, adipokine and inflammatory balance in adipose tissue on the example of isolated adipocytes (in vivo) and in living organism (in vitro) are presented. Effect of statins on the action of insulin, as well as the possibility of developing pathological conditions associated with insulin resistance and the development of type 2 diabetes mellitus (DM 2). The proven clinical effects of cholesterol-lowering action of statins, allow new insights and to further explore their possible impact on other links in the development of obesity, and potentially to use them as therapeutic agents for pharmacological correction of obesity and the fight against cardiovascular diseases.

Given rapid advancements in medical science, it is often challenging for the busy clinician to remain up-to-date on the fundamental and multifaceted aspects of preventive cardiology and maintain awareness of the latest guidelines applicable to cardiovascular disease (CVD) risk factors. The “American Society for Preventive Cardiology (ASPC) Top Ten CVD Risk Factors 2021 Update” is a summary document (updated yearly) regarding CVD risk factors. This “ASPC Top Ten CVD Risk Factors 2021 Update” summary document reflects the perspective of the section authors regarding ten things to know about ten sentinel CVD risk factors. It also includes quick access to sentinel references (applicable guidelines and select reviews) for each CVD risk factor section. The ten CVD risk factors include unhealthful nutrition, physical inactivity, dyslipidemia, hyperglycemia, high blood pressure, obesity, considerations of select populations (older age, race/ethnicity, and sex differences), thrombosis/smoking, kidney dysfunction and genetics/familial hypercholesterolemia. For the individual patient, other CVD risk factors may be relevant, beyond the CVD risk factors discussed here. However, it is the intent of the “ASPC Top Ten CVD Risk Factors 2021 Update” to provide a succinct overview of things to know about ten common CVD risk factors applicable to preventive cardiology.

Preventive cardiology involves understanding and managing multiple cardiovascular disease (CVD) risk factors. Given the rapid advancements in medical science, it may be challenging for the busy clinician to remain up-to-date on the multifaceted and fundamental aspects of CVD prevention, and maintain awareness of the newest applicable guidelines. The “American Society for Preventive Cardiology (ASPC) Top Ten 2020” summarizes ten essential things to know about ten important CVD risk factors, listed in tabular formats. The ten CVD risk factors include unhealthful nutrition, physical inactivity, dyslipidemia, hyperglycemia, high blood pressure, obesity, considerations of select populations (older age, race/ethnicity, and gender), thrombosis/smoking, kidney dysfunction and genetics/familial hypercholesterolemia. For the individual patient, other CVD risk factors may be relevant, beyond the CVD risk factors discussed here. However, it is the intent of the “ASPC Top Ten 2020” to provide a succinct overview of things to know about ten common CVD risk factors applicable to preventive cardiology.

Metabolic syndrome (MS) is a cluster of cardiometabolic factors that are strongly associated with the risk of serious chronic diseases. The prevalence of MS continues to grow, including among children, adolescents and people of active reproductive age. For the sphere of reproductive medicine, the problem of MS is of particular importance not only because of its negative impact on fertility, the frequency of complications of pregnancy and childbirth, but also because of its transgenerative effect on the health of offspring: it is proved that each of the components of the metabolic syndrome is a powerful epigenetic factor. Recent studies have revealed many new facets of the pathogenesis of MS and expanded the range of its etiologic factors beyond the alimentary factors, which determines the possibility of finding new approaches to prevention and treatment of this pathology. The review presents: evolution of diagnostic criteria for MS and reflection of this process in epidemiology and clinical approaches to the disease; epidemiological data on the prevalence of MS in young adults. A brief overview of a large array of scientific research of the last decade on etiology and pathogenesis of MS, in particular the role of adipose tissue dysfunction of visceral, ileofemoral and ectopic depots, causes of the tendency to prevail in one or another adipose tissue depot, new obesity classification, as well as the role of perinatal and epigenetic, ecological (environmental obesogenes, artificial light contamination), composition of intestinal microbiota, state of the sympathetic nervous system, nutritional deficiencies in the development of obesity and MS is provided. The gender differences of pathogenesis and clinical features of MS, as well as the association of MS with dyshormonal and other pathologies (PCOS, hyperprolactinemia, uterine myoma, endometriosis) of female reproductive health are considered.

Abstract Background Metabolic syndrome is defined as a cluster of at least three out of five clinical risk factors: abdominal (visceral) obesity, hypertension, elevated serum triglycerides, low serum high-density lipoprotein (HDL) and insulin resistance. It is estimated to affect over 20% of the global adult population. Abdominal (visceral) obesity is thought to be the predominant risk factor for metabolic syndrome and as predictions estimate that 50% of adults will be classified as obese by 2030 it is likely that metabolic syndrome will be a significant problem for health services and a drain on health economies. Evidence shows that regular and consistent exercise reduces abdominal obesity and results in favourable changes in body composition. It has therefore been suggested that exercise is a medicine in its own right and should be prescribed as such. Purpose of this review This review provides a summary of the current evidence on the pathophysiology of dysfunctional adipose tissue (adiposopathy). It describes the relationship of adiposopathy to metabolic syndrome and how exercise may mediate these processes, and evaluates current evidence on the clinical efficacy of exercise in the management of abdominal obesity. The review also discusses the type and dose of exercise needed for optimal improvements in health status in relation to the available evidence and considers the difficulty in achieving adherence to exercise programmes. Conclusion There is moderate evidence supporting the use of programmes of exercise to reverse metabolic syndrome although at present the optimal dose and type of exercise is unknown. The main challenge for health care professionals is how to motivate individuals to participate and adherence to programmes of exercise used prophylactically and as a treatment for metabolic syndrome.

• 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]

A surge to increase the production via usage of chemicals at both industrial and agricultural arena has forced humans to be routinely and imprudently exposed to a wide variety of endocrine disrupting chemicals. The overall aim of the study was to evaluate possible relation that might exist between bisphenol-A (BPA) and the adipose tissue hormones, and further impact on adiposopathy. In the present study, the role of BPA, an "endocrine disruptor" with respect to adiposopathy was evaluated in type 2 diabetes mellitus patients. For the study, 150 healthy control subjects and 150 newly diagnosed diabetes patients were recruited. Fasting venous blood samples was analyzed for several biochemical parameters such as serum glucose, lipid profile, insulin, adiponectin, leptin, TNF-α, IL-6, IL-1, free fatty acid. Concentrations of BPA were also measured both in control and diabetic subjects. Serum BPA concentration was found to be significantly higher in diabetic subjects in comparison to the control subjects. Levels of BPA were found to be positively correlated with BMI and WC in diabetic subjects. Also, it was found to be positively correlated with leptin and negatively correlated with adiponectin in diabetic subjects. Therefore, the current study suggested more deleterious effect of BPA on diabetes and its pathophysiology. [ABSTRACT FROM AUTHOR]

Background: It is well known that there is a link between obesity and oncogenesis in many sites, including the kidney. Adiposopathy is characterized by an excessive accumulation of adipose tissue, principally visceral, which can lead to adipocyte and adipose tissue-related disorder, promoting metabolic syndrome. Visceral adipocytes secrete growth factors, proinflammatory cytokines and adipokines, regarded as mediating factors associated with the oncogenesis of obesity-related tumors. In this study, we evaluate the relationship between visceral adipose tissue (VAT) and non-clear cell renal cell carcinoma (nccRCC) in male patients. Methods: In this retrospective study, two groups were included: nccRCC group and control group. Total adipose tissue (TAT) area, VAT area and subcutaneous adipose tissue (SAT) area were measured in both groups. VAT/SAT ratio was subsequently calculated. Results: Statistically significant differences between the two groups were found in TAT area (p = 0.05), VAT area (p < 0.01) and VAT/SAT ratio (p < 0.05), while no significant difference was found in SAT area. Conclusions: This study demonstrates an increased visceral adipose tissue in male patients with nccRCC. [ABSTRACT FROM AUTHOR]

Background: 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., Methods: This joint expert review is based upon scientific evidence, clinical perspectives of the authors, and peer review by the OMA and NLA leadership., Results: 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., Conclusions: 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., (© 2024 The Author(s).)

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]

Metabolic syndrome is a group of several risk factors consist of hypertension, dyslipidemia, glucose intolerance disorder, obesity, and has a relationship with CVD pathomechanism. WHO was report in 2003 more than 300 million adult in the world suffered from obesity. The role of adipose tissue in infectious diseases and adipocyte quality changes after exposure to pathogen has not been revealed. On the other hand, the prevalence of infectious diseases in developing country is still high. Previous studies proved a relationship between infection of Toxoplasma gondii and tissue dysfunction. Profilin is a membrane component of Toxoplasma gondii that able to stimulate expression of proinflammation cytokines through TLR-11 upregulation, and predicted able to trigger the adipocyte dysfunction. The aim of this study are to knows the effect of profilin exposure in vitro on subcutaneous adipocyte to the expression of IL-6 and TNF-α. The measurement of IL-6 and TNF-a levels was done by ELISA technique. The result showed profilin exposure doses 5, 15 and 25 ng / ml increasing IL-6. Profilin exposure cause adipocyte dysfunction through the increasing proinflammatory adipocytokine levels as pathomechanism of metabolic syndrome associated with adipose tissue.

Background: Excessive accumulation of adipose tissue, mainly visceral, can determine adipocyte- and adipose tissue-related disorder. Visceral adipocytes secrete mediators associated with carcinogenesis. Several studies have shown a correlation between blood levels of these mediators and clear cell renal cell carcinoma (ccRCC). Indeed, specific biomarkers, including adipokines, have been considered as a possible link between obesity and RCC. Objective: The objective of the study is to test the hypothesis that there is an increase of visceral adipose tissue (VAT) in male patients with ccRCC. Methods: In this retrospective study, two groups were included: A group of patients with ccRCC and a control group without a history of malignancies. Total adipose tissue (TAT) area, VAT area, and subcutaneous adipose tissue (SAT) area were measured in both groups. VAT/SAT ratio was subsequently calculated. Results: Statistically significant differences between the two groups were found in VAT area (P = 0.01) and VAT/SAT ratio (P < 0.05), while no significant difference was found in TAT area and SAT area. Conclusions: This study shows an increased VAT in male patients with ccRCC. [ABSTRACT FROM AUTHOR]

The dysregulation of adipokine secretion owing to adiposopathy can contribute to the pathogenesis of obesity-related disorders. Being that exercise is an advised strategy against obesity-induced adiposopathy, we aimed to analyze the role of physical exercise as a preventive and therapeutic strategy against high-fat diet (HFD)-induced adipokine and ghrelin alterations. Rats were pair-fed the Lieber De Carli standard diet (S, 35 Kcal% fat) or HFD (71 Kcal% fat) over 17 weeks. Animals were assigned into four groups as follows: standard diet sedentary (SS), standard diet voluntary physical activity (SVPA), high-fat diet sedentary (HS), and high-fat diet voluntary physical activity (HVPA). After 9 weeks of dietary treatment, half of the SS and HS animals were submitted to an 8-week endurance training program, standard diet endurance training (SET), and high-fat-diet endurance training (HET) groups, maintaining the respective diets. Although there were no changes in body weight, HFD increased visceral adiposity, percentage of large adipocytes, hypoxia inducible factor (HIF)-1α, and leptin contents in epididymal adipose tissue (eWAT) and decreased plasma content of adiponectin (AdipQ). Both VPA and ET decreased visceral adiposity and percentage of large adipocytes in HFD-fed animals, but ET also increased the percentage of small- to medium-sized adipocytes. VPA increased plasma growth hormone secretagogue receptor (GHS-R) and decreased leptin protein in HVPA group. ET decreased plasma insulin and leptin levels and eWAT HIF-1α and leptin expression in HET group. Moreover, ET improved insulin sensitivity, plasma high molecular weight, and AdipQ and ghrelin levels and increased eWAT and GHS-R expression. Our data suggest that exercise, particularly ET, reverted adiposopathy and related endocrine alterations induced by an isocaloric HFD pair-fed diet. [ABSTRACT FROM AUTHOR]

This article is co-authored by the mother of a child with obesity and insulin resistance, who gives her perspective. It is also co-authored by the treating Obesity Medicine clinician and an investigator in obesity clinical research (both certified in Obesity Medicine), who give their perspectives. The discussion focuses upon the potential clinical use of metformin in managing young patients with obesity and insulin resistance. The article integrates what is scientifically known about the mechanisms of actions of metformin and how these mechanisms are reflected in the clinical response of young patients. [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]

Background: This Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) is intended to provide clinicians with an overview on obesity, thrombosis, venous disease, lymphatic disease, and lipedema., Methods: The scientific support for this CPS is based upon published citations, clinical perspectives of OMA authors, and peer review by the Obesity Medicine Association leadership., Results: Topics in this CPS include obesity, thrombosis, venous disease, lymphatic disease, and lipedema. Obesity increases the risk of thrombosis and cardiovascular disease via fat mass and adiposopathic mechanisms. Treatment of thrombosis or thrombotic risk includes healthful nutrition, physical activity, and the requisite knowledge of how body weight affects anti-thrombotic medications. In addition to obesity-related thrombotic considerations of acute coronary syndrome and ischemic non-hemorrhagic stroke, this Clinical Practice Statement briefly reviews the diagnosis and management of clinically relevant presentations of deep vein thromboses, pulmonary embolism, chronic venous stasis, varicose veins, superficial thrombophlebitis, lipodermatosclerosis, corona phlebectatica, chronic thromboembolic pulmonary hypertension, iliofemoral venous obstruction, pelvic venous disorder, post-thrombotic syndrome, as well as lymphedema and lipedema - which should be included in the differential diagnosis of other edematous or enlargement disorders of the lower extremities., Conclusions: This Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) on obesity, thrombosis, and venous/lymphatic disease is one of a series of OMA CPSs designed to assist clinicians in the care of patients with the disease of obesity., (© 2023 The Authors.)

Background: This Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) provides an overview of the mechanisms and treatment of obesity and hypertension., Methods: The scientific support for this CPS is based upon published citations, clinical perspectives of OMA authors, and peer review by the Obesity Medicine Association leadership., Results: Mechanisms contributing to obesity-related hypertension include unhealthful nutrition, physical inactivity, insulin resistance, increased sympathetic nervous system activity, renal dysfunction, vascular dysfunction, heart dysfunction, increased pancreatic insulin secretion, sleep apnea, and psychosocial stress. Adiposopathic factors that may contribute to hypertension include increased release of free fatty acids, increased leptin, decreased adiponectin, increased renin-angiotensin-aldosterone system activation, increased 11 beta-hydroxysteroid dehydrogenase type 1, reduced nitric oxide activity, and increased inflammation., Conclusions: Increase in body fat is the most common cause of hypertension. Among patients with obesity and hypertension, weight reduction via healthful nutrition, physical activity, behavior modification, bariatric surgery, and anti-obesity medications mostly decrease blood pressure, with the greatest degree of weight reduction generally correlated with the greatest degree of blood pressure reduction., (© 2023 The Authors.)