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Background/Purpose: Metabolic syndrome (MetS) is a chronic pro-inflammatory and pro-thrombotic state associated with increased atherosclerosis, cardiovascular events and type 2 diabetes. It is diagnosed in the presence of at least 3 of 5 metabolic risk factors (obesity, hypertension, hypertriglyceridemia, low high-density lipoproteins (HDL) and insulin resistance [1]). The pathophysiology of MetS remains incompletely understood, but may share mechanisms with inflammatory states such as SLE. Visceral adiposity is known as a source of pro-inflammatory cytokines by adipocytes, the so-called adipokines. The contribution of glucocorticoids to the development of MetS in SLE is not clear, even though their use is associated with cardiovascular comorbidities [2]. We aim to characterize the prevalence and associations of MetS, including serum levels of adipokines, in a multi-ethnic cohort of patients with SLE. Method(s): Using a standardised protocol, baseline demographics, per visit disease activity (SLEDAI2K) and treatment data, and annual recording of organ damage accrual (SLICC damage index (SDI)) were prospectively captured on SLE patients from a single tertiary centre. The presence of MetS,defined using the updated joint consensus criteria [1], was assessed retrospectively at the last recorded visit. Serum levels of adipokines (resistin, lipocalin-2, TNF, MCP-1) and insulin were measured by Quantibody. Result(s): 116 patients (median (IQR) age at enrolment 39.5 (31.4-51.1) years, median disease duration 6.1 (1.4-12) years) were followed for a median of 6.7 (4.1-8.1) years. 80% of patients were exposed to glucocorticoids (median time-adjusted mean dose 3.7 (0.5-7.0) mg/day and 50% accrued organ damage during follow-up. The prevalence of MetS in this cohort was 29%. The prevalence of the components of MetS included: hypertension (59%), low-HDL (51%), hypertriglyceridemia (32%), obesity (16%) and hyperglycaemia (22%). In univariable analysis, MetS was associated with base

Breast cancer is the most common tumor in women worldwide, and an increasing public health concern. Knowledge of both protective and negative risk factors is essential for a better understanding of this heterogenous disease. We undertook a review of the recent literature and evaluated the relationship between obesity mediators and breast cancer development depending on menopausal status. Excess weight is now pandemic and has replaced tobacco as the main lifestyle-related risk factor for premature death. Although the prevalence of obesity/overweight has increased globally over the last 50 years, the potential harm attributable to excess fat has generally been underestimated. The relationship between overweight/obesity, breast cancer and overall risk appears to be highly dependent on menopausal status. Thus, obesity increases the risk of breast cancer in postmenopausal women but, conversely, it appears to be protective in premenopausal women. We evaluate the role of different clinical factors potentially involved in this seemingly contradictory relationship, including estrogen, mammogram density, adipokines, insulin-signaling pathway activation, and inflammatory status. A key focus of this review is to better understand the impact of body mass index and menopausal status on these clinical factors and, hence, provide some clarity into the inter-relationships involved in this controversial issue

Background/Purpose: Metabolic syndrome (MetS) is a chronic pro-inflammatory and pro-thrombotic state associated with increased atherosclerosis, cardiovascular events and type 2 diabetes. It is diagnosed in the presence of at least 3 of 5 metabolic risk factors (obesity, hypertension, hypertriglyceridemia, low high-density lipoproteins (HDL) and insulin resistance [1]). The pathophysiology of MetS remains incompletely understood, but may share mechanisms with inflammatory states such as SLE. Visceral adiposity is known as a source of pro-inflammatory cytokines by adipocytes, the so-called adipokines. The contribution of glucocorticoids to the development of MetS in SLE is not clear, even though their use is associated with cardiovascular comorbidities [2]. We aim to characterize the prevalence and associations of MetS, including serum levels of adipokines, in a multi-ethnic cohort of patients with SLE. Method(s): Using a standardised protocol, baseline demographics, per visit disease activity (SLEDAI2K) and treatment data, and annual recording of organ damage accrual (SLICC damage index (SDI)) were prospectively captured on SLE patients from a single tertiary centre. The presence of MetS,defined using the updated joint consensus criteria [1], was assessed retrospectively at the last recorded visit. Serum levels of adipokines (resistin, lipocalin-2, TNF, MCP-1) and insulin were measured by Quantibody. Result(s): 116 patients (median (IQR) age at enrolment 39.5 (31.4-51.1) years, median disease duration 6.1 (1.4-12) years) were followed for a median of 6.7 (4.1-8.1) years. 80% of patients were exposed to glucocorticoids (median time-adjusted mean dose 3.7 (0.5-7.0) mg/day and 50% accrued organ damage during follow-up. The prevalence of MetS in this cohort was 29%. The prevalence of the components of MetS included: hypertension (59%), low-HDL (51%), hypertriglyceridemia (32%), obesity (16%) and hyperglycaemia (22%). In univariable analysis, MetS was associated with base

Aging and overweight increase the risk of developing type 2 diabetes mellitus. In this cross‐sectional study, we aimed to investigate the potential mediating role of T‐EMRA cells and inflammatory markers in the development of a decreased insulin sensitivity. A total of 134 healthy older volunteers were recruited (age 59.2 (SD 5.6) years). T cell subpopulations were analyzed by flow cytometry. Furthermore, body composition, HOMA‐IR, plasma tryptophan (Trp) metabolites, as well as cytokines and adipokines were determined. Using subgroup and covariance analyses, the influence of BMI on the parameters was evaluated. Moreover, correlation, multiple regression, and mediation analyses were performed. In the subgroup of participants with obesity, an increased proportion of CD8+EMRA cells and elevated concentrations of plasma kynurenine (KYN) were found compared to the lower‐weight subgroups. Linear regression analysis revealed that an elevated HOMA‐IR could be predicted by a higher proportion of CD8+EMRA cells and KYN levels. A mediation analysis showed a robust indirect effect of the Waist‐to‐hip ratio on HOMA‐IR mediated by CD8+EMRA cells. Thus, the deleterious effects of abdominal obesity on glucose metabolism might be mediated by CD8+EMRA cells in the elderly. Longitudinal studies should validate this assumption and analyze the suitability of CD8+EMRA cells as early predictors of incipient prediabetes. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.

Breast cancer is the most common tumor in women worldwide, and an increasing public health concern. Knowledge of both protective and negative risk factors is essential for a better understanding of this heterogenous disease. We undertook a review of the recent literature and evaluated the relationship between obesity mediators and breast cancer development depending on menopausal status. Excess weight is now pandemic and has replaced tobacco as the main lifestyle-related risk factor for premature death. Although the prevalence of obesity/overweight has increased globally over the last 50 years, the potential harm attributable to excess fat has generally been underestimated. The relationship between overweight/obesity, breast cancer and overall risk appears to be highly dependent on menopausal status. Thus, obesity increases the risk of breast cancer in postmenopausal women but, conversely, it appears to be protective in premenopausal women. We evaluate the role of different clinical factors potentially involved in this seemingly contradictory relationship, including estrogen, mammogram density, adipokines, insulin-signaling pathway activation, and inflammatory status. A key focus of this review is to better understand the impact of body mass index and menopausal status on these clinical factors and, hence, provide some clarity into the inter-relationships involved in this controversial issue.

Nutrient sensing plays important roles in promoting satiety and maintaining good homeostatic control. Taste receptors (TAS) are located through the gastrointestinal tract, and recent studies have shown they have a relationship with metabolic disorders. The aim of this study was to analyze the jejunal expression of TAS1R2, TAS1R3, TAS2R14 and TAS2R38 in women with morbid obesity, first classified according to metabolic syndrome presence (MetS; n = 24) or absence (non-MetS; n = 45) and then classified according to hepatic histology as normal liver (n = 28) or nonalcoholic fatty liver disease (n = 41). Regarding MetS, we found decreased expression of TAS2R14 in MetS patients. However, when we subclassified patients according to liver histology, we did not find differences between groups. We found negative correlations between glucose levels, triglycerides and MetS with TAS1R3 expression. Moreover, TAS2R14 jejunal expression correlated negatively with the presence of MetS and ghrelin levels and positively with the jejunal Toll-like receptor (TLR)4, peroxisome proliferator-activated receptor (PPAR)-gamma, and interleukin (IL)-10 levels. Furthermore, TAS2R38 expression correlated negatively with TLR9 jejunal expression and IL-6 levels and positively with TLR4 levels. Our findings suggest that metabolic dysfunctions such as MetS trigger downregulation of the intestinal TASs. Therefore, taste receptors modulation could be a possible therapeutic target for metabolic disorders.

Objective — to assess the vaspin and TNF-α levels in patients with type 2 diabetes mellitus (DM-2), depending on the parameters of carbohydrate metabolism.Materials and methods. Examinations involved 31 patients with DM-2, the mean age 54.8 years, who were treated at the Endocrinology Department of the Municipal non-profit enterprise of the Kharkiv Regional Council «Regional Clinical Hospital». The control group consisted of 20 healthy volunteers. All patients received antihyperglycemic agent of sulfonylurea and/or biguanides types. The body mass index (BMI) was determined by the formula: BMI = weight (kg)/height (m). The fasting glucose, glycated haemoglobin was determined and the insulin resistance index HOMA-IR was calculated. The adipokines levels, vaspin and TNF-α, and level of immunoreactive insulin were evaluated in serum. statistical processing was performed using the Statistica Basic Academic 13 for Windows En package.Results and discussion. The average DM-2 duration of the investigated patients was 9.02 [3—13] years. All parameters of carbohydrate metabolism had significant deviations (FGL 8.18 [6.4—9.7]) mmol/l, HbA1c 7.23 % [6.5—7.89]) compared with the control group.The adipocytokines’ levels were significantly higher in patients with DM-2 (vaspin 3.47 pg/ml, TNF-α 6.87 pg/ml) compared with the control group. The correlation has been established between carbohydrate metabolism and the studied parameters. Vaspin and FGL (r = 0.62; p < 0.01), HOMA-IR (r = 0.45; p < 0.05), IRI (r = 0.6; p < 0.01) and HbA1c (r = 0.56; p < 0.01). The level of TNF-α had the following correlations with FPG (r = 0.35; p < 0.03), HOMA-IR (r = 0.51; p < 0.05), IRI (r = 0.52; p < 0.01), HbA1c (r = 0.32; p = 0.04).Conclusions. On the basis of the obtained results, it can be assumed that vaspin and TNF-α have a significant relationship with the parameters of carbohydrate metabolism, and at least can be biomarkers of carbohydrate metabolism disorders taking into, Цель работы — оценить уровень васпина и TNF-α у пациентов с сахарным диабетом 2 типа (СД-2) в зависимости от показателей углеводного обмена.Материалы и методы. Обследован 31 пациент среднего возраста 54,8 года, находившийся на лечении в эндо­кри­нологическом отделении Коммунального некоммерческого предприятия Харьковского областного совета «Областная клиническая больница», с диагнозом СД-2. Контрольную группу составили 20 практически здоровых добровольцев. Все пациенты получали сахароснижающие препараты класса сульфонилмочевины и/или бигуа­ниды. Индекс массы тела (ИМТ) определялся по формуле: ИМТ = вес (кг) / рост (м2). Определяли глюкозу натощак (ГНТ), гликозилированный гемоглобин (HbA1c), рассчитывался показатель инсулинорезистентности HOMA-IR. Адипокины — васпин, TNF-α и уровень иммунореактивного инсулина (ИРИ) определялись в сыворотке крови. Статистическая обработка проводилась с помощью пакета Statistica Basic Academic 13 for Windows En.Результаты и обсуждение. У обследованных пациентов средняя длительность заболевания СД-2 составила 9,02 [3—13] года. По всем параметрам углеводного обмена были выявлены статистически значимые отклонения (ГНТ 8,18 [6,4—9,7] ммоль/л, HbA1c 7,23 % [6,5—7,89]) по сравнению с контрольной группой.Уровень изучаемых адипоцитокинов был статистически значимо повышен у пациентов с СД-2 (васпин — 3,47 пг/мл, TNF-α — 6,87 пг/мл) по сравнению с группой контроля.Отмечены тесные корреляционные связи между показателями углеводного обмена и изучаемыми показателями. А именно васпина и ГНТ (r = 0,62; p < 0,01), HOMA-IR (r = 0,45; p < 0,05), ИРИ (r = 0,6; p < 0,01) и HbA1c (r = 0,56; p < 0,01). Уровень TNF-α имел следующие корреляции с ГНТ (r = 0,35; p < 0,03), HOMA-IR (r = 0,51; p > 0,05), ИРИ (r = 0,52; p < 0,01), HbA1c (r = 0,32; p = 0,04).Выводы. На основании полученных результатов можно предположить, что васпин и TNF-α имеют значимую взаимосвязь с параметрами углеводного обмена и, по крайней мере, могут быть биомаркерами на, Мета роботи — оцінити рівень васпіну та TNF-α у пацієнтів з цукровим діабетом 2 типу (ЦД-2) залежно від показників вуглеводного обміну.Матеріали та методи. Обстежено 31 пацієнта середнього віку 54,8 року, що перебував на лікуванні в ендокринологічному відділенні Комунального некомерційного підприємства Харківської обласної ради «Обласна клінічна лікарня», з діагнозом ЦД-2. Контрольну групу склали 20 практично здорових волонтерів. Індекс маси тіла (ІМТ) визначали за формулою: ІМТ = вага (кг)/зріст (м2). Пацієнти отримували цукрознижувальні препарати класу сульфонілсечовини або/та бігуаніди. Оцінювалась глюкоза натщесерце (ГНТ), імунореактивний інсулін (ІРІ), глікозильований гемоглобін (HbA1c), розраховувався показник інсулінорезистентності HOMA-IR. Адипоцитокін — васпін, TNF-α та рівень інсуліну визначались у сироватці крові. Статистична обробка проводилась за допомогою пакета Statistica Basic Academic 13 for Windows En.Результати та обговорення. В обстежених пацієнтів середня тривалість захворюваності на ЦД 2 типу складала (9,02 [3—13]) року. Визначено статистично значущі відхилення вуглеводного обміну (ГНТ 8,18 [6,4—9,7] ммоль/л, HbA1c 7,23 % [6,5—7,89]). Рівень досліджуваних адипоцитокінів був статистично значуще підвищеним у пацієнтів з ЦД 2 типу (васпін — 3,47 пг/мл; TNF-α — 6,87 пг/мл) порівняно з групою контролю.Відзначено тісні кореляційні зв’язки між параметрами вуглеводного обміну та досліджуваними показниками. А саме васпіну з ГНТ (r = 0,62; p < 0,01), HOMA-IR (r = 0,45; p < 0,05), ІРІ (r = 0,6; p < 0,01) та HbA1c (r = 0,56; p < 0,01). Рівень TNF-α мав наступні кореляції з ГНТ (r = 0,35; p < 0,03), HOMA-IR (r = 0,51; p < 0,05) ІРІ (r = 0,52; p < 0,01), HbA1c (r = 0,32; p = 0,04).Висновки. На основі отриманих результатів можливо припустити, що васпін та TNF-α мають взаємозв’язок з параметрами вуглеводного обміну та, принаймні, можуть бути біомаркерами порушення вуглеводного обміну, зважаючи на отримані кореляції.

Objective: To examine the role of high-molecular-weight (HMW) adiponectin and its relationship to sympathetic activity in women with polycystic ovary syndrome (PCOS). Design(s): Cross sectional study using biobanked samples. Setting(s): Not applicable. Patient(s): Premenopausal women with PCOS (n = 46, Rotterdam diagnostic criteria) and without PCOS (n = 22). Intervention(s): None. Main Outcome Measure(s): High-molecular-weight adiponectin levels with secondary outcomes of sympathetic activity and leptin levels. Result(s): The high-molecular-weight adiponectin level was lower in women with PCOS (median 2.2 [interquartile range (IQR)2.3] mug/mL) than in controls (median 3 [IQR2.5] mug/mL) (age and BMI adjusted), and it correlated inversely with the values measured for homeostatic model of assessment of insulin resistance (HOMA-IR), fasting insulin, triglycerides, and free androgen index and positively with sex hormone-binding globulin (SHBG) and high-density lipoprotein cholesterol in all participants and in the PCOS group. In the PCOS group, sympathetic activity (burst frequency) was statistically significantly higher than in controls (median 26 [IQR11] vs. median 22 [IQR14], respectively) and correlated inversely with HMW adiponectin (r = -0.230). The leptin levels were similar between the women with PCOS and controls and did not statistically significantly correlate with HMW adiponectin or sympathetic activity. On multiple regression analysis, burst frequency and SHBG explained 40% of the HMW adiponectin variability (B = -0.7; 95% CI -1.2 to -0.2; and B = 0.01; 95% CI 0.004-0.01) in PCOS. Conclusion(s): Alongside insulin resistance, increased sympathetic activity is associated with and may modulate HMW adiponectin levels in women with PCOS.Copyright © 2017 American Society for Reproductive Medicine

Objective: To examine the role of high-molecular-weight (HMW) adiponectin and its relationship to sympathetic activity in women with polycystic ovary syndrome (PCOS). Design(s): Cross sectional study using biobanked samples. Setting(s): Not applicable. Patient(s): Premenopausal women with PCOS (n = 46, Rotterdam diagnostic criteria) and without PCOS (n = 22). Intervention(s): None. Main Outcome Measure(s): High-molecular-weight adiponectin levels with secondary outcomes of sympathetic activity and leptin levels. Result(s): The high-molecular-weight adiponectin level was lower in women with PCOS (median 2.2 [interquartile range (IQR)2.3] mug/mL) than in controls (median 3 [IQR2.5] mug/mL) (age and BMI adjusted), and it correlated inversely with the values measured for homeostatic model of assessment of insulin resistance (HOMA-IR), fasting insulin, triglycerides, and free androgen index and positively with sex hormone-binding globulin (SHBG) and high-density lipoprotein cholesterol in all participants and in the PCOS group. In the PCOS group, sympathetic activity (burst frequency) was statistically significantly higher than in controls (median 26 [IQR11] vs. median 22 [IQR14], respectively) and correlated inversely with HMW adiponectin (r = -0.230). The leptin levels were similar between the women with PCOS and controls and did not statistically significantly correlate with HMW adiponectin or sympathetic activity. On multiple regression analysis, burst frequency and SHBG explained 40% of the HMW adiponectin variability (B = -0.7; 95% CI -1.2 to -0.2; and B = 0.01; 95% CI 0.004-0.01) in PCOS. Conclusion(s): Alongside insulin resistance, increased sympathetic activity is associated with and may modulate HMW adiponectin levels in women with PCOS.Copyright © 2017 American Society for Reproductive Medicine

Accumulating evidence revealed that adipose tissues secrete pro-inflammatory and anti-inflammatory humoral factors, called as adipocytokines. Most of the arteries are surrounded by perivascular adipose tissue (PVAT), which influences adjacent artery by secreting adipocytokines. PVATs are supposed to be athero-protective under healthy conditions, whereas PVATs are athero-promoting in obesity. Recent clinical studies suggested that coronary atherosclerosis is associated with increased volume of epicardial adipose tissue (EAT), PVAT of coronary artery. It was suggested that enhanced inflammation in EAT is also associated with vasospastic angina. In this review article, we will summarize recent findings about potential roles of EAT in the pathogenesis of coronary atherosclerosis.

Traditionally, it is believed that white adipose tissues serve as energy storage, heat insulation, and mechanical cushion, whereas non-shivering thermogenesis occurs in brown adipose tissue. Recent evidence revealed that adipose tissue secretes many types of cytokines, called as adipocytokines, which modulate glucose metabolism, lipid profile, appetite, fibrinolysis, blood pressure, and inflammation. Most of the arteries are surrounded by perivascular adipose tissue (PVAT). PVAT has been thought to be simply a structurally supportive tissue for vasculature. However, recent studies showed that PVAT influences vasodilation and vasocontraction, suggesting that PVAT regulates vascular tone and diameter. Adipocytokines secreted from PVAT appear to have direct access to the adjacent arterial wall by diffusion or via vasa vasorum. In fact, PVAT around atherosclerotic lesions and mechanically-injured arteries displayed inflammatory cytokine profiles, suggesting that PVAT functions to promote vascular lesion formation. Many clinical studies revealed that increased accumulation of epicardial adipose tissue (EAT), which surrounds coronary arteries, is associated with coronary artery disease. In this review article, we will summarize recent findings about potential roles of PVAT in the pathogenesis of atherosclerosis, particularly focusing on a series of basic and clinical studies from our laboratory.

Background: Polycystic ovary syndrome (PCOS) is associated with features linked to metabolic syndrome including visceral obesity, dyslipidemia and impaired glucose homeostasis. Recent studies suggest that these metabolic effects are linked to a low-grade chronic inflammation with the triad of hyperinsulinemia, hyperandrogenism, and low-grade inflammation acting together in a vicious cycle. Adipose tissue produces immunomodulatory adipocytokines which contribute to regulation of insulin sensitivity, reproduction and cardiovascular function. Limited evidence is available on the role of adipocytokines in PCOS. Aim(s): This study investigated the relationships between PCOS status, adipocytokines and aetiological features of PCOS. Method(s): In an observational study of community recruited PCOS and controls, we measured serum HMW-adiponectin, omentin, resistin, interleukin-6 (IL-6), asymmetric dimethylarginine (ADMA), plasminogen activator inhibotir-1(PAI-1), high sensitivity CRP (hs-CRP), androgens, SHBG, fasting glucose and insulin levels. Result(s): Forty-nine women with PCOS (age 29.8 +/- 5.9 years, BMI: 29.0 +/- 5.4 kg/m2) and 25 healthy controls (age 37.6 +/- 7.8 years, BMI: 28.9 +/- 4.0 kg/m2) were recruited. Homeostatic model assessment for insulin resistance (HOMA-IR) (P = 0.006), free androgen index (FAI) (P = 0.01) and Ferriman-Galway score (P < 0.001) were higher in PCOS. For adipocytokines, women with PCOS had lower omentin [median (IQR): 68.76(67.17) vs 112.45(67.42)] (P = 0.01) and higher hs-CRP [median (IQR): 2.15 (3.4) vs 1.00 (2.1)] (P = 0.03) after adjustment for age and BMI. On assessment of non-obese and obese subgroups, HMWadiponectin and omentin were lower in obese women with PCOS compared to obese controls (P = 0.022 and P = 0.034 respectively) and nonobese PCOS (P = 0.028 and P = 0.016 respectively). Among women with PCOS, HMW-adiponectin was negatively correlated with HOMA-IR and FAI, however only the correlation between HMW-adiponectin and FAI

A number of approaches have been utilized in the prevention, management, and treatment of obesity, including, surgery, medication, diet, exercise, and overall lifestyle changes. Despite these interventions, the prevalence of obesity and the various disorders related to it is growing. In obesity, there is a constant state of chronic low-grade inflammation which is characterized by activation and infiltration of pro-inflammatory immune cells and a dysregulated production of high levels of pro-inflammatory cytokines. This pro-inflammatory milieu contributes to insulin resistance, type-2 diabetes, cardiovascular disease, and other related co-morbidities. The roles of the innate (macrophages, neutrophils, eosinophils, mast cells, NK cells, MAIT cells) and the adaptive (CD4 T cells, CD8 T cells, regulatory T cells, and B cells) immune responses and the roles of adipokines and cytokines in adipose tissue inflammation and obesity are discussed. An understanding of the crosstalk between the immune system and adipocytes may shed light in better treatment modalities for obesity and obesity-related diseases. Copyright © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Background: Polycystic ovary syndrome (PCOS) is associated with features linked to metabolic syndrome including visceral obesity, dyslipidemia and impaired glucose homeostasis. Recent studies suggest that these metabolic effects are linked to a low-grade chronic inflammation with the triad of hyperinsulinemia, hyperandrogenism, and low-grade inflammation acting together in a vicious cycle. Adipose tissue produces immunomodulatory adipocytokines which contribute to regulation of insulin sensitivity, reproduction and cardiovascular function. Limited evidence is available on the role of adipocytokines in PCOS. Aim(s): This study investigated the relationships between PCOS status, adipocytokines and aetiological features of PCOS. Method(s): In an observational study of community recruited PCOS and controls, we measured serum HMW-adiponectin, omentin, resistin, interleukin-6 (IL-6), asymmetric dimethylarginine (ADMA), plasminogen activator inhibotir-1(PAI-1), high sensitivity CRP (hs-CRP), androgens, SHBG, fasting glucose and insulin levels. Result(s): Forty-nine women with PCOS (age 29.8 +/- 5.9 years, BMI: 29.0 +/- 5.4 kg/m2) and 25 healthy controls (age 37.6 +/- 7.8 years, BMI: 28.9 +/- 4.0 kg/m2) were recruited. Homeostatic model assessment for insulin resistance (HOMA-IR) (P = 0.006), free androgen index (FAI) (P = 0.01) and Ferriman-Galway score (P < 0.001) were higher in PCOS. For adipocytokines, women with PCOS had lower omentin [median (IQR): 68.76(67.17) vs 112.45(67.42)] (P = 0.01) and higher hs-CRP [median (IQR): 2.15 (3.4) vs 1.00 (2.1)] (P = 0.03) after adjustment for age and BMI. On assessment of non-obese and obese subgroups, HMWadiponectin and omentin were lower in obese women with PCOS compared to obese controls (P = 0.022 and P = 0.034 respectively) and nonobese PCOS (P = 0.028 and P = 0.016 respectively). Among women with PCOS, HMW-adiponectin was negatively correlated with HOMA-IR and FAI, however only the correlation between HMW-adiponectin and FAI

Background: Patients with diabetes have increased risk of developing microvascular complications. Adipocytokines have been variously associated with these complications in observational clinical studies. However, there are no comprehensive data examining the associations between adipocytokines concentrations and the presence of these complications. Method(s): We performed a systematic review of cross-sectional studies comparing circulating adipocytokines in patients with type 2 diabetes (T2D) who were affected by at least one microvascular complication, with T2D patients without these complications. Relevant studies were retrieved from MEDLINE, EMBASE, Scopus and Cochrane databases. Study quality was evaluated using a modified Newcastle-Ottawa Quality Assessment Scale. Meta-analysis was performed using an inverse-variance model. Standardised mean differences (SMD) and 95% confidence intervals (CI) were calculated for leptin and adiponectin. Heterogeneity was determined by Q and I2 statistics, from which fixed or random effects models were applied. Result(s): 554 abstracts were identified; 28 studies satisfied our inclusion/ exclusion criteria. Study quality ranged from 4-10 (out of 11). Higher leptin levels were associated with the presence of microalbuminuria (SMD = 0.41; 95%CI = 0.14, 0.67; n = 901; p = 0.0003) and macroalbuminuria (SMD = 0.68; 95%CI = 0.30, 1.06; n = 406; p = 0.0004). Similarly, higher leptin levels were associated with the presence of neuropathy (SMD = 0.26; 95%CI = 0.07, 0.44; n = 609; p = 0.008). Higher adiponectin levels were associated with the presence of microalbuminuria (SMD = 0.55; 95%CI = 0.29, 0.81, n = 274; p < 0.001) and macroalbuminuria (SMD = 1.37; 95%CI = 0.78, 1.97, n = 246; p < 0.00001). In addition, higher adiponectin levels were associated with neuropathy (SMD = 0.25; 95%CI = 0.14, 0.36; n = 1516; p < 0.00001) and retinopathy (SMD = 0.38; 95%CI = 0.25, 0.51; n = 1306; p < 0.00001). Discussion(s): This systematic review and met

Background: Patients with diabetes have increased risk of developing microvascular complications. Adipocytokines have been variously associated with these complications in observational clinical studies. However, there are no comprehensive data examining the associations between adipocytokines concentrations and the presence of these complications. Method(s): We performed a systematic review of cross-sectional studies comparing circulating adipocytokines in patients with type 2 diabetes (T2D) who were affected by at least one microvascular complication, with T2D patients without these complications. Relevant studies were retrieved from MEDLINE, EMBASE, Scopus and Cochrane databases. Study quality was evaluated using a modified Newcastle-Ottawa Quality Assessment Scale. Meta-analysis was performed using an inverse-variance model. Standardised mean differences (SMD) and 95% confidence intervals (CI) were calculated for leptin and adiponectin. Heterogeneity was determined by Q and I2 statistics, from which fixed or random effects models were applied. Result(s): 554 abstracts were identified; 28 studies satisfied our inclusion/ exclusion criteria. Study quality ranged from 4-10 (out of 11). Higher leptin levels were associated with the presence of microalbuminuria (SMD = 0.41; 95%CI = 0.14, 0.67; n = 901; p = 0.0003) and macroalbuminuria (SMD = 0.68; 95%CI = 0.30, 1.06; n = 406; p = 0.0004). Similarly, higher leptin levels were associated with the presence of neuropathy (SMD = 0.26; 95%CI = 0.07, 0.44; n = 609; p = 0.008). Higher adiponectin levels were associated with the presence of microalbuminuria (SMD = 0.55; 95%CI = 0.29, 0.81, n = 274; p < 0.001) and macroalbuminuria (SMD = 1.37; 95%CI = 0.78, 1.97, n = 246; p < 0.00001). In addition, higher adiponectin levels were associated with neuropathy (SMD = 0.25; 95%CI = 0.14, 0.36; n = 1516; p < 0.00001) and retinopathy (SMD = 0.38; 95%CI = 0.25, 0.51; n = 1306; p < 0.00001). Discussion(s): This systematic review and met

Adipose tissue is an active organ playing a role not only in metabolism but also in immune and inflammatory processes, releasing several pro-inflammatory mediators. This can explain the possible association between obesity and rheumatoid arthritis (RA) and its role in the progression of the disease. Adipose and synovial tissues share common histological features of local inflammation in terms of activation of target tissues infiltrating cells (i.e. myeloid cells). Among the so-called adipocytokines, PEDF and Chemerin orchestrate the cellular cross-talk between adipose and myeloid cells, being possible biomarkers to monitor the effect of weight loss or the decrease of adipose tissue in patients with RA. Moreover, dietary intervention has been demonstrated to reduce Chemerin as well as IL-6 and MCP-1 expression. Finally, epigenetic regulators such as micro-RNAs (i.e. miR-155) are key regulators of myeloid cells activation in RA and obesity as well as in adipocytes. In this review, we will summarize the biological link between obesity/overweight state and RA focusing on pathophysiological mechanisms, consequences and management considerations.

Vitamin D deficiency and dysfunctional adipose tissue are involved in the development of cardiometabolic disturbances (eg, hypertension, insulin resistance, type 2 diabetes mellitus, obesity, and dyslipidemia). We evaluated the relation between vitamin D and adipocytokines derived from adipose tissue. We studied 50 obese individuals who were classified into different subgroups according to medians of observed anthropometric parameters (body mass index, body fat percentage, waist circumference, and trunk fat mass). There was a negative correlation between vitamin D level and leptin and resistin (r = -.61, P LT .01), while a positive association with adiponectin concentrations was found (r = .7, P LT .001). Trend estimation showed that increase in vitamin D level is accompanied by intensive increase in adiponectin concentrations (growth coefficient: 12.13). In conclusion, a positive trend was established between vitamin D and the protective adipocytokine adiponectin. The clinical relevance of this relationship needs to be investigated in larger studies.

Vitamin D deficiency and dysfunctional adipose tissue are involved in the development of cardiometabolic disturbances (eg, hypertension, insulin resistance, type 2 diabetes mellitus, obesity, and dyslipidemia). We evaluated the relation between vitamin D and adipocytokines derived from adipose tissue. We studied 50 obese individuals who were classified into different subgroups according to medians of observed anthropometric parameters (body mass index, body fat percentage, waist circumference, and trunk fat mass). There was a negative correlation between vitamin D level and leptin and resistin (r = -.61, P LT .01), while a positive association with adiponectin concentrations was found (r = .7, P LT .001). Trend estimation showed that increase in vitamin D level is accompanied by intensive increase in adiponectin concentrations (growth coefficient: 12.13). In conclusion, a positive trend was established between vitamin D and the protective adipocytokine adiponectin. The clinical relevance of this relationship needs to be investigated in larger studies.

Background: Adipocytokines are associated with energy homeostasis and mediate various immune responses and inflammatory processes. Vaspin is a novel adipocytokine that is thought to exhibit anti-inflammatory effects. Aim: We aimed to evaluate serum vaspin levels in inflammatory bowel disease (IBD) and determine its possible associations with the course and to clarify its intestinal localization. Methods: Serum samples were obtained from patients with Crohn's disease (CD; n = 30) and ulcerative colitis (UC; n = 33) and from healthy volunteers (controls; n = 26). Enzyme-linked immunosorbent assays were performed for all patients. Vaspin immunohistochemical staining was performed for intestines affected with IBD. Results: Serum vaspin concentrations were significantly higher in patients with UC than in patients with CD and controls (422.9 ± 361.9 vs. 163.4 ± 116.2 vs. 147.5 ± 89.4 pg/mL, respectively; P < 0.01). There was no difference in the serum vaspin concentrations between the patients with CD and controls. There was also no difference in the serum vaspin concentrations between the patients with active IBD and those with inactive IBD. However, the serum vaspin concentrations of most patients with UC increased after remission induction. Vaspin was expressed in the adipocytes of the mesenteric adipose tissues but not in the epithelial or inflammatory cells of large intestines of the patients with IBD. Conclusions: Serum vaspin concentrations are elevated in patients with UC and increase further after remission induction, suggesting that vaspin may aid the auxiliary diagnosis of UC and may be useful for assessing disease activity in patients., Digestive Diseases and Sciences, 59(2), pp.315-321; 2014

Chronic low-grade inflammation has been implicated in the processes leading to the development of type 2 diabetes (T2D) and its progression. Non-Hispanic Blacks bear a disproportionate burden of T2D and are highly susceptible to inflammation. This cross-sectional study assessed and compared the serum levels of established adipocytokines; interleukin-6 (IL-6), C-reactive protein (CRP), leptin, and novel adipocytokines; chemerin and omentin in Haitian and African Americans with and without T2D. The relationships of these adipocytokines with metabolic syndrome (MetS), anthropometric and HOMA2 measures by ethnicity and diabetes status were also assessed. Serum levels of IL-6, CRP, leptin, chemerin and omentin were determined by the ELISA method. HOMA2 measures were calculated for insulin sensitivity (HOMA2-IS) and insulin resistance (HOMA2-IR). Analyses of available data for 230 Haitian Americans and 241 African Americans (240 with and 231 without T2D) for the first study showed that Haitian Americans with and without MetS had lower levels of IL-6 and CRP compared to African Americans with and without MetS (P Ethnic-specific diabetes intervention and treatment programs must be designed to target Haitian Americans and African Americans as separate unique groups, in order to reduce the burden of T2D among the non-Hispanic Black community. Further research is needed to gain better understanding of the role of inflammation and T2D in this population.

Leptin is a cytokine produced by adipocytes, and plays a key role in the regulation of energy balance. In the present study, we measured plasma leptin concentrations of 166 normal and obese dogs visiting veterinary practices, and clarified the influence of age, gender and breed on plasma leptin levels in dogs. Leptin levels were higher in the dogs with higher body condition scores. There was no noticeable influence of age, gender and breed, but those in optimal puppies and obese Miniature Dachshund tended to be lower than those in corresponding groups. We conclude that plasma leptin is a reliable marker of adiposity in dogs regardless of age, gender and breed variations, and thereby useful as a blood biochemistry test for health examinations and treatment of obesity.

Leptin is a cytokine produced by adipocytes, and plays a key role in the regulation of energy balance. In the present study, we measured plasma leptin concentrations of 166 normal and obese dogs visiting veterinary practices, and clarified the influence of age, gender and breed on plasma leptin levels in dogs. Leptin levels were higher in the dogs with higher body condition scores. There was no noticeable influence of age, gender and breed, but those in optimal puppies and obese Miniature Dachshund tended to be lower than those in corresponding groups. We conclude that plasma leptin is a reliable marker of adiposity in dogs regardless of age, gender and breed variations, and thereby useful as a blood biochemistry test for health examinations and treatment of obesity.

Face à l'étendue épidémique, dans le monde industrialisé, du diabète, de l'obésité, du syndrome métabolique et des complications cardiovasculaires qui leurs sont associées, les connaissances acquises dans le domaine de l'athérosclérose se développent elles aussi à très grande allure. Aucune facette de cette problématique n'est négligée, qu'il s'agisse du dépistage des patients à risque, de la caractérisation des lésions ou du développement des armes thérapeutiques. L'hypercholestérolémie familiale représente un modèle judicieux de risque cardiovasculaire élevé, ce qui offre l'opportunité d'étudier les causes et les effets du développement précoce de l'athérosclérose. Dans le cadre du présent projet de recherche, une attention a été portée à l'adiponectine. L'adiponectine est une adipocytokine sécrétée exclusivement par le tissu adipeux dont les propriétés cardioprotectrices sont de plus en plus pertinentes. L'élément principal que révèle cette étude est la nature de la relation entre les bas taux plasmatiques d'adiponectine et la survie sans aucun événement coronarien dans une population de sujets hypercholestérolémiques familiaux. Ce qui suggère que l'adiponectine pourrait être un excellent marqueur du développement de l'athérosclérose et une potentielle cible thérapeutique chez les patients à risque.

Ayonrinde, O. T., Adams, L. A., Mori, T. A., Beilin, L. J., de Klerk, N., Pennell, C. E., . . . Olynyk, J. K. (2018). Sex differences between parental pregnancy characteristics and nonalcoholic fatty liver disease in adolescents. Hepatology, 67(1), 108-122. Available here