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The optimal exercise type of adipokines in children and adolescents was improved by network meta-analysis, and personalized and accurate evidence-based exercise prescription suggestions were proposed accordingly.

Oral cancer is the sixth most commonly diagnosed cancer worldwide, with one-fourth of the cases reported in India. The interlink between immunity, inflammation, and cancer has gained a spotlight in recent years. Adipokine, an inflammatory cytokine, has been studied in Oral cancer. This scoping review aims to summarize various adipokines studied in oral squamous cell carcinoma patients and their role in pathogenesis.

Obesity and type 2 diabetes mellitus (T2DM) are intricately linked metabolic disorders with global health implications. The crosstalk between adipose and skeletal muscle tissues, primarily mediated through secreted signaling molecules like adipokines and myokines which plays a pivotal role in the development and progression of these diseases. Adipokines such as leptin, adiponectin, resistin, and visfatin influence systemic insulin sensitivity and inflammatory responses. Concurrently, myokines like irisin, interleukin-6 (IL-6), and myostatin regulate muscle metabolism, glucose homeostasis, and adipose tissue function. This manuscript explores the complex interplay between adipokines and myokines in obesity-induced insulin resistance and the pathogenesis of T2DM. Understanding this inter-organ communication network reveals novel therapeutic targets and strategies for the integrated management of obesity and T2DM. 

This article is from Diabetes & Metabolism Journal , volume 36 . Abstract The incidence of obesity has increased dramatically during recent decades. Obesity increases the risk for metabolic and cardiovascular diseases and may therefore contribute to premature death. With increasing fat mass, secretion of adipose tissue derived bioactive molecules (adipokines) changes towards a pro-inflammatory, diabetogenic and atherogenic pattern. Adipokines are involved in the regulation of appetite and satiety, energy expenditure, activity, endothelial function, hemostasis, blood pressure, insulin sensitivity, energy metabolism in insulin sensitive tissues, adipogenesis, fat distribution and insulin secretion in pancreatic β-cells. Therefore, adipokines are clinically relevant as biomarkers for fat distribution, adipose tissue function, liver fat content, insulin sensitivity, chronic inflammation and have the potential for future pharmacological treatment strategies for obesity and its related diseases. This review focuses on the clinical relevance of selected adipokines as markers or predictors of obesity related diseases and as potential therapeutic tools or targets in metabolic and cardiovascular diseases.

This article is from Nutrition & Metabolism , volume 9 . Abstract Background: The soluble cell adhesion molecules and adipokines are elevated in patients with obesity, hypertension, type 2 diabetes mellitus, breast cancer and atherosclerosis. Objective: To investigate the relationship between anthropometric profile, dietary intake, lipid profile and fasting glycemia with serum levels of adipokines (adiponectin and PAI-1) and adhesion molecules (ICAM-1 and VCAM-1) in women without breast cancer undergoing routine mammographic screening. Design: Transversal study. Subjects: One hundred and forty-five women over 40-years old participated in this study. Results: In 39.3% of cases the BMI was above 30 kg/m2; 46.9% had hypertension, 14.5% had type 2 Diabetes Mellitus, 31.7% had dyslipidemia and 88.3% presented a waist-to-hip ratio ≥ 0.8. A linear correlation was found between serum levels of PAI-1 and triglycerides, between serum levels of PAI-1 and WHR and between serum levels of VCAM-1 and BMI. Conclusion: We found a high prevalence of obesity and metabolic syndrome. PAI-1 and VCAM-1 levels were correlated with clinical indicators of obesity and overweight.

This article is from BMC Infectious Diseases , volume 14 . Abstract Background: Lipodystrophies are characterized by adipose tissue redistribution, insulin resistance (IR) and metabolic complications. Adipokines and hormones related to body composition may play an important role linking these alterations. Our aim was to evaluate adipocyte-derived hormones (adiponectin, leptin, resistin, TNF-α, PAI-1) and ghrelin plasma levels and their relationship with IR in HIV-infected patients according to the presence of lipodystrophy and fat redistribution. Methods: Anthropometric and metabolic parameters, HOMA-IR, body composition by DXA and CT, and adipokines were evaluated in 217 HIV-infected patients on cART and 74 controls. Fat mass ratio defined lipodystrophy (L-FMR) was defined as the ratio of the percentage of the trunk fat mass to the percentage of the lower limb fat mass by DXA. Patient’s fat redistribution was classified into 4 different groups according the presence or absence of either clinical lipoatrophy or abdominal prominence: no lipodystrophy, isolated central fat accumulation (ICFA), isolated lipoatrophy and mixed forms (MXF). The associations between adipokines levels and anthropometric, metabolic and body composition were estimated by Spearman correlation. Results: Leptin levels were lower in patients with FMR-L and isolated lipoatrophy, and higher in those with ICFA and MXF. Positive correlations were found between leptin and body fat (total, trunk, leg, arm fat evaluated by DXA, and total, visceral (VAT), subcutaneous adipose tissue (SAT), and VAT/SAT ratio evaluated by CT) regardless of FMR-L, and with HOMA-IR only in patients with FMR-L. Adiponectin correlated negatively with VAT, and its mean levels were lower in patients with ICFA and higher in those with no lipodystrophy. Resistin was not correlated with adipose tissue but positively correlated with HOMA-IR in FMR-L patients. PAI-1 levels were higher in MXF-patients and their levels were positively correlated with VAT in those with FMR-L. Ghrelin was higher in HIV-infected patients than controls despite BMI-matching. Conclusion: The overall body fat reduction in HIV lipoatrophy was associated with low leptin plasma levels, and visceral fat accumulation was mainly associated with decreased plasma levels of adiponectin.

This article is from Journal of the International Society of Sports Nutrition , volume 11 . Abstract Background: The present study investigated the effects of a multi-ingredient dietary supplement (MIDS) containing caffeine, conjugated linoleic acid (CLA), green tea, and branched-chain amino acids (BCAA) taken for 8 weeks on body composition, blood lipid profile, glucose, insulin, adiponectin, leptin, and high-sensitivity C-reactive protein (hs-CRP) in overweight and obese men and women. Methods: Twenty-two participants completed the study (PL, n = 11; 7 women, 4 men; age, 34 ± 3.5 years; height, 169.2 ± 3.3 cm; body mass, 96.9 ± 6.8 kg; BMI, 34.1 ± 1.8 kg/m2; MIDS, n = 11; 9 women, 2 men; age, 36 ± 3.4 years; height, 173.2 ± 2.9 cm; body mass, 91.9 ± 5.6 kg; BMI, 30.0 ± 1.5 kg/m2). Participants were randomly assigned and stratified by body fat percentage to two groups: 1) a soybean oil placebo (PL) or 2) MIDS. Each group consumed two pills with breakfast and two pills with lunch. Body composition and android fat, waist and hip circumferences, blood pressure and heart rate were measured at baseline and after 8 weeks of supplementation. Results: There were no significant changes for any of the variables of body composition. Feelings of hunger were significantly higher in MIDS versus PL with no changes observed in satiety or desire to eat. Heart rate and blood pressure were unaltered in MIDS after 8 weeks of supplementation. Furthermore, lipid profile, food intake, mood state variables, fasting blood glucose, and endocrine markers did not significantly change regardless of group. Conclusion: MIDS intake does not appear to alter body composition or markers of cardiovascular health versus PL. Moreover, MIDS may actually increase feelings of hunger versus PL.

This article is from BMC Nephrology , volume 15 . Abstract Background: Dietary sodium restriction is a key management strategy in chronic kidney disease (CKD). Recent evidence has demonstrated short-term reduction in blood pressure (BP) and proteinuria with sodium restriction, however the effect on other cardiovascular-related risk factors requires investigation in CKD. Methods: The LowSALT CKD study involved 20 hypertensive Stage III-IV CKD patients counselled by a dietitian to consume a low-sodium diet (

This article is from Cardiovascular Diabetology , volume 13 . Abstract Background: Cardiovascular diseases (CVD) are a leading cause of death worldwide including the Middle East. This is caused in part by the dysregulation of adipose tissue leading to increased production of pro-inflammatory adipokines and reduction in cardio-protective adipokines such as adiponectin. Ethnicity has been recognized as a major factor in the association between CVD risk factors and the different circulating adipokines. In this study, for the first time, the relationship between traditional cardiovascular risk factors, Metabolic Syndrome (MetS) and circulating level of adipokines in Arab ethnicity was investigated. Methods: We conducted a population-based cross-sectional survey on 379 adult Arab participants living in Kuwait. Traditional cardiovascular risk factors such as blood pressure (BP), low density lipoprotein (LDL) and triglyceride (TG) were measured. Plasma levels of circulating Leptin, Plasminogen Activator Inhibitor (PAI-1) visfatin, adiponectin, resistin and adipsin were assessed using the multiplexing immunobead-based assay. Results: Circulating levels of High sensitivity C-Reactive Protein (hsCRP), Leptin, PAI-1 and adiponectin were significantly higher in Arab women than men (p < 0.0001). In multi-variate analysis, the homeostasis model assessment-insulin resistance (HOMA-IR) and body mass index (BMI) showed strong association with most of the biomarkers (p < 0.05). HsCRP showed significant association with all risk factors (p < 0.05). Leptin, PAI-1 and adipsin showed significant positive correlation with BMI, unlike adiponectin which showed inverse correlation (p < 0.05). Subjects in the highest tertile of leptin, PAI-1 and hsCRP had higher odds of having Metabolic Syndrome (MetS) (odd ratio [OR] = 3.02, 95% confidence interval [CI] = 1.47 – 6.19) and (OR = 2.52, 95% CI = 1.45 – 4.35), (OR = 4.26, 95% CI = 2.39 – 7.59) respectively. On the other hand subjects with highest tertile of adiponectin had lower odds of having MetS (OR = 0.22, 95% CI = 0.12 – 0.40). Leptin, PAI-1 and hsCRP showed significant positive association with increased MetS components (P-trend

There is extensive evidence supporting the relationship between sex-hormones in immune and inflammatory processes, the accumulation and distribution of adipose tissue, and energy homeostasis. Oestrogens favour visceral lipolysis and subcutaneous adipogenesis, driving the accumulation of subcutaneous fat mass in females prior to menopause. However, the sudden withdrawal of oestrogens through the menopausal transition, shifts the direction of fat mass accumulation, and adipose tissue begins to favour visceral deposition. Visceral fat mass is closely associated with a persisting state of low-grade inflammation, metabolic syndromes such as type 2 diabetes, cardiovascular disease and certain cancers. Therefore, post-menopause females are at a higher risk of developing such conditions in comparison with their pre-menopausal counterparts, even after confounding for age. The mechanisms behind the association between oestrogens, fat mass distribution, chronic inflammation and disease state are currently unclear, and no systematic review and meta-analysis has compared markers of visceral adiposity and chronic inflammation in pre- and post-menopausal women to date.

This article is from Adipocyte , volume 2 . Abstract Epigenetics generates a considerable interest in the field of research on complex traits, including obesity and diabetes. Recently, we reported a number of epipolymorphisms in the placental leptin and adiponectin genes associated with maternal hyperglycemia during pregnancy. Our results suggest that DNA methylation could partly explain the link between early exposure to a detrimental fetal environment and an increased risk to develop obesity and diabetes later in life. This brief report discusses the potential importance of adipokine epigenetic changes in fetal metabolic programming. Additionally, preliminary data showing similarities between methylation variations of different tissues and cell types will be presented along with the challenges and future perspectives of this emerging field of research.

By the light of new studies, new adipokines and cytokines are being defined and their functions showed. Besides their endocrinological effects, they have very important roles on inflammation, inflamatuar response, regulation of appetite, sleep, triggering important illness and being useful biomarker for them. This review collected current information about new adipokines and cytokines. 

This article is from Frontiers in Endocrinology , volume 4 . Abstract For many years, adipose tissue was considered as an inert energy storage organ that accumulates and stores triacylglycerols during energy excess and releases fatty acids in times of systemic energy need. However, over the last two decades adipose tissue depots have been established as highly active endocrine and metabolically important organs that modulate energy expenditure and glucose homeostasis. In rodents, brown adipose tissue plays an essential role in non-shivering thermogenesis and in energy dissipation that can serve to protect against diet-induced obesity. White adipose tissue collectively referred too as either subcutaneous or visceral adipose tissue is responsible for the secretion of an array of signaling molecules, termed adipokines. These adipokines function as classic circulating hormones to communicate with other organs including brain, liver, muscle, the immune system, and adipose tissue itself. The dysregulation of adipokines has been implicated in obesity, type 2 diabetes, and cardiovascular disease. Recently, inflammatory responses in adipose tissue have been shown as a major mechanism to induce peripheral tissue insulin resistance. Although leptin and adiponectin regulate feeding behavior and energy expenditure, these adipokines are also involved in the regulation of inflammatory responses. Adipose tissue secretes various pro- and anti-inflammatory adipokines to modulate inflammation and insulin resistance. In obese humans and rodent models, the expression of pro-inflammatory adipokines is enhanced to induce insulin resistance. Collectively, these findings have suggested that obesity-induced insulin resistance may result, at least in part, from an imbalance in the expression of pro- and anti-inflammatory adipokines. Thus we will review the recent progress regarding the physiological and molecular functions of adipokines in the obesity-induced inflammation and insulin resistance with perspectives on future directions.

This article is from Arquivos brasileiros de cardiologia , volume 102 . Abstract Background: The impact of blood pressure (BP) during adolescence on other cardiovascular risk factors in young adults is important for the primary prevention. Objective: To evaluate BP, anthropometric indexes, metabolic and inflammatory profiles in young individuals stratified by their BP behavior recorded for 18 years. Methods: A total of 116 individuals, of whom 63 were males, from the Rio de Janeiro study (follow-up of 17.76 ± 1.63 years), were assessed at two moments: A1 (12.40 ± 1.49 years) and A2 (30.09 ± 2.01 years). The 116 individuals were divided into two groups: GN (n = 71), of participants with normal BP at A1; and GH (n = 45), of those with abnormal BP at A1. BP, weight, height and body mass index (BMI) were measured at A1 and A2. At A2, abdominal circumference (AC) and laboratory, metabolic and inflammatory variables were included. Results: 1) No difference was observed between the groups as regards age and gender; 2) At A2, GH showed higher mean weight, BMI, BP, insulin, HOMA-IR (p < 0.001), leptin (p < 0.02), apolipoprotein B100 and A1 (p < 0.02), apolipoprotein B100 / apolipoprotein A1 ratio (p < 0.010); and higher prevalences of overweight/obesity (p < 0.001), of increased AC (p < 0.001) and of hypertension (p < 0.02); 3) No difference was observed between the groups as regards the inflammatory variables; 4) There was a positive correlation of BP at A1 with BP, BMI, insulin, leptin and HOMA-IR at A2 (p < 0.05). Conclusion: BP in adolescence was associated with higher values of BP, and anthropometric and metabolic variables in young adulthood, but not with inflammatory variables.

This article is from Diabetes Care , volume 36 . Abstract OBJECTIVE: To study the effects of high-protein versus high-carbohydrate diets on various metabolic end points (glucoregulation, oxidative stress [dichlorofluorescein], lipid peroxidation [malondialdehyde], proinflammatory cytokines [tumor necrosis factor-α and interleukin-6], adipokines, and resting energy expenditure [REE]) with high protein–low carbohydrate (HP) and high carbohydrate–low protein (HC) diets at baseline and after 6 months of dietary intervention. RESEARCH DESIGN AND METHODS: We recruited obese, premenopausal women aged 20–50 years with no diabetes or prediabetes who were randomized to HC (55% carbohydrates, 30% fat, and 15% protein) or HP (40% carbohydrates, 30% fat, and 30% protein) diets for 6 months. The diets were provided in prepackaged food, which provided 500 kcal restrictions per day. The above metabolic end points were measured with HP and HC diet at baseline and after 6 months of dietary intervention. RESULTS: After 6 months of the HP versus HC diet (12 in each group), the following changes were significantly different by Wilcoxon rank sum test for the following parameters: dichlorofluorescein (−0.8 vs. −0.3 µmol/L, P < 0.0001), malondialdehyde (−0.4 vs. −0.2 μmol/L, P = 0.0004), C-reactive protein (−2.1 vs. −0.8 mg/L, P = 0.0003), E-selectin (−8.6 vs. −3.7 ng/mL, P = 0.0007), adiponectin (1,284 vs. 504 ng/mL, P = 0.0011), tumor necrosis factor-α (−1.8 vs. −0.9 pg/mL, P < 0.0001), IL-6 (−1.3 vs. −0.4 pg/mL, P < 0.0001), free fatty acid (−0.12 vs. 0.16 mmol/L, P = 0.0002), REE (259 vs. 26 kcal, P < 0.0001), insulin sensitivity (4 vs. 0.9, P < 0.0001), and β-cell function (7.4 vs. 2.1, P < 0.0001). CONCLUSIONS: To our knowledge, this is the first report on the significant advantages of a 6-month hypocaloric HP diet versus hypocaloric HC diet on markers of β-cell function, oxidative stress, lipid peroxidation, proinflammatory cytokines, and adipokines in normal, obese females without diabetes.

This article is from PLoS ONE , volume 9 . Abstract Objectives: Intermittent hypoxia (IH), resulted from recurring episodes of upper airway obstruction, is the hallmark feature and the most important pathophysiologic pathway of obstructive sleep apnea (OSA). IH is believed to be the most important factor causing systemic inflammation. Studies suggest that insulin resistance (IR) is positively associated with OSA. In this study, we hypothesized that the recurrence of IH might result in cellular and systemic inflammation, which was manifested through the levels of proinflammatory cytokines and adipokines after IH exposure, and because IR is linked with inflammation tightly, this inflammatory situation may implicate an IR status. Methods: We developed an IH 3T3-L1 adipocyte and rat model respectively, recapitulating the nocturnal oxygen profile in OSA. In IH cells, nuclear factor kappa B (NF-κB) DNA binding reactions, hypoxia-inducible factor-1α (HIF-1α), glucose transporter-1 (Glut-1), necrosis factor alpha (TNF-α), interleukin (IL) -6, leptin, adiponectin mRNA transcriptional activities and protein expressions were measured. In IH rats, blood glucose, insulin, TNF-α, IL-6, leptin and adiponectin levels were analyzed. Results: The insulin and blood glucose levels in rats and NF-κB DNA binding activities in cells had significantly statistical results described as severe IH>moderate IH>mild IH>sustained hypoxia>control. The mRNA and protein levels of HIF-1α and Glut-1 in severe IH group were the highest. In cellular and animal models, both the mRNA and protein levels of TNF-α, IL-6 and leptin were the highest in severe IH group, when the lowest in severe IH group for adiponectin. Conclusions: Oxidative stress and the release of pro-inflammatory cytokines/adipokines, which are the systemic inflammatory markers, are associated with IH closely and are proportional to the severity of IH. Because IR and glucose intolerance are linked with inflammation tightly, our results may implicate the clinical relationships between OSA and IR.

This article is from Frontiers in Endocrinology , volume 5 . Abstract None

In this first year of funding we characterized the direct actions of adiponectin on murine T lymphocytes in vitro. Adiponectin induced lymphocyte proliferation in the absence of the specific antigen against which they were activated in vivo (MOG35-55). We will further study the mechanisms leading to these phenomena in the next year by silencing expression of adiponectin receptors on murine T cells. We have also performed experiments an in vitro model of blood brain barrier (BBB). We demonstrated expression of adiponectin receptors on astrocytes and endothelial cells, the two BBB components. Next, we tested adiponectin effects on the BBB. In vitro barrier integrity was assessed by measurement of transendothelial electrical resistance (TEER) or diffusion of fluorescently labeled solutes (fluorescein-dextran). Treatment with adiponectin significantly increases TEER and decreases the diffusivity of fluorescein-dextran compared to treatment with vehicle (PBS). These findings suggest that adiponectin in vitro decreases BBB permeability. No significant effects of adiponectin were observed on level of expression of the endothelial molecules VCAM and VE-cadherin. Furthermore, we have started studying expression of adiponectin receptors on peripheral blood immune cells in MS patients and controls by flow cytometry and on autopsied human MS and non-MS tissues by immunohistochemistry.

Obesity increases the risk of breast cancer in post-menopausal women. The degree of risk increases proportionally with an increase in adiposity. There is mounting evidence that stromal cells in the tumor microenvironment make pivotal contributions to tumor progression. Adipocytes have been shown to exert their influence on breast cancer cells via two secreted adipocytokines, leptin and adiponectin. Leptin stimulates proliferation and invasiveness of breast cancer cell lines. Conversely, adiponectin is down-regulated in obese individuals, and there is an inverse relationship between adiponectin levels and risk of breast cancer. Therefore, in breast cancer development, it is important to know if there are significant interactions or tumorigenic effects of excess adipose tissue on mammary epithelium. The question of how adipocytes exert their influence on pre-malignant mammary epithelial cells had not been resolved until now. Adiponectin was found to suppress the effects of oncogenic ras or Myc in p53-/- MMECs. These cells slowed their rate of growth in response to adiponectin, and were better able to maintain genomic stability. This lead to reduced transformation potential in a soft agar assay. Conversely, the effects of leptin were very striking. The presence of p53 was able to suppress the oncogenic effects of ras and Myc. However, when leptin was present, oncogene-expressing WT-MMECs behaved just like p53-/- MMECs. These cells had a greatly enhanced rate of growth and became highly aneuploid. Furthermore, p53 was no longer able to function as a tumor suppressor in the presence of leptin, allowing oncogenic transformation.

Hypermetabolism is universal in the severely burned and is characterized by catabolism of lean mass and body fat with associated insulin resistance. Adipokines are likely to play a role in these changes but have not been identified to date in burn patients. From a single burn ICU, 17 burn patients with an expected stay greater than 14 days were studied. Study period began within 14 days of admission. Over 7 days, plasma samples were collected for measurement of leptin, adiponectin, resistin, ghrelin, insulin, and cortisol by ELISA. For comparison, samples from 15 healthy controls of similar age, BMI, and blood glucose were obtained. Patients with burns, who are characteristically hypermetabolic with hypercortisolism and insulin resistant, have significant changes in adipokine levels that appear independent of the magnitude of initial injury or metabolic derangement. In addition, suppression of ghrelin in the presence of decreased leptin and adiponectin levels in combination with increased insulin and resistin levels represent unexpected changes in the metabolic milieu of the injured patient possibly due to dramatic activation of inflammatory pathways, indicating strategies for treatment.

This study aims to comprehensively evaluate whether adipokines and gut hormones are associated with cognitive decline (i.e. mild cognitive impairment (MCI), general dementia, and Alzheimer’s disease (AD)). We will perform a systematic review of the available literature and/or a meta-analysis focusing on three adipokines (leptin, adiponectin, and resistin) and one gut hormone (ghrelin), and their associations with the presence of general dementia, AD, and MCI. We will include cross-sectional and longitudinal results in humans, and we will put emphasis on clarifying the possible effects of potential confounding factors such as age.

This article is from Allergy, Asthma & Immunology Research , volume 4 . Abstract Purpose: The aim of this study was to evaluate serum levels of leptin, ghrelin, and adiponectin in obese and non-obese children with asthma and in healthy non-asthmatic children, and analyze their relationships with clinical outcomes. Methods: This study enrolled 40 obese and 51 non-obese children with asthma and 20 healthy children. Body mass index and serum leptin, ghrelin, and adiponectin levels were determined in all children. Asthma symptom scores and lung function test results were recorded for subjects with asthma. Results: Serum leptin levels (11.8±7.9, 5.3±6.8, and 2.1±2.4 ng/mL in the obese asthmatic, non-obese asthmatic, and control groups, respectively) and adiponectin levels (12,586.2±3,724.1; 18,089.3±6,452.3; and 20,297.5±3,680.7 ng/mL, respectively) differed significantly among the groups (P

This article is from Indian Journal of Endocrinology and Metabolism , volume 16 . Abstract Background:: The clustering of cardiovascular risk factors is termed the metabolic syndrome (MS), which strongly predicts the risk of diabetes and cardiovascular disease (CVD). Adipokines may contribute to the development of obesity and insulin resistance and may be a causal link between MS, diabetes and CVD. Hence, we studied the adipokines – adiponectin and plasminogen activator inhibitor-1 (PAI-1) – in subjects with MS. Materials and Methods:: We studied 50 subjects with MS diagnosed by International Diabetes Federation (IDF) criteria and 24 healthy age- and sex-matched controls. Clinical evaluation included anthropometry, body fat analysis by bioimpedance, highly sensitive C-reactive protein, insulin, adiponectin, and PAI-1 measurement. Results:: Subjects with MS had lower adiponectin (4.01 ± 2.24 vs. 8.7 ± 1.77 μg/ml; P < 0.0001) and higher PAI-1 (53.85 ± 16.45 vs. 17.35 ± 4.45 ng/ml; P < 0.0001) levels than controls. Both were related with the number of metabolic abnormalities. Adiponectin was negatively and PAI-1 was positively associated with body mass index, waist hip ratio (WHR), body fat mass, percent body fat, and all the parameters of MS, except HDL where the pattern reversed. WHR and triglycerides were independent predictors of adipokines in multiple regression analysis. Receiver operating characteristic curve analysis showed that adiponectin (6.7 μg/ml) and PAI-1 (25.0 ng/ml) levels predicted the MS with high sensitivity, specificity and accuracy in Indian population. Conclusions:: Subjects with MS have lower adiponectin and higher PAI-1 levels compared to healthy controls. Lifestyle measures have been shown to improve the various components of MS, and hence there is an urgent need for public health measures to prevent the ongoing epidemic of diabetes and CVD.

This article is from BMC Medical Genetics , volume 12 . Abstract Background: Vaspin and omentin are recently described molecules that belong to the adipokine family and seem to be related to metabolic risk factors. The objectives of this study were twofold: to evaluate vaspin and omentin circulating levels and mRNA expression in subcutaneous and visceral adipose tissues in non-diabetic morbidly obese women; and to assess the relationship of vaspin and omentin with anthropometric and metabolic parameters, and other adipo/cytokines. Design: We analysed vaspin and omentin circulating levels in 71 women of European descent (40 morbidly obese [BMI ≥ 40 kg/m2] and 31 lean [BMI ≤ 25]). We assessed vaspin and omentin gene expression in paired samples of visceral and subcutaneous abdominal adipose tissue from 46 women: 40 morbidly obese and 6 lean. We determined serum vaspin and plasma omentin levels with an Enzyme-Linked Immunosorbent Assay and adipose tissue mRNA expression by real time RT-PCR. Results: Serum vaspin levels in the morbidly obese were not significantly different from those in controls. They correlated inversely with levels of lipocalin 2 and interleukin 6. Vaspin mRNA expression was significantly higher in the morbidly obese, in both subcutaneous and visceral adipose tissue.Plasma omentin levels were significantly lower in the morbidly obese and they correlated inversely with glucidic metabolism parameters. Omentin circulating levels, then, correlated inversely with the metabolic syndrome (MS). Omentin expression in visceral adipose tissue was significantly lower in morbidly obese women than in controls. Conclusions: The present study indicates that vaspin may have a compensatory role in the underlying inflammation of obesity. Decreased omentin circulating levels have a close association with MS in morbidly obese women.

This article is from Cardiovascular Diabetology , volume 12 . Abstract Background: It is a matter of debate whether metabolic syndrome (MS) improves cardiovascular risk prediction beyond the risk associated with its individual components. The present study examined the association of MS score with high sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), resistin, adiponectin, and angiographic coronary artery disease (CAD) severity according to the presence of DM. In addition, the predictive value of various clinical and biochemical parameters were analyzed, including the MS score for angiographic CAD. Methods: The study enrolled 363 consecutive patients (196 men, 62 ± 11 years of age) who underwent coronary angiography for evaluation of chest pain. Blood samples were taken prior to elective coronary angiography. MS was defined by the National Cholesterol Education Program criteria, with MS score defined as the numbers of MS components. CAD was defined as > 50% luminal diameter stenosis of at least one major epicardial coronary artery. CAD severity was assessed using the Gensini score. Results: Of the 363 patients studied, 174 (48%) had CAD and 178 (49%) were diagnosed with MS. When the patients were divided into 4 subgroups according to MS score (0–1, 2, 3, 4–5), IL-6 levels and the CAD severity as assessed by the Gensini score increased as MS scores increased. In contrast, adiponectin levels decreased significantly as MS scores increased. When subjects were divided into two groups according to the presence of DM, the relationships between MS score and IL-6, adiponectin, and Gensini score were maintained only in patients without DM. Age, smoking, DM, MS score, and adiponectin independently predicted angiographic CAD in the whole population. However, age is the only predictor for angiographic CAD in patients with DM. Conclusions: In the presence of DM, neither adipokines nor MS score predicted angiographic CAD. However, in non-diabetic patients, IL-6 and adiponectin showed progressive changes according to MS score, and MS score was an independent predictor of CAD in patients without DM.

Background: Hepatitis C virus (HCV) continues to be a major disease burden on the world, especially in Egypt, which may progress to cirrhosis. Adipokines are implicated in regulation of the inflammatory response, angiogenesis and fibrogenesis . Some adipokines have a protective effect while others have negative effect in chronic hepatitis C (CHC). Aim of the study: We aimed to study the new adipokines (visfatin, chemerin and omnetin1) in CHC patients to find out its relation to the biochemical liver functions tests and liver histopathology in non-obese chronic hepatitis C patients Patients and methods: This study included 70 patients with CHC and 20 healthy individuals as a control group. Liver function tests, serum visfatin, chemerin and omentin1 levels were measured. Percutaneous liver biopsy was performed in CHC patients. Results: The three adipokines levels were significantly increased in CHC patients comparing to control group (P

This article is from Frontiers in Immunology , volume 4 . Abstract Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are inflammatory rheumatic diseases that may modify body composition. Adipose tissue has the ability to release a wide range of products involved in physiologic functions, but also in various pathological processes, including the inflammatory/immune response. RA and AS are both associated with the development of cardiovascular complications. It is has been established that central/abdominal, and particularly intra-abdominal or visceral adiposity is closely linked to cardiovascular events. Thus, in this study, we aimed to evaluate the body composition of patients with RA or AS compared to healthy controls (HC), with a special emphasis on the visceral region. In parallel, we measured adipose products or adipokines, namely leptin, adiponectin and its high molecular weight (HMW) isoform, resistin, and ghrelin, a gastric peptide that plays a role in energetic balance. The homeostasis model assessment for insulin resistance (HOMA-IR) and atherogenic index were used to evaluate cardiovascular risk. One hundred and twelve subjects were enrolled (30 patients with RA, 31 with AS, and 51 HC). Body composition was measured using dual-energy X-ray absorptiometry to determine total fat mass and lean mass, adiposity, fat in the android and gynoid regions, and visceral fat. Patients and HC did not differ in terms of body mass index. On the contrary, adiposity was increased in RA (p = 0.01) while visceral fat was also increased, but only in women (p = 0.01). Patients with AS tended to have lower total fat mass (p = 0.07) and higher lean mass compared to HC (p = 0.07). Leptin and leptin/fat mass were decreased in male patients with AS (p 

This article is from PLoS ONE , volume 9 . Abstract Objective: Coronary artery disease (CAD) is associated with abdominal obesity and metabolic syndrome. Adipocytes secrete adipokines, including the newly discovered adipocyte fatty acid binding protein (A-FABP) and chemerin. Adipokines contribute to the pathogenesis of CAD. In patients with CAD, the presence of significant ischemia predicts adverse outcomes. It is unknown whether adipokines can be better predictors of the presence of significant myocardial ischemia than conventional risk factors. This study aimed to compare adipokines with clinical risk factors and abdominal obesity as predictive factors for significant myocardial ischemia. Methods: One hundred and ninety-six adults with suspected, but unproven, CAD were consecutively enrolled. The main measures were clinical and biochemical parameters and stress myocardial perfusion imaging with gated myocardial perfusion single-photon emission computed tomography (SPECT), with computed tomography (CT) attenuation correction. The abdominal visceral fat area was examined using a hybrid SPECT/CT scanner. Serum levels of high-sensitivity C-reactive protein (hs-CRP) and adipokines (adiponectin, A-FABP, and chemerin) were evaluated. Results: A-FABP levels correlated significantly with adiponectin, hs-CRP, body mass index, waist circumference, and visceral fat area. A-FABP was significantly associated with metabolic syndrome (OR 3.2, 95% CI 1.6–6.4, p = 0.001), significant myocardial ischemia (OR 1.9, 95% CI 1.0–3.4, p = 0.05), and stress lung-to-heart ratio (β = 0.03, p = 0.03) on SPECT. Chemerin was significantly associated with serum triglyceride levels but not with metabolic syndrome, significant ischemia, or stress lung-to-heart ratio on SPECT. A-FABP was better at detecting significant inducible ischemia than other biomarkers, although this was a modest improvement (area under ROC curve 0.579, 95% CI 0.46–0.69). Conclusions: Serum A-FABP concentrations correlate significantly with visceral fat area, metabolic syndrome, and predicted significant myocardial ischemia on SPECT. This may help to more accurately assess CAD risk, especially in patients with metabolic syndrome.

This article is from Arthritis Research & Therapy , volume 14 . Abstract Introduction: The current markers of disease activity in Takayasu arteritis (TA) are insufficient for proper assessment. We investigated circulating levels of unacylated and acylated ghrelin, leptin and adiponectin and their relationships with disease activity in patients with TA. Methods: This study included 31 patients with TA and 32 sex-, age- and body mass index-matched healthy controls. Disease activity was assessed in TA patients using various tools, including Kerr's criteria, disease extent index-Takayasu, physician's global assessment, radiological parameters, and laboratory markers. Plasma unacylated and acylated ghrelin, and serum leptin and adiponectin levels were measured using an enzyme-linked immunosorbent assay. Results: Unacylated and acylated ghrelin levels were found to be significantly lower in TA patients than that in healthy controls. Patients with active disease had lower unacylated ghrelin levels than those with inactive disease and had lower acylated ghrelin levels than healthy controls. Ghrelin levels were negatively correlated with various parameters of disease activity. The leptin/ghrelin ratio was significantly higher in TA patients than controls. It was positively correlated with disease activity. There was a positive correlation between unacylated and acylated ghrelin and a negative correlation between leptin and ghrelin. There was no statistical difference in adiponectin levels between TA patients and controls. The radiological activity markers were positively correlated with other parameters of disease activity. Conclusions: This study suggests that plasma unacylated and acylated ghrelin levels may be useful in monitoring disease activity and planning treatment strategies for patients with TA. The serum leptin level and leptin/ghrelin ratio may also be used to help assess the disease activity.

This article is from Arthritis Research & Therapy , volume 15 . Abstract Introduction: Cardiovascular (CV) morbidity and mortality are increased in patients with rheumatoid arthritis (RA). Inflammation is thought to be an important factor in accelerated atherosclerosis in RA, whereas insulin resistance is a known risk factor for atherosclerosis in RA. We hypothesised that adipokines could be a link between inflammation, insulin resistance, and atherosclerosis in RA. Methods: The common carotid artery (CCA) intima-media thickness (IMT), CCA resistive index (RI), and carotid plaques were measured by ultrasonography in 192 patients with RA. Insulin resistance was assessed by the homeostasis model assessment for insulin resistance (HOMA-IR). Serum adiponectin, leptin, resistin, tumor necrosis factor-α, and interleukin (IL)-6 concentrations were determined. Results: The CCA RI was associated with CCA IMT and the estimated total plaque volume after adjustment for conventional CV risk factors. Among adipokines, resistin and IL-6 were correlated with inflammatory parameters. Leptin and leptin:adiponectin (L:A) ratio were correlated with metabolic risk factors, including HOMA-IR. And L:A ratio was related to the CCA RI after adjustment for conventional and nonconventional CV risk factors, including HOMA-IR, erythrocyte sedimentation rate and C-reactive protein. Conclusion: L:A ratio was associated with HOMA-IR and carotid RI. L:A ratio might be an independent factor for predicting cardiovascular risk in patients with RA.

This article is from International Journal of Molecular Sciences , volume 15 . Abstract Accumulating evidence indicates that obesity is closely associated with an increased risk of metabolic diseases such as insulin resistance, type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease. Obesity results from an imbalance between food intake and energy expenditure, which leads to an excessive accumulation of adipose tissue. Adipose tissue is now recognized not only as a main site of storage of excess energy derived from food intake but also as an endocrine organ. The expansion of adipose tissue produces a number of bioactive substances, known as adipocytokines or adipokines, which trigger chronic low-grade inflammation and interact with a range of processes in many different organs. Although the precise mechanisms are still unclear, dysregulated production or secretion of these adipokines caused by excess adipose tissue and adipose tissue dysfunction can contribute to the development of obesity-related metabolic diseases. In this review, we focus on the role of several adipokines associated with obesity and the potential impact on obesity-related metabolic diseases. Multiple lines evidence provides valuable insights into the roles of adipokines in the development of obesity and its metabolic complications. Further research is still required to fully understand the mechanisms underlying the metabolic actions of a few newly identified adipokines.

This article is from International Journal of Molecular Sciences , volume 15 . Abstract Accumulating evidence indicates that obesity is closely associated with an increased risk of metabolic diseases such as insulin resistance, type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease. Obesity results from an imbalance between food intake and energy expenditure, which leads to an excessive accumulation of adipose tissue. Adipose tissue is now recognized not only as a main site of storage of excess energy derived from food intake but also as an endocrine organ. The expansion of adipose tissue produces a number of bioactive substances, known as adipocytokines or adipokines, which trigger chronic low-grade inflammation and interact with a range of processes in many different organs. Although the precise mechanisms are still unclear, dysregulated production or secretion of these adipokines caused by excess adipose tissue and adipose tissue dysfunction can contribute to the development of obesity-related metabolic diseases. In this review, we focus on the role of several adipokines associated with obesity and the potential impact on obesity-related metabolic diseases. Multiple lines evidence provides valuable insights into the roles of adipokines in the development of obesity and its metabolic complications. Further research is still required to fully understand the mechanisms underlying the metabolic actions of a few newly identified adipokines.

This article is from International Journal of Molecular Sciences , volume 15 . Abstract Accumulating evidence indicates that obesity is closely associated with an increased risk of metabolic diseases such as insulin resistance, type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease. Obesity results from an imbalance between food intake and energy expenditure, which leads to an excessive accumulation of adipose tissue. Adipose tissue is now recognized not only as a main site of storage of excess energy derived from food intake but also as an endocrine organ. The expansion of adipose tissue produces a number of bioactive substances, known as adipocytokines or adipokines, which trigger chronic low-grade inflammation and interact with a range of processes in many different organs. Although the precise mechanisms are still unclear, dysregulated production or secretion of these adipokines caused by excess adipose tissue and adipose tissue dysfunction can contribute to the development of obesity-related metabolic diseases. In this review, we focus on the role of several adipokines associated with obesity and the potential impact on obesity-related metabolic diseases. Multiple lines evidence provides valuable insights into the roles of adipokines in the development of obesity and its metabolic complications. Further research is still required to fully understand the mechanisms underlying the metabolic actions of a few newly identified adipokines.

Obesity increases the risk of breast cancer in post-menopausal women. The degree of risk increases proportionally with an increase in adiposity. There is mounting evidence that stromal cells in the tumor microenvironment make pivotal contributions to tumor progression. Stromal adipocytes have been shown to exert their influence on breast cancer cells via two secreted adipocytokines, leptin and adiponectin. Leptin stimulates proliferation and invasiveness of breast cancer cell lines. Conversely, adiponectin is down-regulated in obese individuals, and there is an inverse relationship between adiponectin levels and risk of breast cancer. Therefore, in breast cancer development, it is important to know if there are significant interactions or tumorigenic effects of excess adipose tissue on mammary epithelium. The question of how adipocytes exert their influence on pre-malignant mammary epithelial cells has not been resolved. Adiponectin was found to suppress the effects of oncogenic ras or Myc in p53-/- MMECs. These cells slowed their rate of growth in response to adiponectin, and was better able to maintain genomic stability. This lead to reduced transformation potential in a soft agar assay. Conversely, the effects of leptin was very striking. The presence of p53 was able to suppress the oncogenic effects of ras and Myc. However, when leptin was present, oncogene-expressing WT-MMECs behaved just like p53-/- MMECs. These cells had a greatly enhanced rate of growth and became highly aneuploid. Furthermore, p53 was no longer able to function as a tumor suppressor in the presence of leptin, allowing oncogenic transformation.

Severe trauma is accompanied by a period of hypermetabolism and disuse. In this study, a rat model was used to determine the effects of burn and disuse independently and in combination on body composition, food intake and adipokines. SA had a progressive increase in body mass (BM), SH and BA no change and BH a reduction. Compared to SA, BM was reduced by 10% in both SH and BA and by 17% when combined in BH. Compared to SA, all groups had reductions in lean and fat body mass with BH being greater. The decrease in lean mass was associated with the rate of urinary corticosterone excretion. The loss in fat mass was associated with decreases in plasma leptin and adiponectin and an increase in ghrelin. Following the acute response to injury, BH had a greater food intake per 100 g BM. Food intake was associated with the levels of leptin, adiponectin and ghrelin. The effects of the combination of burn and disuse in this animal model were additive, therefore in assessing metabolic changes with severe trauma both injury and disuse should be considered. Furthermore, the observed changes in adipokines, corticosterone and ghrelin provide insights for interventions to attenuate the hypermetabolic state following injury, possibly reducing catabolism and muscle loss and subsequent adverse effects on recovery and function.

This article is from Clinical and Translational Gastroenterology , volume 1 . Abstract OBJECTIVES:: Leptin and adiponectin (APN) are adipokines produced by adipocytes that participate in the modulation of immune and inflammatory responses. In Crohn's disease (CD), fat wrapping surrounding the inflamed intestine produces high levels of leptin and APN. In inflammatory bowel disease (IBD), apoptosis resistance of lamina propria T lymphocytes (LPL-T) is one of the mechanisms that maintains chronic inflammation. We addressed the mechanism by which leptin and APN regulate inflammation and apoptosis in IBD. METHODS:: Immune cell infiltration, several factors expressed by adipose tissue (AT), and spontaneous release of cytokines by adipocytes were measured. The presence of APN and leptin in intestinal mucosa was detected and their effect on LPL-T apoptosis, signal transducer and activator of transcription 3 (STAT3), Suppressor of Cytokine Signaling 3 (SOCS3), Bcl-2 and Bcl-xL expression, and cytokine production was studied. In addition, the effects of globular and high-molecular-weight (HMW) APN on LPL-T cytokine production and apoptosis were studied. RESULTS:: Higher levels of several chemokines, cytokines, and growth factors were present in AT near active than near inactive disease. A significantly higher amount of inflammatory infiltrate was present in AT near active CD than near ulcerative colitis, controls, and near the inactive area of CD. There were no changes in the ratios of APN molecular weight in control and IBD adipocyte products. Leptin and APN inhibited anti-CD3-stimulated-LPL-T apoptosis and potentiated STAT3 phosphorylation, Bcl-2, and Bcl-xL expression in IBD and control mucosa. However, SOCS3 expression was suppressed only in IBD. Both globular and HMW APN have similar effects on LPL-T cytokine production and apoptosis. Leptin and APN enhanced interleukin (IL)-10 production by anti-CD3-stimulated LPL-T in IBD only. APN, but not leptin, increased anti-CD3-induced IL-6 levels in LPL-T only in IBD patients. IL-10 exerts its anti-inflammatory activity in the presence of SOCS3 suppression by leptin or APN. CONCLUSION:: Leptin and APN maintain the inhibition of anti-CD3-stimulated LPL-T apoptosis by enhancing Bcl-2 and Bcl-xL overexpression and promoting STAT3 phosphorylation while suppressing SOCS3.

This article is from Adipocyte , volume 1 . Abstract Adenosine A1 receptor-deficient mice develop a phenotype of insulin resistance and grow fat. Participating pathophysiological pathways are not understood in detail yet, as discussed in our recent manuscript. This commentary further explores possible pathophysiological mechanisms with emphasis on the roles of the adipokines resistin, retinol-binding protein 4, adiponectin and the function of the gastric hormone ghrelin in adenosine mediated central regulation of energy balance. The postulate of an important function of ghrelin/A1AR axis provides a good hypothetical basis for further investigations to clarify the mechanism of A1AR-dependent metabolic homeostasis.

This article is from Molecular Metabolism , volume 3 . Abstract Prevention of obesity and therapeutic weight loss interventions have provided only limited long term success. Therefore there is an urgent need to develop novel pharmacological treatment strategies, which target mechanisms underlying positive energy balance, excessive fat accumulation and adverse fat distribution. Adipokines may have potential for future pharmacological treatment strategies of obesity and metabolic diseases, because they are involved in the regulation of appetite and satiety, energy expenditure, endothelial function, blood pressure, insulin sensitivity, adipogenesis, fat distribution and insulin secretion and others. There are important road blocks on the way from an adipokine candidate to the clinical use a therapeutic compound. Such road blocks include an incomplete understanding of the mechanism of action, resistance to a specific adipokine, side effects of the adipokine and others. This review focuses on the potential of selected adipokines as therapeutic tools or targets and discusses important road blocks, which currently prevent their clinical use.

This article is from Frontiers in Endocrinology , volume 5 . Abstract White and brown adipose tissues (BATs), which store and burn lipids, respectively, play critical roles in energy homeostasis. Fibroblast growth factors (FGFs) are signaling proteins with diverse functions in development, metabolism, and neural function. Among 22 FGFs, FGF1, FGF10, and FGF21 play roles as adipokines, adipocyte-secreted proteins, in the development and function of white and BATs. FGF1 is a critical transducer in white adipose tissue (WAT) remodeling. The peroxisome proliferator-activated receptor γ–FGF1 axis is critical for energy homeostasis. FGF10 is essential for embryonic white adipocyte development. FGF21 activates BAT in response to cold exposure. FGF21 also stimulates the accumulation of brown-like cells in WAT during cold exposure and is an upstream effector of adiponectin, which controls systemic energy metabolism. These findings provide new insights into the roles of FGF signaling in white and BATs and potential therapeutic strategies for metabolic disorders.

This article is from Critical Care , volume 17 . Abstract Introduction: Severe trauma is accompanied by a period of hypermetabolism and disuse. In this study, a rat model was used to determine the effects of burn and disuse independently and in combination on body composition, food intake and adipokines. Methods: Male rats were assigned to four groups 1) sham ambulatory (SA), 2) sham hindlimb unloaded (SH), 3) 40% total body surface area full thickness scald burn ambulatory (BA) and 4) burn and hindlimb unloaded (BH). Animals designated to the SH and BH groups were placed in a tail traction system and their hindlimbs unloaded. Animals were followed for 14 days. Plasma, urine, fecal and tissue samples were analyzed. Results: SA had a progressive increase in body mass (BM), SH and BA no change and BH a reduction. Compared to SA, BM was reduced by 10% in both SH and BA and by 17% when combined in BH. Compared to SA, all groups had reductions in lean and fat body mass with BH being greater. The decrease in lean mass was associated with the rate of urinary corticosterone excretion. The loss in fat mass was associated with decreases in plasma leptin and adiponectin and an increase in ghrelin. Following the acute response to injury, BH had a greater food intake per 100 g BM. Food intake was associated with the levels of leptin, adiponectin and ghrelin. Conclusions: The effects of the combination of burn and disuse in this animal model were additive, therefore in assessing metabolic changes with severe trauma both injury and disuse should be considered. Furthermore, the observed changes in adipokines, corticosterone and ghrelin provide insights for interventions to attenuate the hypermetabolic state following injury, possibly reducing catabolism and muscle loss and subsequent adverse effects on recovery and function.