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Endovascular stenting is a safer alternative to open surgery for use in treating cerebral arterial stenosis and significantly reduces the recurrence of ischemic stroke, but the widely used bare-metal stents (BMSs) often result in in-stent restenosis (ISR). Although evidence suggests that drug-eluting stents are superior to BMSs in the short term, their long-term performances remain unknown. Herein, we propose a potential vascular stent modified by immobilizing clickable chemerin 15 (C15) peptides on the stent surface to suppress coagulation and restenosis. Various characterization techniques and an animal model were used to evaluate the surface properties of the modified stents and their effects on endothelial injury, platelet adhesion, and inflammation. The C15-immobilized stent could prevent restenosis by minimizing endothelial injury, promoting physiological healing, restraining the platelet-leukocyte-related inflammatory response, and inhibiting vascular smooth muscle cell proliferation and migration. Furthermore, in vivo studies demonstrated that the C15-immobilized stent mitigated inflammation, suppressed neointimal hyperplasia, and accelerated endothelial restoration. The use of surface-modified, anti-inflammatory, endothelium-friendly stents may be of benefit to patients with arterial stenosis. Endovascular stenting is increasingly used for cerebral arterial stenosis treatment, aiming to prevent and treat ischemic stroke. But an important accompanying complication is in-stent restenosis (ISR). Persistent inflammation has been established as a hallmark of ISR and anti-inflammation strategies in stent modification proved effective. Chemerin 15, an inflammatory resolution mediator with 15-aa peptide, was active at picomolar through cell surface receptor, no need to permeate cell membrane and involved in resolution of inflammation by inhibiting inflammatory cells adhesion, modulating macrophage polarization into protective phenotype, and reducing inflammatory factors release. The implications of this study are that C15 immobilized stent favors inflammation resolution and rapid re-endothelialization, and exhibits an inhibitory role of restenosis. As such, it helps the decreased incidence of ISR. [Display omitted] [ABSTRACT FROM AUTHOR]

Obesity-induced insulin resistance (IR) is known to influence hepatic cytokines (hepatokines), including fibroblast growth factor (FGF-21), fetuin-A, and chemerin. This study aimed to investigate the association between hepatokines and markers of endothelial dysfunction and vascular reactivity in obese adolescents. A total of 45 obese adolescents were categorized into three groups based on glucose tolerance: normal glucose tolerance (NGT), prediabetes (PD), and type 2 diabetes (T2D). We examined the relationships between FGF-21, fetuin-A, and chemerin with endothelial markers (plasminogen activator inhibitor-1 [PAI-1], intercellular adhesion molecule-1 [ICAM-1], and vascular cell adhesion marker-1 [VCAM-1]) and vascular surrogates (brachial artery reactivity testing [BART] and peak reactive hyperemia [PRH]). Obese adolescents (age 16.2±1.2 years; 62 % female, 65 % Hispanic) with NGT (n=20), PD (n=14), and T2D (n=11) had significant differences between groups in BMI; waist-hip ratio (p=0.05), systolic BP (p=0.008), LDL-C (p=0.02), PAI-1 (p<0.001). FGF-21 pg/mL (mean±SD: NGT vs. PD vs. T2D 54±42; 266±286; 160±126 p=0.006) and fetuin-A ng/mL (266±80; 253±66; 313±50 p=0.018), were significantly different while chemerin ng/mL (26±5; 31±10; 28±2) did not significantly differ between the groups. Positive correlations were found between chemerin and both PAI-1 (r=0.6; p=0.05) and ICAM-1 (r=0.6; p=0.05), FGF-21 and PAI-1 (r=0.6; p<0.001), and fetuin-A with TNFα (r=−0.4; p=0.05). Negative correlations were found between chemerin and PRH (r= −0.5; p=0.017) and fetuin-A and PRH (r=−0.4; p=0.05). In our cohort, IR predicted higher FGF-21 levels suggesting a linear relationship may exist between the two parameters. Hepatokines can augment alterations in the microvascular milieu in obese adolescents as demonstrated by their associations with the markers PAI-1, ICAM-1, and PRH. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to investigate if inflammation biomarkers elabela, visfatin, and chemerin will be useful in the diagnosis of patients with COVID-19. PATIENTS AND METHODS: This prospective case-control study included 33 patients with COVID-19 and 30 healthy matched controls. 33 patients, aged 18 years and older, diagnosed with COVID-19 and followed up for one month were included in the study. Blood samples were taken from the patients on the first day they were diagnosed with COVID-19, and levels of elabela (ELA), visfatin, chemerin, white blood cells (WBC), C-reactive protein (CRP) and procalcitonin (PCT) were assessed. Blood samples were also taken from 30 healthy volunteers for the control group. The ELA, visfatin and chemerin levels measured in the patients on day one were compared with those measured in the control group and with the WBC, CRP and PCT levels measured in the patients. RESULTS: Visfatin levels measured in COVID-19 patients were significantly higher than in the healthy control group. There was no significant difference in ELA and chemerin levels between the two groups. A significant positive correlation was found between chemerin and visfatin levels in the patients. A significant negative correlation was found between the levels of ELA-chemerin and ELA-visfatin in the patients. There was no significant correlation between elabela, visfatin and chemerin levels and WBC, CRP, PCT levels. CONCLUSIONS: Measurement of visfatin levels may be helpful in patients with COVID-19. However, two other biomarkers in our study, ELA and chemerin, were found not to be useful in diagnosing COVID-19. New inflammatory biomarkers may help to diagnose a disease in which the inflammatory response is at the forefront, such as COVID-19. New studies are needed on this subject. [ABSTRACT FROM AUTHOR]

Copyright of Pediatric Endocrinology, Diabetes & Metabolism is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Konuralp Medical Journal / Konuralp Tip Dergisi is the property of Duzce University Medical School and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Chemerin is an adipocytokine whose concentration in blood correlates positively with blood pressure (BP). We have recently revealed that acute intracerebroventricular (i.c.v.) injection of chemerin-9, an active fragment of human chemerin, increased systemic BP in normal Wistar rats, suggesting that chemerin is involved in the central nervous control of peripheral BP. After secreted as an inactive form as prochemerin, a mature form of active chemerin is produced through the cleavage of its carboxyl (C)-terminus by proteases. Although the activity of cleaved products of chemerin has been examined in vitro, in vivo effects remained to be elusive. In order to explore them, we performed acute i.c.v. injection of mouse chemerin-9 (mChemerin-9; 148F-156S), mouse chemerin-8 (mChemerin-8; 148F-155F), and mouse chemerin-7 (mChemerin-7; 148F-154A) into Wistar rats, and examined the effects on systemic BP. After chemerin fragment (1-30 nmol/head, i.c.v.) was cumulatively administered, systemic BP was measured by a cannulation method under an isoflurane anesthesia. mChemerin-9 but not mChemerin-8 and -7 induced a pressor response, which was concentration-dependent. In conclusion, we for the first time demonstrated that mChemerin-9 that corresponds to the C-terminal nine amino acids of active mouse chemerin156S increased systemic BP in rats, and also that chemerin fragments showed different effects on systemic BP dependent on how their C-terminus was cleaved. [ABSTRACT FROM AUTHOR]

Copyright of China Journal of Oral & Maxillofacial Surgery is the property of Shanghai Jiao Tong University, College of Stomatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The adipokines, visfatin, chemerin, and its receptor are expressed in the testis. It has also been shown that heat-stress alters the secretion and expression of other adipokines. Testicular heat-stress is now well known to cause the impairment in the testis. It has also been documented that heat-stress changes the expression of genes and proteins in the testis. To the best of our knowledge, the expression and localization of visfatin chemerin and its receptor have not been investigated in the heat-stressed testis. Therefore, the present study has investigated the expression and localization of these proteins in the heat-stressed testis. The expression of visfatin and chemerin and receptor exhibits a differential repossess against the heat stress. Visfatin expression was up-regulated while chemerin and chemerin receptor was down-regulated in the heat-stressed testis as shown by western blot analysis. The immunolocalization of visfatin and chemerin showed increased abundance in the seminiferous tubules of heat-stressed mice testis. Furthermore, abundance of visfatin, chemerin, and its receptor showed a decrease in abundance in the Leydig cells of heat-stressed testis. The decreased abundance of these proteins in the Leydig cells coincides with decreased 3β-HSD immunostaining along with decreased testosterone levels. These results suggest that heat-stress might decrease testosterone secretion by modulating visfatin and chemerin in the Leydig cells. The increased abundance of visfatin and chemerin in the primary spermatocytes, round spermatid, and multinucleated germ cells also coincides with increased immunostaining of active caspase-3. Moreover, expression of Bcl-2 was down-regulated, and expression of active caspase-3 and HSP70 were up-regulated along with increased oxidative stress in the heat-stressed testis, suggesting stimulated apoptosis. In conclusion, our results showed that visfatin, chemerin, and its receptor are differentially expressed in the testis under heat-stress and within the testis also it might differentially regulate testosterone biosynthesis in the Leydig cells and apoptosis in the seminiferous tubules. • Heat-stress up-regulates visfatin and down-regulates chemerin and its receptor (CMKLR1) in the testis. • However, abundance of visfatin, chemerin and CMKLR1 decreases in the Leydig cells of heat-stressed testis. • The decreased abundance of visfatin and chemerin in Leydig cells coincides with decreased testosterone. • Elevated immunostaining of visfatin and chemerin in the seminiferous tubules coincides with increased apoptosis. • Heat-stressed differentially regulates the expression of visfatin and chemerin system. [ABSTRACT FROM AUTHOR]

The study aimed to contribute to understanding the role of CRP, chemerin, fetuin-A and osteopontin and to assess their suitability as biomarkers of early stages of cardiovascular diseases in psoriasis vulgaris. Serum levels measured in 28 patients and 22 controls. Patients: increased levels of CRP (p<0.001), chemerin (p<0.05), osteopontin (p<0.05) and decreased levels of fetuin-A (p<0.05), significant relationships between CRP and fetuin-A (rho=0.530, p<0.01), CRP and chemerin (rho=0.543, p<0.01), CRP and age (rho=0.590, p<0.001), osteopontin and fetuin-A (r=-0.415, p<0.05), chemerin and PASI score (rho=-0.424, p<0.05). We confirmed specific roles of the biomarkers in psoriasis. CRP, fetuin-A and osteopontin could be considered appropriate markers for the detection of early stages of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Copyright of Arquivos de Neuro-Psiquiatria is the property of Thieme Medical Publishing Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Elevated chemerin level is observed in patients with arterial hypertension. The aim of the study was to determine the relationship between chemerin level, and parameters of blood pressure and arterial stiffness in children and adolescents with obesity but without arterial hypertension. Methods: In 23 children with obesity (13 girls, mean age 9.3, SD 1.9, mean BMI SDS 3.9, SD 1.7) 24 h ABPM (Spacelabs 90,217, USA), common carotids and abdominal aorta intima media thickness measurements (Voluson 730, GE Medical System 8.5 and 3.5 MHz probes), body composition analysis (Tanita BC 418 S MA, Tokyo, Japan) were performed. Glucose, triglycerides, total, LDL and HDL cholesterol, liver enzymes, uric acid, creatinine, sodium, insulin and chemerin levels were assessed in blood sample taken after a 12-h fasting period. Results: There was a significant correlation of circulating chemerin level with systolic blood pressure load in ABPM (r=0.5, p<0.05). Conclusion: Elevated chemerin level may be associated with increased systolic blood pressure in obese children. [ABSTRACT FROM AUTHOR]

Objective: Low-grade inflammation is a characteristic of various conditions, including obesity. Diet is regarded as a strong modifier of inflammation. The potential links between inflammatory properties of diet and adipokines as well as insulin resistance (IR) warrant further investigation. Therefore, this study aimed to examine the associations of the dietary inflammatory index (DII) with serum chemerin, omentin, and lipopolysaccharide-binding protein (LBP) as well as IR among apparently healthy obese adults.Design: In this cross-sectional study, 171 abdominally obese subjects were recruited in the northwest of Iran. Demographic data, dietary intake, anthropometric indices, and physical activity (PA) were assessed. DII scores were calculated based on dietary intake, using a validated 168-item food frequency questionnaire (FFQ). Basal blood samples were collected to determine the biochemical parameters. A linear regression test with adjusted beta estimates was applied for data analysis.Result: Compared to those with higher DII score, the group with lower DII score (anti-inflammatory diet) had higher protein (83.62 ± 36.42 g vs. 71.61 ± 25.94 g) and lower carbohydrate (325.00 ± 125.76 g vs. 378.19 ± 137.69 g) intake. Participants with higher DII score had lower consumption of polyunsaturated and monounsaturated fats as well as fiber and higher saturated fats (p < .001). Those with elevated DII score had higher levels of chemerin (p = .034) and LBP (p = .040), compared to those with lower DII. Omentin showed no significant differences between groups with different DII scores. Additionally, people with a more proinflammatory diet had higher FBS (p = .005); however, other markers of IR did not differ by DII scores.Conclusions: The results suggest that increased inflammatory potential of diet, as indicated by higher DII score, is associated with elevated levels of chemerin and LBP. While DII was positively associated with FBS, no significant correlation was found for insulin and other indices of IR. [ABSTRACT FROM AUTHOR]

Introduction. In Poland, an increasing number of patients are hospitalized due to liver diseases. One of the common liver diseases is cirrhosis, which can be caused by alcohol, viral hepatitis, autoimmune processes and metabolic diseases. Materials and method. The study included 99 patients with alcoholic cirrhosis from the Lublin region of Eastern Poland. The control group consisted of 20 healthy individuals without liver disease who did not abuse alcohol. The concentrations of serum kallistatin and chemerin were determined using ELISA kits. Objective. The aim of the study is to evaluate serum levels of kallistatin and chemerin in patients with different stages of alcoholic liver cirrhosis. Results. The highest chemerin level was found in the control group - 182.6±80.4 ng/ml. In other stages of liver cirrhosis, the following levels were observed: 175.7±62.7 ng/ml in Child-Pugh stage A (Ch-P A), 150.2±59.7 ng/ml in Ch-P B and 110.3±73.6 ng/ml in Ch-P C. Significant differences in chemerin levels between controls and Ch-P C patients (p=0.01), as well as between the Ch-P A patients and Ch-P C patients (p=0.02), were demonstrated. The highest kallistatin level was demonstrated in the control group - 8.2±3.5 µg/ml. In other stages of liver cirrhosis, the following concentrations were found: 7.2±27 µg/ml in Ch-P A, 4.4±2.2 µg/ml in Ch-P B and 3.5±1.9 µg/ml in Ch-P C (Tab. 3). Statistically significant differences were observed between controls and Ch-P B patients (p<0.001), controls and Ch-P C patients (p<0.001), Ch-P A and Ch-P B patients (p=0.01), as well as Ch-P A and Ch-P C patients (<0.001). Conclusions. The levels of chemerin and kallistatin decrease with progression of liver damage during alcoholic liver cirrhosis. The impairment of its synthetic function leads to reductions in levels of the adipokines studied. [ABSTRACT FROM AUTHOR]

Limited studies investigated the effects of long-term ozone exposure on cardiometabolic health. We aimed to examine the association of long-term ozone exposure with a range of cardiometabolic diseases, as well as the subclinical indicators in Eastern China. The study included 202,042 adults living in 11 prefecture-level areas in Zhejiang Province between 2014 and 2021. Using a satellite-based model with a 1 × 1 km spatial resolution, we estimated residential 5-year average ozone exposures for each subject. Mixed-effects logistic and linear regression models were applied to explore the associations of ozone exposure with cardiometabolic diseases and subclinical indicators, respectively. We found that a 9% [95% confidence interval (95% CI): 7–12%] higher in odds of cardiometabolic disease per 10 μg/m3 increase in ozone exposure. Specifically, we also found higher prevalence of cardiovascular diseases (15%), stroke (19%), hypertension (7%), dyslipidemia (15%), and hypertriglyceridemia (9%) associated with ozone exposure. However, we did not find significant associations between ozone exposure and coronary heart disease, myocardial infarction, or diabetes mellitus. Long-term ozone exposures were also significantly associated with adverse changes in systolic blood pressure, diastolic blood pressure, total serum cholesterol, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, glucose concentration, and body mass index. Our results showed that people with lower education levels, those over 50 years old, and those who were overweight or obese were more susceptible to the effects of ozone on cardiometabolic diseases. Our findings demonstrated the detrimental effects of long-term ozone exposure on cardiometabolic health, emphasizing the need for ozone control strategies to reduce the burden of cardiometabolic diseases. [Display omitted] • Increase risk of some cardiometabolic diseases associated with O 3 exposure. • Ozone exposures were associated with adverse changes in some subclinical indicators. • More prominent odds of cardiometabolic diseases under higher ozone concentration. • People with characteristics such as aged 50 years and older were more susceptible. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The purpose of the present study was to explore the mechanism of action of the adipokine chemerin in osteoarthritis (OA) by means of an in vitro OA model. MATERIALS AND METHODS: Primary chondrocytes were isolated from normal rats. The chondrocytes were stimulated with interleukin 1 beta (IL-1β, 10 μg/L) to establish a model of induced OA. Chemerin was administered to cells of this model. After culture of the chondrocytes in the presence of chemerin for 48 h, the expression of the genes related to OA occurrence and protection, matrix metalloproteinase-1 (MMP-1), matrix metalloproteinase-3 (MMP-3), and matrix metalloproteinase-13 (MMP-13) was examined. Western blot was then performed to analyze the phosphorylation of the AKT and extracellular signal-regulated kinase (ERK) proteins in chondrocytes. RESULTS: Stimulation of chondrocytes with IL-1β markedly reduced the proliferative capability of chondrocytes. Chemerin (5 μM) also significantly decreased the proliferative capability of chondrocytes. The combined administration of IL-1β and chemerin induced an even greater reduction in the proliferative capability of chondrocytes. Polymerase chain reaction (PCR) results showed that both IL-1β and chemerin reduced the expression of the protective genes in OA (MMP-1, MMP-3, and MMP-13). Also, the stimulation with IL-1β and chemerin significantly enhanced the phosphorylation of AKT/ERK in chondrocytes. CONCLUSIONS: This adipokine induces changes in the metabolic and proliferative capabilities of chondrocytes by increasing the phosphorylation of AKT/ERK, thereby inducing OA or aggravating the symptoms of OA. [ABSTRACT FROM AUTHOR]

Copyright of Pediatric Endocrinology, Diabetes & Metabolism is the property of Termedia Publishing House and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Shanghai Physical Education Institute / Shanghai Tiyu Xueyuan Xuebao is the property of Shanghai Physical Education Institute and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

OBJECTIVE: Chemerin is believed to be a mediator for the adipose tissue inflammation that occurs in obesity. The present study compared chemerin levels between healthy and type 2 diabetic women matched for age and body composition. We also aimed to assess the relationship of serum chemerin levels with body composition, insulin resistance, dyslipidemia, and diabesity. PATIENTS AND METHODS: This observational case-control study was conducted at the Departments of Physiology and Medicine, Saud University Riyadh, Saudi Arabia, from September 2013 to April 2014. A total of 100 subjects were recruited, including 51 adult diabetic females, and a control group consisting of 49 healthy females. Finally, 80 subjects were selected as per inclusion criteria. In the finally selected group, 45 of were type 2 diabetics and 35 were healthy subjects matched for age, body mass index (BMI) and body composition with age ranging between 30-65 years. Body composition analysis was estimated using bioelectrical impendence analyzer. Fasting venous blood samples were analyzed for glycemic markers, lipids, and chemerin. Insulin resistance and sensitivity indices were calculated by HOMA-IR and QUICKI using standard formulas. RESULTS: The two groups were matched for age, BMI, body fat percentage (BF%), basal metabolic rate (BMR), truncal fat and waist hip ratio (WHR). Serum chemerin levels were higher in diabetics than controls (p=0.001). Systolic blood pressure, weight, fat mass and visceral fat were found to be significantly higher in diabetics when compared to controls. Fasting blood glucose (FBG), glycosylated hemoglobin (HbA1c), low-density lipoprotein (LDL), triglycerides (TG), insulin and HOMA-IR were significantly higher in diabetics compared to controls. While QUICKI and HDL were significantly lower in diabetics compared to controls. Chemerin levels correlated positively with age (r=0.300, p=0.007), waist hip ratio (r=0.250, p=0.026), weight (r=0.270, p=0.016), BMI (r=0.334, p=0.003), BF% (r=0.325, p=0.003), fat mass (r=0.250, p=0.026), visceral fat (r=0.356, p=0.001), truncal fat mass (r=0.245, p=0.030), truncal fat % (r=0.249, p=0.027), serum basal insulin levels (r=0.354, p=0.001) and HOMA IR (0.275, p=0.015), while it correlated inversely with QUICKI (r=-0.283*, p=0.012). In multiple linear regression analysis age (r=0.236, p=0.023), BF% (r=0.265, p=0.014) and basal insulin levels (r=0.265, p=0.014) were independent predictors of chemerin. CONCLUSIONS: Serum chemerin levels are elevated in patients with type 2 DM compared to healthy control subjects and are positively correlated with adiposity and Insulin resistance in patients with type 2 DM. [ABSTRACT FROM AUTHOR]

Purpose: Chemerin has been suggested to be linked to insulin resistance and type 2 diabetes mellitus (T2DM). However, the relationship between visceral adiposity and chemerin levels remains unclear in subjects with T2DM. In this study, we investigated the relationship between serum chemerin levels and visceral adiposity. Materials and Methods: This study included 102 subjects newly diagnosed with T2DM. The relationships between serum chemerin levels and clinical and biochemical parameters were examined. Multiple linear regression analysis was performed to determine the predictable factors of serum chemerin levels. Results: Serum chemerin levels showed significant positive correlations with body mass index (BMI), waist circumference (WC), visceral fat thickness (VFT), insulin levels, the homeostasis model assessment of insulin resistance, and levels of triglycerides (log-transformed) and high-sensitivity C-reactive protein, while showing significant negative correlations with high-density lipoprotein cholesterol. After adjusting for BMI and WC, VFT showed a significant relationship with serum chemerin levels (r=0.222, p=0.027). Moreover, VFT was an independent predictive factor of serum chemerin levels (β=0.242, p=0.041). Conclusion: We demonstrated that chemerin is linked to metabolic syndrome components. Moreover, serum chemerin levels were associated significantly with obesity, especially visceral adipose tissue, in subjects with T2DM. [ABSTRACT FROM AUTHOR]

Cholesterol efflux capacity (CEC) as a measure of high-density lipoprotein functionality is independently and inversely associated with increased risk of cardiovascular events and mortality, and advanced plaque morphology. Adipokines, adipose tissue-derived factors, can influence systemic lipoprotein metabolism, and participate in the regulation of vascular function and inflammation. We aimed to investigate the association between CEC and circulating adipokine levels (anti-inflammatory adiponectin, and pro-inflammatory chemerin and resistin) in subjects with severe carotid atherosclerotic disease and evaluate its impact on post-surgical outcomes. This is a cross-sectional study with a 5-year follow-up component. Consecutive patients with severe carotid atherosclerosis scheduled for a carotid endarterectomy were recruited from hospital-based centres in Montreal, Canada (n = 285). Fasting blood samples were collected pre-operatively and used to measure plasma total and high-molecular weight (HMW) adiponectin, chemerin, and resistin, and to perform cholesterol efflux assays in J774 macrophage-like cells. Five-year post-surgery outcomes were obtained through medical chart review. Subjects had a mean age of 70.1 ± 9.4, were 67.0 % male, had various comorbidities (hypercholesterolemia [85.3 %], hypertension [83.5 %], type 2 diabetes [34.5 %], coronary artery disease [38.6 %]), and previously experienced cerebrovascular symptomatology (77.9 %). CEC was independently and positively associated with total and HMW adiponectin levels (ß [95 % confidence interval]; 0.216 [0.134–0.298] and 0.107 [0.037–0.176], respectively) but not with chemerin or resistin. Total adiponectin had the greatest association accounting for 8.3 % of the variance in CEC. Interaction regression models demonstrated a significant interaction between adiponectin and chemerin in increasing CEC. Notably, with each unit increase in CEC there was a 93.9 % decrease in the odds of having an ischemic cerebrovascular event 5 years post-surgery (0.061 [0.007–0.561]). Our findings demonstrated circulating adiponectin to have a strong association with increased CEC in subjects with severe carotid atherosclerosis and high CEC to be associated with more favourable post-surgical outcomes. These findings reflect the importance of adipose tissue health in influencing CEC levels and atherosclerotic cardiovascular disease risk. Adipose tissue secretes anti-inflammatory (adiponectin) and pro-inflammatory factors (chemerin and resistin). Circulating levels of lower- and higher-molecular weight (LMW and HMW) isoforms of adiponectin were significantly and positively associated with increased cholesterol efflux capacity (CEC). In contrast, chemerin and resistin exhibited a negative, however non-significant association with increased CEC. Significant and positive interactions between adiponectin and chemerin were observed in increasing CEC. In addition, increased CEC was significantly associated with reduced post-surgical risk for ischemic cerebrovascular events (stroke, transient ischemic attack, amaurosis fugax), MACE (total death, myocardial infarction [MI], any ischemic cerebrovascular event), and total adverse events (total death, MI, any ischemic cerebrovascular event, and restenosis) 5 years post-surgery. CEC is depicted as lipid-poor apoA-I acquiring free cholesterol through ABCA1 to generate HDL particles to alleviate the cellular lipid overload in macrophages. Asterix (*) denotes statistically significant associations. [Display omitted] • CEC is positively associated with total and HMW adiponectin, but not with chemerin or resistin. • Total adiponectin had the greatest association accounting for 8.3 % of the variance in CEC. • A synergistic interaction between adiponectin and chemerin was observed in raising efflux levels. • High CEC was associated with more favourable post-surgical outcomes. [ABSTRACT FROM AUTHOR]

Summary Aims Serum chemerin concentrations are elevated in obese individuals and may play a role in type 2 diabetes. Exercise improves insulin sensitivity, which may be related to changes in chemerin. This study explored how an acute bout of aerobic exercise affected chemerin levels in non-diabetic obese adults. Methods Blood samples from 11 obese adults were obtained during two separate conditions: sedentary (SED) and exercise (EX; 60–65% VO 2peak ). Samples were drawn at baseline, immediately following exercise and hourly for an additional 2 h. ANOVA was used to test for differences in chemerin between conditions. Results Unadjusted analysis showed no difference in overall change (baseline to 2 h post) in chemerin between conditions. During the 2-h post-exercise period, chemerin decreased to 12% below baseline, compared to a 2.5% increase above baseline during that time period on the sedentary day ( p = 0.06, difference in post-to-2 h change between conditions). Controlling for homeostatic model assessment of insulin resistance (HOMA-IR), a significant difference existed between EX and SED in the change in chemerin from baseline to 2-h post ( p = 0.02). Stratified analyses showed a consistent exercise-induced decrease in chemerin among non-insulin resistant subjects, while chemerin increased during exercise among insulin resistant subjects, and then decreased post-exercise. Conclusion An acute bout of exercise in obese individuals may elicit a drop in chemerin levels during the post-exercise period, and this response may vary based on insulin resistance. [ABSTRACT FROM AUTHOR]

Summary Background “Chemerin” is a multifuntional peptide involved in lipid and glucose metabolism. Elevated levels of this peptide have been associated with insulin resistance and systemic inflammation. This study aims to identify whether Chemerin along with other inflammatory markers (TNFα and hsCRP) can discriminate subjects with subclinical diabetes. Methodology/findings Fifty-two asymptomatic healthy volunteers and 22 chronic diabetics (T2DM) were enrolled in a cross sectional study design. They were subjected to a 75 g oral glucose tolerance test [OGTT (2-h glucose > 200 mg/dL)] and were then classified as either newly diagnosed diabetics (NDM) ( n = 23) or healthy controls ( n = 29). Our results showed a higher Chemerin level in NDM ( p < 0.01; MWU) compared to controls and previously diagnosed DM. Using ROC analysis, Chemerin level in NDM and T2DM had AUC of 0.963 and 0.764 respectively, compared to healthy controls. We suggest that the cut off of 13.7 ng/ml of Chemerin can discriminate 73% of NDM subjects with impaired glucose level with 91% and 96% of sensitivity and specificity respectively. Elevated serum Chemerin in NDM group is a surrogate of impairment in glucose metabolism in obese individual. Conclusions Chemerin along with other inflammatory biomarkers suggest an ongoing inflammatory process in a high risk obese group that indicates a pre-diabetic state. [ABSTRACT FROM AUTHOR]

Objective: Our objective was to evaluate the relationship of plasma level of chemerin and vaspin to early atherosclerotic changes and cardiac autonomic neuropathy (CAN) in adolescent type 1 diabetic patients. Patients and methods: The study included 62 type 1 diabetic patients and 30 healthy volunteers of the same age and sex. Blood samples were taken for assessment of chemerin, vaspin, asymmetric dimenthylarginine (ADMA), and oxidized low-density lipoprotein (OxLDL) by enzyme-linked immunosorbent assay (ELISA) technique. Also, blood samples were taken for analysis of glycosylated hemoglobin; lipid profiles and urine samples were taken for assessment of albumin/creatinine ratio. Twenty-four-hour holter [for assessment of time domain heart rate variability (HRV)] and carotid intima-media thickness (CIMT) were also done. The t-test or Mann-Whitney U-test for independent variables, Pearson's or Spearman's correlation, and stepwise multiple regression analysis were used. Results: The mean age of diabetic patients was 16.3±1.5 years, and mean duration of diabetes was 9.4±2.9 years. Chemerin, vaspin, OxLDL, and albumin/creatinine ratio were significantly higher, whereas ADMA was significantly lower than the controls. By stepwise multiple regression analysis, vaspin had a relation with a standard deviation difference RR (SDARR) and waist/height ratio. Conversely, chemerin had a relation with OxLDL. Albumin/creatinine ratio had a significant positive correlation with chemerin and OxLDL, and a negative correlation with ADMA. Conclusions: Type 1 diabetic patients had impaired time domain HRV associated with increased CIMT. Vaspin had a significant relation to CAN, whereas chemerin, ADMA, and OxLDL had a significant correlation with albumin/creatinine ratio that reflects their role in renal affection. [ABSTRACT FROM AUTHOR]

Background Psoriasis is a chronic inflammatory dermatosis that affects about 2–3% of the general population. We aimed to investigate the relationship between serum chemerin and calprotectin levels and the inflammatory markers that can lead to oxidative damage. Methods Fifty patients with psoriasis and 30 healthy controls were included in the study. Levels of chemerin and calprotectin were measured in addition to levels of C-reactive protein, the erythrocyte sedimentation rate, and the white blood cell count to evaluate inflammation. Results According to our findings, chemerin and calprotectin levels in the patient group were significantly higher than in the control group ( p < 0.01 and p < 0.001, respectively). Patients with psoriasis were divided into three groups based on the Psoriasis Area and Severity Index: mild, moderate, and severe. The chemerin levels in the severe and moderate groups were significantly higher than in the mild group ( p < 0.01 and p < 0.05, respectively). The calprotectin levels in the severe psoriasis group were also significantly higher than in the mild group ( p < 0.05). Similarly, the erythrocyte sedimentation rate and levels of fibrinogen and C-reactive protein were significantly higher in patients with psoriasis than in the control group ( p < 0.05, p < 0.01, and p < 0.001, respectively). Stepwise regression analysis was used to assess the individual contributing factors. Among these contributing factors, the chemerin levels were observed to be positively correlated with both the Psoriasis Area and Severity Index ( R 2 = 0.111) and the calprotectin level ( R 2 = 0.445). Calprotectin was observed to be positively correlated with both the C-reactive protein ( R 2 = 0.119) and chemerin levels ( R 2 = 0.315). Conclusion The chemerin and calprotectin levels in patients with psoriasis showed that there is an inflammatory process in psoriasis and that these markers are useful indicators of the severity of psoriasis. [ABSTRACT FROM AUTHOR]

Objective To know the difference between chemerin and adipocyte fatty acid-binding protein (AFABP) levels in obese individuals with positive Toxoplasma gondii ( T. gondii ) immunoglobulin G (IgG) compared with negative T. gondii IgG. Methods This study is a cross-sectional study by using consecutive sampling methods conducted from January to April 2013. The subjects were 57 obese individuals who were divided into obese group of positive and negative T. gondii IgG. The level of chemerin, AFABP and T. gondii IgG was done by ELISA. The data were analyzed by independent t test. Results The results showed that the level of chemerin of positive T. gondii IgG group was significantly higher than the negative T. gondii IgG group [(70.0 ± 16.5) vs. (64.4 ± 16.1) pg/mL; P = 0.003], but there was not significant AFABP difference between seropositive and negative IgG groups [(83.6 ± 41.9) vs. (74.2 ± 36.7) pg/mL; P = 0.598]. Conclusions It can be concluded that the level of chemerin of seropositive T. gondii IgG was higher than that in the negative T. gondii IgG group. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Chemerin is a recently identified adipocytokine that has been positively correlated with the presence and severity of coronary artery disease (CAD). However, no studies have examined circulating chemerin levels as a predictor of acute coronary syndrome (ACS). The purpose of this study is to evaluate whether chemerin levels predict the onset of ACS. Materials/Methods: We studied 90 men whose serum had been collected at least 2years before the development of ACS, and 162 controls matched with the cases in a 1:2 fashion for age and year of collection. The mean age of the cohort was 66.3±9.6years (range 34–84years). Serum chemerin levels were measured with a commercially available enzyme-linked immunosorbent assay. Results: Age was positively associated with chemerin levels (r=0.39, p<0.001). Logistic regression analysis, adjusting for years since blood collection, demonstrated a null association between chemerin levels and the odds ratio for development of ACS (OR: 0.99, 95% CI [0.99–1.001]). This association remained null after adjusting for age (OR: 0.99 95% CI [0.99–1.001]). Conclusions: Although cross-sectional and case–control studies suggest a positive association between chemerin levels and CAD, we demonstrate that chemerin levels do not predict the development of ACS. [Copyright &y& Elsevier]

Abstract: Introduction: Adipose tissue secretes numerous bioactive peptides, collectively termed “adipocytokines” or “adipokines”. Adipokines act in a paracrine, autocrine, or endocrine manner and regulate several physiological and pathological processes. Increasing evidence indicates that adipokines are implicated also in several malignancies, including lung cancer as well. Aim: The aim of this study is to summarize data concerning adipokines in lung cancer pathogenesis, prognosis and survival; the role of adipokines in lung cancer cachexia is also examined. Materials and Methods: A systematic literature search was performed in the electronic database of Medline. Several studies and review articles met the inclusion criteria. Results: Leptin and adiponectin are the best studied adipokines. The majority of the relevant studies has investigated the potential correlations mainly between leptin, adiponectin, and sometimes also resistin, and nutritional status, systemic inflammation of lung cancer or lung cancer cachexia and have also assessed their prognostic significance. Few other studies have studied genetic variations in leptin, leptin receptor and adiponectin genes and their association with lung cancer susceptibility and prognosis. The ongoing list of adipokines associated with lung cancer also includes resistin, chemerin, and visfatin. Conclusions: Increasing evidence points to the involvement of certain adipocytokines in lung cancer development, progression and prognosis. No conclusive evidence exists so far with regards to the role of adipocytokines in lung cancer cachexia. Future, longitudinal studies are warranted in order to clarify the role of adipocytokines in lung cancer and also uncover adipocytokines as novel therapeutic targets. [Copyright &y& Elsevier]

Objective: Irisin is a recently discovered myokine proposed to increase thermogenesis-related energy expenditure and improve metabolism. We aimed to comparatively evaluate serum irisin levels in patients with biopsy-proven nonalcoholic fatty liver disease (NAFLD) vs. controls and study their association with disease severity. Methods: Fifteen and 16 consecutively enrolled patients with biopsy-proven nonalcoholic simple steatosis (NAFL) and steatohepatitis (NASH), respectively, and 24 lean and 28 obese controls without NAFLD were recruited. Irisin, established adipokines and biochemical tests were measured. Results: Serum irisin levels were statistically different in obese controls (33.7±2.7ng/mL; p<0.001) and patients with NAFL (30.5±1.5ng/mL; p<0.001) and NASH (35.8±1.9ng/mL; p=0.001) compared with lean controls (47.7±2.0ng/mL), but were similar among patients with NAFL, NASH and obese controls. This difference remained significant after adjustment for body mass index (or waist circumference), gender, age, insulin resistance (assessed by HOMA-IR or QUICKI), exercise and time since blood collection. Serum leptin and adiponectin, but not irisin, levels were independently from BMI correlated with insulin resistance and cardiometabolic factors. Serum irisin tended to be higher in patients with (36.7±2.4ng/mL) than without (30.8±1.2ng/mL; p=0.02) portal inflammation and independently associated with the latter; these data need to be confirmed by future studies. Conclusions: Serum irisin levels differ between lean controls and obese controls or NAFLD patients. Despite similar circulating irisin levels between NAFL and NASH groups, irisin may be independently and positively associated with the presence of portal inflammation. Future clinical and mechanistic studies are needed to confirm and extend these data. [ABSTRACT FROM AUTHOR]

Once considered a passive reservoir for lipid storage and an inert provider of thermal/ mechanical insulation, white adipose tissue (WAT) is presently seen as a highly dynamic endocrine organ that actively modulates a variety of physiologic processes, including energy balance, food intake, inflammation, immunity, metabolism, as well as cardio-vascular (CV) and neuroendocrine homeostasis. Actually, other than fatty acids and lipid moieties, WAT secretes a wide range of bioactive factors, considerably different in therms of structure and functions, including cytokines, chemokines, growth factors, complement system molecules, acute phase reactants, and hormones, among which the products predominantly or exclusively synthesized by and released from adipocytes are categorized as "adipokines". The adipokine expression is intimately linked to various parameters of adiposity (such as total bodyfat, percentage of bodyfat, and fat distribution), resulting generally (with very few exceptions, such as adiponectin, omentin, and zinc-α2-glycoprotein) in positive correlation with WAT mass. The adipokine profiles undergo opposite changes in WAT excess or deficiency/dystrophy. In obese subjects, the altered adipokine network strikingly contributes to the development of systemic low-grade inflammation, as well as of obesity-related metabolic/CV comorbidities, that collectively define the so called metabolic syndrome. Adipokine dysregulation has been also observed in patients with chronic inflammatory / autoimmune disorders, such as connective tissue diseases, and adipokine pathway targeting has been thought to represent a potential innovative therapeutic perspective. Comprehensive advances in understanding the WAT biology and signaling may provide crucial insights into the physiopathology of the whole body homeostasis. [ABSTRACT FROM AUTHOR]

Obesity is one of the risk factors of metabolic diseases. Decreased sensitivity to insulin or impairment of the insulin signaling pathway may affect the metabolism of adipose tissue. Bisphenol F (BPF) has been widely used in various products as a substitute for bisphenol A (BPA). BPA has been defined as "obesogen". However, knowledge about the correlation between BPF and obesity is very limited. This study was aimed to explore the effects of BPF on glucose metabolism and insulin sensitivity in mammalian tissues, using a mouse 3T3-L1 adipocyte line as the model. Differentiated 3T3-L1 adipocytes were treated with BPF at various concentrations for 24 h or 48 h, followed by the measurement of cell viability, lipid accumulation, expression levels of adipocytokines, glucose consumption, and impairment of the insulin signaling pathway. The results indicated that BPF had no effect on the size of 3T3-L1 adipocytes, but the expression of leptin, adiponectin and apelin was decreased, while that of chemerin and resistin was increased after 48 h of BPF treatment. Moreover, BPF inhibited the glucose consumption, the expression of GLUT4, and its translocation to the plasma membranes in 3T3-L1 adipocytes. Western blot analysis indicated that the activation of IRS-1/PI3K/AKT signaling pathway was inhibited by BPF, which resulted in reduced GLUT4 translocation. In conclusion, our data suggest that exposure of adipocytes to BPF may alter the expression of calorie metabolism-related adipokines and suppress insulin-stimulated glucose metabolism by impairing the insulin signaling (IRS-1/PI3K/AKT) pathway. • Bisphenol F had no effect on the lipid accumulation of 3T3-L1 adipocytes. • Bisphenol F influenced the expression of adipokines in 3T3-L1 adipocytes. • Bisphenol F could inhibit glucose metabolism in 3T3-L1 adipocytes. • Bisphenol F could inhibit the glucose metabolism via glucose transporter type 4. • Bisphenol F could inhibit the IRS-1/PI3K/AKT pathway in insulin-treated adipocytes. [ABSTRACT FROM AUTHOR]

Abstract: Background: Chemerin is a novel adipokine that regulates adipocyte development and metabolic function and glucose metabolism. Our aim was to determine the effect of chemerin and its receptor, chemokine-like receptor-1, in obesity-associated low-grade chronic inflammation, exploring its circulating and gene expression levels in obesity and the effect of weight loss and to analyze the effect of the stimulation with tumor necrosis factor-α in human visceral adipocytes at a University hospital. Methods: We included 52 women (16 lean and 36 obese) in the present study. The plasma concentrations of chemerin and the expression levels of chemerin and its receptor in visceral adipose tissue were analyzed. The chemerin concentrations were also measured before and after weight loss achieved by Roux-en-Y gastric bypass (n = 26). Results: The circulating concentrations and visceral adipose tissue expression of chemerin were increased in obese patients (P < .01) and were associated with well-established markers of inflammation (P < .001). Gene expression levels of chemokine-like receptor-1 followed the same trend and were upregulated (P < .05) in human obesity. Elevated chemerin levels in obese patients did not change after Roux-en-Y gastric bypass weight loss. Tumor necrosis factor-α treatment significantly enhanced (P < .05) the mRNA levels of chemerin in human visceral adipocytes, but the gene expression levels of chemokine-like receptor-1 were not affected. Conclusion: The increased levels of chemerin in obesity and its positive association with inflammation suggest a role for this chemoattractant protein in the changes that take place in visceral adipose tissue in the presence of energy surplus, establishing a link between inflammation and the greater risk of the development of metabolic disease. [Copyright &y& Elsevier]

Abstract: Background: Chemerin is an adipocytokine that is expressed in different fat deposits and has been shown to play an important role in adaptive and innate immunity due to its activity as a chemoattractant. Chemerin acts as a ligand for the G protein-coupled receptor chemokine - like receptor 1 (CMKLR1). Chemerin has been shown to regulate the development and metabolic function of adipocytes, liver and muscle tissue. Objective: There is evidence indicating that several adipocytokines play an important role in placenta. This study aimed to investigate the regulation of chemerin in rat and human placentas throughout gestation. Design and setting: Chemerin was examined in rat and human placentas using immunohistochemistry. The chemerin expression pattern in the placenta and adipose tissue of female Sprague Dawley rats on days 12, 16, 19 and 21 of gestation (each of these days represents a group of 12 rats) was determined using TaqMan probe-based quantitative real-time PCR. Rat chemerin serum levels were analyzed with ELISA on days 8, 12, 16, 19 and 21 and compared to virgin controls. Results: Chemerin expression was detected in the cytoplasm of rat placental trophoblastic cells and third trimester human placental cytotrophoblast and Hofbauer’s cells. The serum chemerin levels of rats decreased significantly as gestation progressed. Furthermore, placental chemerin mRNA levels rose significantly at day 16 of gestation and decreased significantly towards the end of the gestation period. Conclusion: Taken together, this data suggests that chemerin may be an important regulator of maternal-fetal metabolism and metabolic homeostasis during pregnancy. [Copyright &y& Elsevier]

Background and objective Chemerin was recently found a chemoattractant just like a chemotatic factor. It can induce immune chemotaxis to dendritic cells and macrophages by binding to its receptor ChemR23. It has been known that the activation of Chemerin could enhance the phagocytosis and antigen presentation of APC. Along with this observation, the contribution of Chemerin in the genesis and development of a tumor attracts more attention. We explored the relation between Chemerin and lung cancer through detecting the expression of Chemerin in peripheral blood of patients. Methods The experiment selected samples of lung cancer patients and normal people. The concentration of Chemerin in peripheral blood was detected by ELISA method. T test was used to compare the statistic difference. We compared the concentration of Chemerin in peripheral blood with age, sex, pathological type, degree of differentiation, metastasis of lymphonode, UICC staging and other clinicopathological index, and analyzed by t test and one-way ANOVA. Results The concentration of Chemerin in peripheral blood of 42 patients with lung cancer (1 965.81 pg/mL±374.03 pg/mL) were significantly higher than the concentration of 31 healthy examination (1 111.44 pg/mL±250.72 pg/mL)(P<0.001). The concentration of Chemerin in peripheral blood of patients with lung cancer had no relationship with clinicopathological factors. Conclusion Chemerin has the potential to lung cancer diagnosis as a marker. [ABSTRACT FROM AUTHOR]

Background: Chemerin is a novel adipokine that has been suggested to play an important role in the pathogenesis of the metabolic syndrome. The aim of our study was to evaluate serum chemerin as a marker of the metabolic syndrome and to assess its predictive accuracy in a Caucasian population. Methods: The study was designed as a cross-sectional study. Anthropometric measurements and serum analyses were done for Body Mass Index, waist circumference, chemerin, insulin, triacylglycerides, total cholesterol, HDLcholesterol, LDL-cholesterol, uric acid, and glucose in 55 non-obese healthy subjects and 181 subjects at risk for the metabolic syndrome. ROC curves were determined and the Chi-squared test was used to analyse the data. Results: Compared with healthy controls, subjects with suspected metabolic syndrome had significantly higher chemerin serum levels (medians: 266.0 vs.192.5 μg/l; P < 0.01). After further chemerin adjustment, the difference between the subgroups persisted. Chemerin serum levels correlated with age (r = 0.23), serum glucose (r = 0.23), HDL-cholesterol (r = -0.19), triacylglycerides (r = 0.22), systolic and diastolic blood pressure (r = 0.40; r = 0.24) and the number of metabolic syndrome risk factors (r = 0.47). At a serum chemerin cut-off level of 240 μg/l, the presence of the metabolic syndrome was diagnosed with 75 % sensitivity and 67 % specificity. Conclusion: In conclusion, serum chemerin levels are associated with the characteristics of the metabolic syndrome and could be an independent marker of this disorder in a Caucasian population. [ABSTRACT FROM AUTHOR]

It was reported that chemerin as an adipocyte-secreted protein could regulate bone resorption and bone formation. However, the specific molecular and gene mechanism of the chemerin role is unclear. The aim of this study is to evaluate the role of chemerin in bone metabolism. In the present study, we investigated the effects of chemerin on bone remodeling in rarres2 knockout (Rarres2−/−) mice and examined the role of chemerin as a determinant of osteoblast and osteoclast differentiation in Mc3t3-E1 and Raw264.7 cell lines. The results showed that the bone mineral density and volume score, trabecular thickness, weight and bone formation marker BALP increased, but Tb.Sp and bone resorption marker TRACP-5b decreased in Rarres2−/− mice. Furthermore, the mRNA and protein expression of biomarkers of osteoblasts (β-catenin, RANKL and OPG) significantly increased, but those of osteoclasts (CTSK and RANK) decreased in Rarres2−/− mice. In vitro, chemerin markedly suppressed β-catenin and OPG, but increased RANKL, CTSK and RANK expression. Moreover, knockdown of chemerin using RNA interference enhanced osteoblastogenesis genes and inhibited osteoclastogenesis genes in Mc3t3-E1 and Raw264.7 cells. Taken together, these data suggest an inhibitive effect of chemerin on osteoblast differentiation and proliferation through inhibition of Wnt/β-catenin signaling, as well as a stimulative effect of chemerin on osteoclast differentiation and proliferation via activation of RANK signaling. The maintenance of a low chemerin level may be a strategy for the prevention and treatment of osteoporosis. [Display omitted] • The bone mineral density and volume score and the trabecular thickness were significantly increased in Rarres2−/− mice. • Chemerin markedly suppressed β-catenin and OPG, and increased RANKL, CTSK as well as RANK expression. • The enhancement of osteoclastogenesis genes by chemerin were blocked by knockdown of chemerin in Raw264.7 cells. • An inhibitive effect of chemerin on osteoblast differentiation through inhibition of Wnt/β-catenin signaling. • The stimulative effect of chemerin on osteoclast differentiation and proliferation via activation of RANK signaling. [ABSTRACT FROM AUTHOR]

Fibronectin type IIIdomain-containing protein 4 (FNDC4) constitutes a secreted factor showing a high homology in the fibronectin type III and transmembrane domains with the exercise-associated myokine irisin (FNDC5). We sought to evaluate whether FNDC4 mimics the anti-obesity effects of FNDC5/irisin in human adipose tissue. Plasma and adipose tissue samples of 78 patients with morbid obesity undergoing bariatric surgery and 26 normal-weight individuals were used in the present study. Plasma FNDC4 was decreased in patients with morbid obesity, related to obesity-associated systemic inflammation and remained unchanged six months after bariatric surgery. Visceral adipose tissue from patients with morbid obesity showed higher expression of FNDC4 and its putative receptor GPR116 regardless of the degree of insulin resistance. FNDC4 content was regulated by lipogenic, lipolytic and proinflammatory stimuli in human visceral adipocytes. FNDC4 reduced intracytosolic lipid accumulation and stimulated a brown-like pattern in human adipocytes, as evidenced by an upregulated expression of UCP-1 and the brown/beige adipocyte markers PRDM16, TMEM26 and CD137. Moreover, FNDC4 treatment upregulated mitochondrial DNA content and factors involved in mitochondrial biogenesis (TFAM, NRF1 and NRF2). Human FNDC4 -knockdown adipocytes exhibited an increase in lipogenesis and a reduction of brown/beige-specific fat markers as well as factors involved in mitochondrial biogenesis. Taken together, the novel adipokine FNDC4 reduces lipogenesis and increases fat browning in human visceral adipocytes. The upregulation of FNDC4 in human visceral fat might constitute an attempt to attenuate the adipocyte hypertrophy, inflammation and impaired beige adipogenesis in the obese state. • Plasma FNDC4 levels are decreased in patients with obesity and type 2 diabetes. • FNDC4 and its receptor GPR116 are increased in visceral fat from obese patients. • Lipogenic, lipolytic and proinflammatory factors regulate FNDC4 in adipocytes. • FNDC4 inhibits lipogenesis, stimulates fat browning and mitochondrial biogenesis. [ABSTRACT FROM AUTHOR]

Preeclampsia represents a major pregnancy complication, associated with high rates of perinatal morbidity. The aim of this systematic review is to accumulate current literature evidence in order to examine the pattern of serum adipokine levels among preeclamptic women and asses their potential efficacy in the prediction of the disease. Medline, Scopus, CENTRAL, Clinicaltrials.gov and Google Scholar databases were systematically searched from inception. All observational studies reporting serum adipokine values among preeclamptic and healthy pregnant women were held eligible. A total of 163 studies were included, comprising 23,482 women. Leptin was evaluated in 91 studies and its values were found to be significantly elevated in preeclamptic women during all pregnancy trimester, independently of disease onset and severity. Preeclampsia was also associated with increased serum fatty acid binding protein-4 and chemerin levels, when measured both during the 1st and 3rd trimester. Data concerning the rest adipokines were either conflicting or limited to reach firm conclusions. Quality of evidence was evaluated to be high for leptin, moderate for serum fatty acid binding protein-4 and chemerin and low for the other adipokines. The existing evidence suggests that preeclampsia is linked to increased levels of leptin, chemerin and fatty acid binding protein-4 in all pregnancy trimesters and forms of the disease. Inconsistent data currently exists concerning the role of the other adipokines. Large-scale prospective studies should longitudinally evaluate the serum concentration of novel adipokines and define the optimal threshold and timing of measurement to be widely applied in clinical practice. • Current evidence suggests that leptin levels are higher in preeclamptic pregnancies. • Leptin increase is observed in all pregnancy trimesters and forms of the disease. • Serum fatty acid binding protein-4 and chemerin are increased in preeclampsia. • The existing evidence regarding the other adipokines is inconsistent. • Future cohorts should define the optimal thresholds to be widely applied. [ABSTRACT FROM AUTHOR]

Endothelium damage caused by Treponema pallidum is the key step in the systemic dissemination and pathophysiology of syphilis, particularly cardiovascular syphilis and neurosyphilis. However, the molecular mechanisms supporting endothelium damage of syphilis are undefined. The outer membrane proteins were thought to be involved. Tp92 was first identified as an outer membrane protein of T. pallidum. Homologous proteins to Tp92 play important roles in cell attachment, inflammation, and tissue destruction in other bacterial species. In this study, we investigated the effect of Tp92 on endothelial cells activation. The data showed that Tp92 induced chemerin production in activated endothelial cells. Endothelial cell-derived chemerin upregulated the expression of TNF-α and ICAM-1 in endothelial cells via CMKLR1. In addition, endothelial cell-derived chemerin promoted THP-1-derived macrophage migration towards endothelial cells. These findings suggest that Tp92 may play an important role in mediating endothelial cell activation by inducing the secretion of chemerin. [ABSTRACT FROM AUTHOR]

Timely resolution of pulp inflammation is a prerequisite for the healing of inflamed dental pulp. Stromal cells, particularly fibroblasts, play a critical role in the inflammation resolution process. Resolvin E1 (RvE1) is a lipid-derived endogenous proresolution molecule that mediates this resolution process. In the present study, we investigated the effects of RvE1 on dental fibroblasts during the pathogenesis of pulpitis. The pulp tissues in maxillary incisors of male Sprague-Dawley rats (N = 50) were exposed to the oral environment for 0, 9, 24, and 48 hours, after which they were treated with RvE1 or its vehicle. The inflammatory changes after 24 hours were assessed using hematoxylin-eosin staining, immunohistochemistry, enzyme-linked immunosorbent assay, and quantitative polymerase chain reaction. Chemerin receptor 23 (ChemR23) expression in rat pulp tissues and human dental fibroblasts was detected by immunofluorescence, Western blot analysis, and quantitative polymerase chain reaction. Finally, small interfering RNA-based knockdown studies were performed to evaluate the effects of RvE1 inhibition on proinflammatory genes and nuclear factor kappa B signaling of human dental pulp fibroblasts. Early treatment (within 24 hours after pulp exposure) with RvE1 promoted a decline in the number of inflammatory cells and gene expression of proinflammatory cytokines. Moreover, it reduced ChemR23 expression in the fibroblastlike cells of inflamed pulp tissues. In vitro , ChemR23 was widely expressed in human dental fibroblasts. RvE1 significantly suppressed cytokine production by fibroblasts, with down-regulation of the nuclear translocation of nuclear factor kappa B p65 in these cells. Knockdown of ChemR23 almost abolished the anti-inflammatory effect of RvE1. RvE1 can suppress the activation of dental pulp fibroblasts in a ChemR23-dependent manner and inhibit inflammation in the relevant early stages of pulpitis. [ABSTRACT FROM AUTHOR]

Aims The growing prevalence of obesity and its related metabolic disorders in adolescents shows the necessity of urgent focus on the related factors. Adipocytes secretions and their pro- or anti-inflammatory roles play effective roles in adipocytes metabolism. We assessed the relation between adiponectin, chemerin and lipid profile in hit phase of life. Methods This case–control study conducted on 78 adolescent girls, divided based on BMI percentile. Serum chemerin, adiponectin, lipid profile and body fat mass were measured. Data were analyzed using Pearson correlation test. The interactive relation between these variables was assessed using Structural Equation Modeling (SEM). Data were analyzed using SPSS software and AMOS software. Results Chemerin were correlated significantly with triglyceride ( r = 0.584 versus r = 0.319), HDL-cholestrol ( r = −0.323 versus r = −0.335), LDL-cholestrol ( r = 0.368 versus r = 0.327) and fat mass ( r = 0.372 versus r = 0.357) in obese versus non-obese girls; while the mentioned correlation were non-significant with total cholesterol in obese group ( r = 0.233 versus r = 0.336). Furthermore, there were significant association between adiponectin and triglyceride ( r = −0.404 versus r = −0.317), HDL-cholesterol ( r = 0.332 versus r = 0.316) and fat mass ( r = −0.529 versus r = −0.346) in obese versus non-obese girls, respectively. Conclusion There were positive associations between lipid profile components and serum chemerin levels. Adiponectin levels were in positive correlation with HDL-cholesterol concentrations. Chemerin showed positive correlations with potent health threatening components of lipid profile including triglyceride and cholesterol levels in adolescents. [ABSTRACT FROM AUTHOR]

Objective: Chemerin, a novel adipokine, has been implicated in adipogenesis, inflammation, and metabolism. The aims of this study were to determine the presence of chemerin in cord blood and its association with birthweight. Study Design: This cross-sectional study included the following: (1) twins with (n = 24) or without (n = 28) birthweight discordancy; and (2) singletons subclassified into small-for-gestational-age (SGA; n = 18); appropriate for gestational age (AGA; n = 33); and large-for-gestational-age (LGA; n = 8). Cord blood chemerin was determined. Parametric and nonparametric statistics were used for analysis. Results: The results of the study included the following: (1) within the discordant twins group, the median chemerin concentration was significantly lower in the SGA group than in their cotwins; (2) within singletons, the median chemerin concentration was significantly higher in the LGA than the AGA newborns; and (3) the regression model revealed that chemerin was independently associated with birthweight. Conclusion: Cord blood chemerin is present in cord blood and its concentrations are positively correlated with birthweight. These novel findings support a role of adipokines in fetal growth. [ABSTRACT FROM AUTHOR]