Role Of Chemerin Research Articles

The Role of Chemerin in Upper Gastrointestinal Cancer

The Role of Chemerin in Upper Gastrointestinal Cancer

Role of chemerin in the metabolic regulation of type 1 diabetes in children

Introduction and objective: Type 1 diabetes is one of the most common chronic diseases of childhood, leading to the development of chronic micro- and macrovascular complications. Recently, many researchers have been focusing their efforts on identifying new markers for the progression of this disease. It is known that adipokines play a significant role in the regulation of lipid and carbohydrate metabolism. The aim of this study was to evaluate the level of serum chemerin in children with type 1 diabetes and assess their correlation with body mass index, glycated haemoglobin, and lipid profile. Materials and methods: The study group included 40 children with newly diagnosed, 40 with long-term diabetes, and 14 children without diabetes as a control group. Chemerin levels were measured using a sandwich enzyme-linked immunosorbent assay. Results: We did not find any statistically differences in chemerin levels in the studied groups of children. In the group of patients with long-term, metabolically well-controlled diabetes, chemerin levels were higher in girls than in boys (p = 0.028). Moreover, no difference in chemerin levels was observed between the studied groups of children depending on the body mass index percentiles. A negative correlation was found between chemerin level and age in children with newly diagnosed diabetes and metabolically well-controlled diabetes. Conclusions: Our study provides new insights into the status of chemerin among paediatric patients with varying degrees of type 1 diabetes control. However, further research is needed involving larger groups of patients with differing degrees of sexual maturation and with the presence of microvascular complications.

Comparison of adipokines expression in adipose tissues of patients with coronary artery disease - Role of chemerin

Comparison of adipokines expression in adipose tissues of patients with coronary artery disease - Role of chemerin

Chemerin in caudal division of nucleus tractus solitarius increases sympathetic activity and blood pressure.

Chemerin is an adipokine that contributes to metabolism regulation. Nucleus tractus solitarius (NTS) is the first relay station in the brain for accepting various visceral afferent activities for regulating cardiovascular activity. However, the roles of chemerin in the NTS in regulating sympathetic activity and blood pressure are almost unknown. This study aimed to determine the role and potential mechanism of chemerin in the NTS in modulating sympathetic outflow and blood pressure. Bilateral NTS microinjections were performed in anaesthetized adult male Sprague-Dawley rats. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate (HR) were continuously recorded. Chemerin and its receptor chemokine-like receptor 1 (CMKLR1) were highly expressed in caudal NTS (cNTS). Microinjection of chemerin-9 to the cNTS increased RSNA, MAP and HR, which were prevented by CMKLR1 antagonist α-NETA, superoxide scavenger tempol or N-acetyl cysteine, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitors diphenyleneiodonium or apocynin. Chemerin-9 increased superoxide production and NADPH oxidase activity in the cNTS. The increased superoxide production induced by chemerin-9 was inhibited by α-NETA. The effects of cNTS microinjection of chemerin-9 on the RSNA, MAP and HR were attenuated by the pretreatment with paraventricular nucleus (PVN) microinjection of NMDA receptor antagonist MK-801 rather than AMPA/kainate receptor antagonist CNQX. These results indicate that chemerin-9 in the NTS increases sympathetic outflow, blood pressure and HR via CMKLR1-mediated NADPH oxidase activation and subsequent superoxide production in anaesthetized normotensive rats. Glutamatergic inputs in the PVN are needed for the chemerin-9-induced responses.

The role of chemerin in patients with reduced ovarian reserve and its impact on IVF success

The role of chemerin in patients with reduced ovarian reserve and its impact on IVF success

Neutrophils regulate tumor angiogenesis in oral squamous cell carcinoma and the role of Chemerin.

Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of the oral cavity. Tumor angiogenesis plays a crucial role in tumor progression. Studies have established the correlation between neutrophils and tumor angiogenesis in the tumor microenvironment. A previous study found that overexpression of Chemerin- in OSCC increased the infiltration of neutrophils in tumor tissues. This study aims to investigate the mechanisms underlying the regulation of the development and progression of OSCC, which have great significance in enhancing the postoperative survival of patients with OSCC. This study evaluated the accuracy of neutrophil count combined with MVD in predicting patients' survival time and its relationship with clinicopathological parameters and prognosis. Additionally, the study explored the effects of the Chemerin-neutrophil interaction on the angiogenic function of HUVECs. In OSCC, the overexpression of Chemerin promoted the angiogenesis of HUVECs through neutrophils. Moreover, Chemerin upregulated pro-angiogenic factors (e.g., VEGF-A, MMP-9, MMP-2, and S100A9) in neutrophils by activating MEK/ERK signaling pathway. In vivo experiments demonstrated that Chemerin may promote tumor growth by regulating tumor angiogenesis. In conclusion, the results suggest that neutrophil count and MVD serve as poor prognostic factors for patients with OSCC, and their combination is a more effective factor in predicting the survival time of OSCC patients. Neutrophils potentially contribute to angiogenesis through MEK/ERK signaling pathway via Chemerin and participate in the progression and metastasis of OSCC.

Expression and protective effect of chemerin in idiopathic pulmonary fibrosis

Objective: To explore the expression and the role of chemerin in idiopathic pulmonary fibrosis (IPF). Methods: Quantitative PCR and Western blotting were used to determine the mRNA and protein levels of chemerin in lung tissues from IPF patients and the controls. Clinical serum level of chemerin was analyzed by enzyme-linked immunosorbent assay. The mouse lung fibroblasts isolated and cultured in vitro were divided into the control, TGF-β, TGF-β+chemerin and chemerin groups. Immunofluorescence staining was used to observe the expression of α-smooth muscle actin (α-SMA). C57BL/6 mice were randomly divided into the control, bleomycin, bleomycin+chemerin, and chemerin groups. Masson and immunohistochemical staining were performed to evaluate the severity of pulmonary fibrosis. Expression of epithelial to mesenchymal transition (EMT) markers was detected by quantitative PCR and immunohistochemical staining in the in vitro and in vivo models of pulmonary fibrosis, respectively. Results: Compared with the control group, the expression of chemerin was downregulated in both the lung tissue and the serum of IPF patients. Immunofluorescence showed that treatment of fibroblasts with TGF-β alone resulted in a robust expression of α-SMA, whereas treatment with TGF-β and chemerin together exhibited the similar expression levels of α-SMA as the control group. Masson staining indicated that the bleomycin-induced pulmonary fibrosis model was constructed successfully, while treatment of chemerin partially alleviated the damage of lung tissue. Immunohistochemical staining showed that the expression of chemerin in the lung tissue was significantly decreased in the bleomycin group. Quantitative PCR and immunohistochemistry showed that chemerin attenuated EMT induced by TGF-β and bleomycin both in vitro and in vivo. Conclusions: The expression of chemerin was reduced in patients with IPF. Chemerin may play a protective role in the development of IPF by regulating EMT, providing a new idea for the clinical treatment of IPF.

The Role of Chemerin in Metabolic and Cardiovascular Disease: A Literature Review of Its Physiology and Pathology from a Nutritional Perspective.

Chemerin is a novel adipokine that plays a major role in adipogenesis and lipid metabolism. It also induces inflammation and affects insulin signaling, steroidogenesis and thermogenesis. Consequently, it likely contributes to a variety of metabolic and cardiovascular diseases, including atherosclerosis, diabetes, hypertension and pre-eclampsia. This review describes its origin and receptors, as well as its role in various diseases, and subsequently summarizes how nutrition affects its levels. It concludes that vitamin A, fat, glucose and alcohol generally upregulate chemerin, while omega-3, salt and vitamin D suppress it. Dietary measures rather than drugs acting as chemerin receptor antagonists might become a novel tool to suppress chemerin effects, thereby potentially improving the aforementioned diseases. However, more detailed studies are required to fully understand chemerin regulation.

Role of Chemerin and Perivascular Adipose Tissue Characteristics on Cardiovascular Risk Assessment by Arterial Stiffness Markers in Patients with Morbid Obesity.

The development of arterial stiffness (AS) in obesity is a multifactorial and complex process. The pleomorphic actions of adipokines and their local activity in perivascular adipose tissue (PVAT) are potential modulators of AS appearance and progression. We aimed to assess the correlations between two adipokines (chemerin, adiponectin), PVAT morphological changes (adipocyte size, blood vessel wall thickness) and AS parameters in the special subgroup of patients with morbid obesity. We enrolled 25 patients with morbid obesity and 25 non-obese patients, who were age- and gender-matched, untreated for cardiovascular risk factors, and admitted to hospital for laparoscopic surgical procedures (bariatric surgery for morbid obesity and non-inflammatory benign pathology surgery for non-obese patients). Before the surgical procedures, we evaluated demographic and anthropometric data and biochemical parameters including the studied adipokines. Arterial stiffness was evaluated using a Medexpert ArteriographTM TL2 device. In both groups, adipocyte size and vascular wall thickness as well as local adiponectin activity were analyzed in PVAT from intraoperative biopsies. In our study, adiponectin (p = 0.0003), chemerin (p = 0.0001) and their ratio (p = 0.005) had statistically significant higher mean values in patients with morbid obesity compared to normal-weight patients. In patients with morbid obesity there were significant correlations between chemerin and AS parameters such as aortic pulse wave velocity (p = 0.006) and subendocardial viability index (p = 0.009). In the same group adipocyte size was significantly correlated with another AS parameter, namely, aortic systolic blood pressure (p = 0.030). In normal-weight patients, blood vessel wall thickness positively correlated with AS parameters such as brachial (p = 0.023) and aortic augmentation index (p = 0.023). An important finding was the negative adipoR1 and adipoR2 immunoexpression in PVAT adipocytes of patients with morbid obesity. Additionally, we found significant correlations between blood vessel wall thickness and blood fasting glucose (p < 0.05) in both groups. Chemerin and adipocyte size could be predictive biomarkers for AS in patients with morbid obesity. Given the small number of patients included, our results need further validation.

The role of chemerin in the regulation of cGAS-STING pathway in gestational diabetes mellitus placenta.

Recent studies already confirmed that placenta mitochondrial dysfunction is associated with the progression of gestational diabetes mellitus (GDM). Besides, a possible relationship between adipokine chemerin and disulfide-bond A oxidoreductase-like protein (DsbA-L) had been revealed, whereas the potential interaction remains unclear. In addition, very little is still known about the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway and its mechanisms of action in the context of GDM. The present study aims to investigate the underlying mechanism of cGAS-STING pathway and its regulatory relationship with chemerin in GDM. A total of 50 participants, including 25 cases of GDM patients and 25 pregnant women with normal glucose tolerance, were enrolled, and their placenta tissues at term labor were collected. Besides, an insulin resistance cell model was established on the human trophoblastic cell line to explore the molecular mechanism of chemerin on cGAS-STING pathway. Results showed that there were mitochondrial pathological changes in GDM placenta, accompanied by the decreased expression of DsbA-L, increased level of chemerin, and the activation of cGAS-STING pathway. In the insulin resistant cell model, overexpression of chemerin upregulated protein expression of DsbA-L, and recombinant chemerin presented time-dependent inhibition on the cGAS-STING pathway, but this effect was not dependent on DsbA-L. In conclusion, elevated chemerin is probably a protective mechanism, which may be a potential therapeutic strategy for GDM.

Effects of Non-surgical Periodontal Therapy on Saliva and Gingival Crevicular Fluid Levels of Chemerin in Periodontitis Subjects With and Without Type 2 Diabetes Mellitus.

Background Evidencehad shown a bi-directional link between diabetes mellitus and periodontitis. Chemerin, an adipose tissue-specific adipokine plays a significant role in adipocyte initiation and differentiation that directly influences glucose metabolism, lipid metabolism, and inflammatory mediators. Non-surgical periodontal therapy (NSPT) for patients with periodontitis and diabetes mellitus improves the periodontal condition and regulates glycemic level. Aims and objectives To assess the impact of chemerin on periodontal disease and diabetes mellitus pathogenesis and to analyze the impact of NSPT on saliva and gingival crevicular fluid (GCF) chemerin levels in patients with periodontitis with and without type 2 diabetes mellitus (T2DM). Materials and methods A total of 60 patients were divided into four groups: Group I: Systemically and periodontally healthy subjects (n=15), Group II: Systemically healthy subjects with periodontitis (n=15), Group III: Subjects with periodontitis and T2DM (n=15), Group IV: Periodontally healthy subjects with T2DM (n=15). Indices and parameters like plaque index (PI), gingival index (GI), periodontal probing depth (PPD), and clinical attachment level (CAL) were assessed at baseline in all four groups and six weeks after NSPT in Group II and Group III. A glycated hemoglobin (HbA1c) test was taken to assess the patient's blood glucose level. Fasting blood sugar (FBS) level was taken at baseline in all the groups and six weeks after NSPT in Group II and Group III subjects. Saliva and GCF chemerin levels were assessed at baseline in all four groups and six weeks after NSPT in Group II and Group III subjects. Results A statistically significant difference was observed in comparing chemerin levels at baseline with all four groups (p < 0.001). After NSPT, there was a reduction in clinical parameters, FBS, and chemerin levels in Group II and Group III. A positive correlation was observed between salivary chemerin and FBS in Group II, GCF chemerin, PI, and FBS in Group II, and PPD and FBS in Group III. A negative correlation was observed between salivary chemerin and all parameters in Group II and between salivary chemerin and GCF chemerin in Group III. Conclusion Based on the observed relationship between chemerin and the parameters, their utility as a dual biomarker for diagnosis and prognosis in periodontal disease seems promising. However, further studies with a larger sample size on the role of chemerin in health and various states of diseases are required to substantiate the result of the study.

Chemerin affects the expression of angiogenesis-related factors in the porcine endometrium during early pregnancy and the oestrous cycle: an in vitro study.

The appropriate course of angiogenesis in the endometrium is crucial for pregnancy establishment and maintenance. Very little is known about the factors linking vessel formation and immune system functioning. We hypothesised that chemerin, an adipokine known for its involvement in the regulation of energy balance and immunological functions, may act as a potent regulator of endometrial angiogenesis during early pregnancy in pigs. Porcine endometrial tissue explants were obtained from pregnant pigs on days 10-11, 12-13, 15-16 and 27-28, and on days 10-12 of the oestrous cycle. The explants were in vitro cultured for 24h in the presence of chemerin (100, 200ng/mL) or in medium alone (control). We evaluated the in vitro effect of chemerin on the secretion of vascular endothelial growth factors A-D (VEGF-A-D), placental growth factor (PlGF), basic fibroblast growth factor (bFGF) and angiopoietin 1 and 2 (ANG-1, ANG-2) with the ELISA method. The protein abundance of angiogenesis-related factor receptors, VEGF receptors 1-3 (VEGFR1-3), FGF receptors 1 and 2 (FGFR1-2) and ANG receptor (TIE2) was evaluated with the Western blot (WB) method. We also analysed the influence of chemerin on the phosphorylation of AMPK using WB. We found that in the studied endometrial samples, chemerin up-regulated the secretion of VEGF-A, VEGF-B and PlGF, and protein expression of VEGFR3. The adipokine caused a decrease in VEGF-C, VEGF-D and ANG-1 release. Chemerin effect on bFGF and ANG-2 secretion, and protein content of VEGFR1, VEGFR2, FGFR1, FGFR2 and TIE2 were dependent on the stage of pregnancy. Chemerin was found to down-regulate AMPK phosphorylation. The obtained in vitro results suggest that chemerin could be an important factor in the early pregnant uterus by its influence on angiogenic factors' secretion and signalling. The obtained results on the role of chemerin in the process of endometrial angiogenesis may, in the long term perspective, contribute to the elaboration of more effective methods of modifying reproductive processes and maintaining energy homeostasis in farm animals.

Circulating Chemerin and Its Kinetics May Be a Useful Diagnostic and Prognostic Biomarker in Critically Ill Patients with Sepsis: A Prospective Study.

Chemerin, a novel adipokine, is a potent chemoattractant molecule with antimicrobial properties, implicated in immune responses. Our aim was to investigate circulating chemerin and its kinetics, early in sepsis in critically ill patients and its association with severity and prognosis. Serum chemerin was determined in a cohort of 102 critically ill patients with sepsis during the first 48 h from sepsis onset and one week later, and in 102 age- and gender-matched healthy controls. Patients were followed for 28 days and their outcomes were recorded. Circulating chemerin was significantly higher in septic patients at onset compared to controls (342.3 ± 108.1 vs. 200.8 ± 40.1 μg/L, p < 0.001). Chemerin decreased significantly from sepsis onset to one week later (342.3 ± 108.1 vs. 308.2 ± 108.5 μg/L, p < 0.001), but remained higher than in controls. Chemerin was higher in patients presenting with septic shock than those with sepsis (sepsis onset: 403.2 ± 89.9 vs. 299.7 ± 99.5 μg/L, p < 0.001; one week after: 374.9 ± 95.3 vs. 261.6 ± 91.9 μg/L, p < 0.001), and in nonsurvivors than survivors (sepsis onset: 427.2 ± 96.7 vs. 306.9 ± 92.1 μg/L, p < 0.001; one week after: 414.1 ± 94.5 vs. 264.2 ± 79.9 μg/L, p < 0.001). Moreover, patients with septic shock and nonsurvivors, presented a significantly lower absolute and relative decrease in chemerin one week after sepsis onset compared to baseline (p < 0.001). Based on ROC curve analyses, the diagnostic performance of chemerin (AUC 0.78, 95% CI 0.69–0.87) was similar to C-reactive protein (CRP) (AUC 0.78, 95% CI 0.68–0.87) in discriminating sepsis severity. However, increased chemerin at sepsis onset and one week later was an independent predictor of 28-day mortality (sepsis onset: HR 3.58, 95% CI 1.48–8.65, p = 0.005; one week after: HR 10.01, 95% CI 4.32–23.20, p < 0.001). Finally, serum chemerin exhibited significant correlations with the severity scores, white blood cells, lactate, CRP and procalcitonin, as well as with biomarkers of glucose homeostasis, but not with cytokines and soluble urokinase-type plasminogen activator receptor (suPAR). Circulating chemerin is increased early in sepsis and its kinetics may have diagnostic and prognostic value in critically ill patients. Further studies are needed to shed light on the role of chemerin in sepsis.

Functional disability is related to serum chemerin levels in rheumatoid arthritis

Adipokines, especially chemerin, can interact with cytokines and other molecules in inflammation. To date, there is insufficient information regarding a possible correlation between functional disability and chemerin and other pro-inflammatory molecules in rheumatoid arthritis (RA). To identify the association of functional disability with serum chemerin and other pro-inflammatory molecules, including other adipokines, cytokines and E-selectin, in patients with RA. Cross-sectional study. Assessment: disease activity (DAS28-ESR) and functional disability (HAQ-DI). We compared the adipokines (chemerin, leptin, adiponectin, resistin, and visfatin), cytokines (TNF-α, IL-6, IL-1β, and IL-18) and E-selectin levels between RA with functional disability and RA non-disabled patients. Of 82 patients with RA, 43 (52%) had functional disability. The RA with functional disability group had higher chemerin (140 vs. 112 ng/mL, p = 0.007) than the non-disabled RA group. Chemerin correlated with the HAQ-DI (rho = 0.27, p = 0.02) and DAS28-ESR (rho = 0.21, p = 0.05). Severe activity correlated with IL-6 (rho = 0.33, p = 0.003) and E-selectin (rho = 0.23, p = 0.03) but not with disability. No other pro-inflammatory molecules correlated with HAQ-DI. High chemerin levels were associated with functional disability in RA, whereas no other molecules correlated with loss of function. These results encourage further studies assessing new roles of chemerin as a marker of impairment in RA.

Impact of chemerin, lipid profile, and insulin resistance on disease parameters in patients with multiple sclerosis.

Plasma chemerin, which has chemotactic and adipogenic functions, is increased in several inflammatory diseases. However, its relationship with multiple sclerosis (MS) has not been explored yet. In this study, we aimed to determine chemerin levels and their possible role in MS. Chemerin serum concentrations were evaluated by using ELISA kit in 91 clinically definite MS patients and 52 healthy controls. The mean serum chemerin, insulin, and cholesterol levels were compared. Patients were divided into two groups according to the body mass index (BMI), and the relationships between clinical and metabolic parameters were evaluated. Serum chemerin levels were 10.46 ± 1.65ng/mL in MS patients and 10.26 ± 2.14ng/mL in the control group. No significant difference was found between patients and controls (p = 0.55). We found no difference regarding age, gender, and BMI between two groups (p = 0.053, p = 0.54, p = 0.41). However, female patients with MS had higher chemerin levels than male patients. There were no associations between serum chemerin levels and EDSS score, annualized relapse rate, BMI, insulin resistance, and serum cholesterol levels in MS patients. In this study, we aimed to determine serum chemerin levels in patients with MS. However, in our study, there was no significant difference between serum chemerin levels of MS patients and healthy controls'. Additionally, chemerin levels were not associated with other metabolic parameters, as well as cognitive dysfunction. Further studies are needed to evaluate the role of chemerin in MS patients.

P1042CHEMERIN, INFLAMMATION AND DIABETIC KIDNEY DISEASE PROGRESSION IN PATENTS WITH TYPE 2 DIABETES MELLITUS

Abstract Background and Aims Diabetic kidney disease (DKD) is the leading cause of end-stage renal diseases worldwide. The development of DKD includes immunologic and inflammatory mechanisms which involve activation of the innate immune system and participation of inflammatory cytokines such as tumor necrosis factor (TNF)-α. Chemerin is an adipokine that has been suggested to be related to inflammation and has been correlated with the development of diabetic complications.We aimed to explore the potential links between chemerin, inflammation and the development of DKD in patients with type 2 diabetes mellitus (DM). Method The study population included 94 subjects: 84 patients with type 2 DM (89.4%), classified into 3 groups according to the 24 hr urinary albumin, and 10 normoalbuminuric non-diabetic controls (10.6%). Demographic, clinical and analytical data, and chemerin and TNF-α levels were collected. Results A total of 84 diabetic patients were enrolled, 32 males (38.1%) and 52 females (61.9%), mean age 57.9±10.7 years. They were divided into 3 groups: 14 with normalbuminuria, 27 with microalbuminuria, and 43 with macroalbuminuria (24 h urinary albumin &amp;lt;30, 30-300 and &amp;gt;300 mg/dl respectively). Chemerin levels increased significantly with the rise in albuminuria (control: 21.3 (10.8 –180), normoalbuminuria: 794 (556.9-1066), microalbuminura: 1155.5 (718 – 1877) and macroalbuminuria: 1619 (705 – 8067) ng/ml; p&amp;lt; 0.001, Kruskal Wallis test), yet with no significant difference between the control and normoalbuminuria groups. Serum TNF-α was significantly elevated in macroalbuminuria compared to control groups (p=0.017) with no significant difference between normoalbuminuria, microalbuminuria and macroalbumenuria groups (control: 77.85 (59 – 124.7), normoalbuminuria: 85.15 (59-146), microalbumenuria: 89 (68 – 180) and macroalbuminuria: 100 (66 – 556) pg/ml) (Figure). Among the diabetics, a significant association was evident between serum chemerin and serum TNF-α (r= 0.84; p&amp;lt;0.001). Both biomarkers were significantly associated with the inflammatory markers ESR and CRP, serum creatinine, BUN, 24 hour urine albumin, HbA1c, and diabetes duration and negatively with eGFR and serum albumin (p&amp;lt;0.05). On linear stepwise regression analysis, chemerin was significantly associated with TNF-α (unstandardized β 9.954, p&amp;lt;0.001) and ESR (unstandardized β 19.596, p&amp;lt;0.001); and TNF-α was significantly correlated with chemerin (unstandardized β 0.059, p&amp;lt;0.001), 24 hour urine albumin (unstandardized β 0.004, p&amp;lt;0.001) and HbA1c (unstandardized β -13.699, p=0.014). Conclusion Chemerin increased progressively with the rise in albuminuria, and was associated with the inflammatory milieu in patients with DKD, given the significant association with the inflammatory markers TNF-α and ESR. TNF-α, as surrogate of inflammation, was strongly associated with albuminuria. As such, our results suggest a potential role of Chemerin and TNF-α in the development and progressions of DKD. Larger studies are warranted to further explore the potential links between chemerin, inflammation and DKD.

Beneficial effect of symbiotic supplementation during pregnancy in high fat diet-induced metabolic disorder in rats: Role of Chemerin

ObjectiveMetabolic disorders during pregnancy have detrimental effect on mother and her fetus. Symbiotic supplementation can improve metabolic disorders. The aim of this study was to assess the impact of symbiotic supplementation on the levels of Chemerin, lipid profile, glucose, and insulin resistance in pregnant rats fed a high-fat diet (HFD). Materials and methodsThirty female Wistar rats (weighing 200–220 g) were randomly assigned into three groups: control group, HFD group, and HFD + symbiotic group. The control group received the regular diet (fed lab chow); the HFD group received HFD alone; and the HFD + symbiotic group that in addition to taking HFD, was gavaged daily during pregnancy with a symbiotic solution, which contained Lactobacillus rhamnosus and Bacillus coagulans at a concentration of 108 CFU/ml and fructooligosaccharide 10%. On the 10th day of the experiment, the animals became pregnant. At the end of pregnancy period, birth weight of offspring, levels of blood glucose, total cholesterol, triglyceride (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), insulin, and chemerin level were measured. ResultsBirth weight of offspring in the HFD + symbiotic group was significantly lower than in the HFD group (P < 0.02). Similarly, insulin, insulin resistance, TG, total cholesterol, and LDL levels in the HFD + symbiotic group were significantly lower than in the HFD group (all P < 0.01). Symbiotic supplementation significantly reduced chemerin concentration in HFD + symbiotic group than HFD group (P < 0.008). Chemerin levels had a significant and positive correlation with food intake in the first ten days of the experiment and gestation period (P < 0.01, P < 0.04), fasting blood sugar (FBS) (P < 0.01), Total cholesterol (P < 0.05) and homeostatic model assessment (HOMA) index (P < 0.01). Moreover, chemerin levels had a significant and negative correlation with HDL (P < 0.01) and insulin (P < 0.02) levels. ConclusionBased on our results, symbiotic supplementation has beneficial effects on metabolic disorders and improves weight gain during pregnancy, pup birth weight, FBS, insulin resistance and lipid profile. These advantages of symbiotic supplementation could be mediated by change in chemerin secretion.

Role of Chemerin as a Putative Biomarker of Cardiovascular Risk in Metabolic Syndrome: A Brief Review

Cardiovascular disease (CVD) is one of the major alarming causes of morbidity and mortality with widespread prevalence around the world. The major risk factor for cardiovascular disease is metabolic syndrome (MetS) and is most prevalent among obesity-related comorbidities. The main causative factors linking metabolic syndrome and cardiovascular disease are assumed to involve the expansion of adipose tissue and chronic inflammation. In addition to storing surplus fat, adipose tissue also produces adipokines which act through autocrine, paracrine and endocrine functions in the body. Increasing evidence suggests that the altered secretion of adipokines may play a role in the pathogenesis of metabolic syndrome but the mechanisms underlying are not fully known. To date, only leptin and adiponectin are the best-studied adipokines among the variety of adipokines secreted by adipose tissue. However, recent studies have implicated the novel adipokine chemerin as a regulator of adipogenesis, inflammation and glucose metabolism which demonstrates its multifaceted actions. Furthermore, they also found that elevated circulating levels of chemerin in metabolic syndrome acts as a significant risk factor for cardiovascular disease. Chemerin has gained considerable interest due to its role as a pro- or anti-inflammatory mediator is still controversial and the effect of chemerin on glucose metabolism is a matter of debate. Thus, the purpose of this review is to focus primarily on chemerin expression, processing, signaling of receptors, biological actions and pathophysiological implications and the role of chemerin as a biomarker of cardiovascular disease in metabolic syndrome.

Abstract 113: Chemerin Regulates Adipocyte Size in Mesenteric Perivascular Adipose Tissue When on a Normal but Not High Fat Isocaloric Diet

Chemerin is an adipokine, positively associated with blood pressure, and used as a marker for metabolic syndrome. We hypothesized that a global knockout (KO) of chemerin in the rat would lead to a global decrease in white visceral fat mass in both control (C) and high-fat (HF) diets. Wild-type (WT) and KO rats on a Sprague-Dawley background were fed a C (10% kcal fat) or HF (60% kcal fat) diet with weekly monitoring of body weight and food consumption. MicroCT was performed at 8 weeks and 25 weeks of age to measure subcutaneous and intrabdominal fat. Blood pressure was measured by radiotelemetry measuring for 10 seconds every 10 minutes for 24 hours/day. At the end of 25 weeks, fats were dissected and flash frozen for PCR analysis or fixed with paraformaldehyde for histology. There were no physiologically relevant differences in blood pressure (table). Within each diet, there were no significant differences in final total body weight (table). KO-C had reduced intrabdominal fat when compared to WT-C. Histology of the KO-C intrabdominal white fat components revealed a significant leftward shift in mesenteric adipocyte area compared to WT-C (table; p = 0.01 by the Kolmogorov-Smirnov test) but no changes in retroperitoneal adipocytes. RNA expression of perilipin, adiponectin, and fatty acid synthase normalized to beta-2 microglobulin were all undetectable only in the mesenteric fat, not retroperitoneal fat, of KO-C animals compared to WT-C (table). These data are the first to provide in vivo support for the role of chemerin in adipogenesis but also indicates that chemerin’s role in adipocyte development specific to a location vital for blood pressure regulation.

Ovarian Expression of Adipokines in Polycystic Ovary Syndrome: A Role for Chemerin, Omentin, and Apelin in Follicular Growth Arrest and Ovulatory Dysfunction?

Adipokines are a potential link between reproduction and energy metabolism and could partly explain some infertilities related to some pathophysiology, such as polycystic ovary syndrome (PCOS). However, adipokines were predominantly assessed in blood samples, while very little is known concerning their variations in follicular fluid (FF) and ovarian granulosa cells (GCs) of PCOS women. Thus, the objectives of our study were to investigate adiponectin, chemerin, resistin, visfatin, omentin, and apelin ovarian expression in PCOS women in comparison with controls and women with only a polycystic ovary morphology. In total, 78 women undergoing an in vitro fertilization procedure were divided into three groups: 23 PCOS women, 28 women presenting only ≥12 follicles per ovary (ECHO group), and 27 control women. Each group almost equally included normal weight and obese women. Follicular fluid (FF) concentration and granulosa cells (GCs) mRNA expression of adipokines and their receptors were assessed by ELISA and RT-qPCR, respectively. Omentin levels in FF and GC were higher in PCOS than in ECHO and control women, while apelin expression was increased in both PCOS and ECHO groups. FF chemerin concentration was predominant in normal-weight PCOS women compared to BMI (Body Mass Index)-matched ECHO and control women, while GC mRNA levels were higher in the obese PCOS group than in the ECHO one. Compared to PCOS, ECHO women had increased FF adiponectin concentrations and lower plasma AMH levels. The FF concentration of all adipokines was higher in obese subjects except for adiponectin, predominant in normal-weight women. In conclusion, women with PCOS expressed higher GC chemerin and omentin, whereas the ECHO group presented higher levels of FF adiponectin and apelin and lower plasma AMH and LH concentrations. Chemerin, omentin, and apelin expression was differently regulated in women with PCOS, suggesting their possible role in follicular growth arrest and ovulatory dysfunction characterizing PCOS pathogenesis.