Plasma Visfatin Research Articles

Visfatin/pre-B cell colony-enhancing factor immunohistochemical overexpression in oral cancers

Increased visfatin expression has been shown to increase gene expression, which promotes cell survival and increases SirT1 activity thereby promoting angiogenesis. Previous studies have shown that oral squamous cell carcinomas (OSCCs) express high levels of activated signal transducer and activator of transcription 3 (Stat3). Since visfatin expression is increased by Stat3, we hypothesized that visfatin protein may be highly expressed in OSCCs. Immunohistochemistry was the technique used to examine the expression of visfatin in 19 OSCCs and 4 hyperplastic lesions. The results indicated that visfatin was detected in the cytoplasm and nuclei of the OSCCs and epithelial hyperplasia as well as in the stromal tissues of patients with OSCC and oral hyperplasia. Furthermore, co-expression of visfatin and proliferating cell nuclear antigen proteins was noted in verrucous epithelial hyperplasia, and co-expression of visfatin and CD68 in the inflammatory cells of the stromal region was noted in the OSCCs. In addition, enzyme-linked immunosorbent assay showed that plasma visfatin concentrations were significantly increased in the patients with OSCC and oral hyperplasia compared to those of the control subjects. In conclusion, visfatin expression and concentrations were higher in OSCCs and oral hyperplasia, suggesting that visfatin may play a role in the pathogenesis of oral cancers.

Plasma Visfatin Levels in Adolescents with Polycystic Ovary Syndrome: A Prospective Case-Control Study

Study ObjectiveWe evaluated the plasma visfatin levels in hirsute female adolescents with polycystic ovary syndrome. Design, Setting, and ParticipantsThis prospective case-control study included 87 female patients who were seen in our adolescence department. Demographic characteristics and hormonal and biochemical parameters were evaluated between patients with and without polycystic ovary syndrome. Next, we divided the patients with polycystic ovary syndrome into the following subgroups: overweight or obese (body mass index [BMI] ≥ 25 kg/m2) vs normal weight (BMI < 25 kg/m2) and hirsute vs nonhirsute. ResultsThere were statistically significant differences in the BMI, serum androgen levels, homeostasis model assessment–insulin resistance (HOMA-IR) levels, and insulin levels between patients with and without polycystic ovary syndrome (P < .05). The mean visfatin levels showed no statistically significant difference between these 2 groups (P > .05). The serum visfatin levels were similar between the 2 subgroups classified by BMI (P > .05). However, there were statistically significant differences in the total and free testosterone levels, 17-hydroxylase progesterone level, HOMA-IR level, and visfatin level between the 2 subgroups classified by hirsutism (P < .05). The plasma visfatin level was higher in hirsute PCOS than in nonhirsute PCOS patients. ConclusionSignificantly higher visfatin levels were found in hirsute than in nonhirsute adolescents with PCOS. According to these results, plasma visfatin levels may be a useful marker in hirsute adolescents with PCOS.

Elevated plasma visfatin levels correlate with conversion of laparoscopic cholecystectomy to open surgery in acute cholecystitis

Visfatin correlates with inflammation and its levels in peripheral blood are associated with some inflammatory diseases. This study aimed to assess the relationship between plasma visfatin levels and conversion of laparoscopic cholecystectomy to open surgery in acute cholecystitis. One hundred and forty-six acute cholecystitis patients and 146 sex- and age-matched healthy controls were recruited and their plasma visfatin levels were determined using an enzyme immunoassay. 17 patients (11.6%) underwent conversion. Plasma visfatin levels were statistically significantly elevated in all patients (97.2±41.8ng/mL), those with (161.4±71.3ng/mL) or without conversion (88.7±26.9ng/mL), compared to controls (40.3±13.3ng/mL, all P<0.001). A linear regression analysis showed that plasma visfatin levels were positively associated with plasma C-reactive protein levels (t=0.510, P<0.001). A logistic-regression analysis showed that age [odds ratio (OR) 1.160, 95% confidence interval (CI) 1.011–1.332, P=0.035] and plasma visfatin levels (OR 1.035, 95% CI 1.005–1.066, P=0.022) appeared to be the independent predictors of conversion. A receiver operating characteristic curve analysis found that plasma visfatin levels predicted conversion with high area under curve (AUC) (AUC, 850; 95% CI, 0.781–0.903). The AUC of the visfatin concentration was similar to that of age (AUC, 0.738; 95% CI, 0.659–0.807) (P=0.188). Visfatin improved the AUC of age to 0.914 (95% CI, 0.856–0.954) (P=0.011) using a combined logistic-regression model. Thus, high plasma levels of visfatin are associated with systemic inflammation, and may independently predict conversion of laparoscopic cholecystectomy to open surgery in acute cholecystitis.

Elevated plasma visfatin levels correlate with poor prognosis of gastric cancer patients

Visfatin is a proinflammmatory cytokine with accumulating evidence for its rise in circulation of cancer patients. This study aimed to evaluate the relationship between preoperative plasma visfatin level and prognosis of gastric cancers. Preoperative plasma visfatin levels of 262 patients with gastric cancers and plasma visfatin levels of 262 healthy individuals were determined using enzyme-linked immunosorbent assay. Preoperative plasma visfatin level was substantially higher in patients than in healthy subjects. Plasma visfatin levels were associated with invasion depth, lymph node metastasis, distant metastasis, peritoneal dissemination, tumor size and tumor node metastasis stage. Multivariate analysis revealed that high plasma visfatin level was an independent factor for death. Receiver operating characteristic curve analysis showed that plasma visfatin level predicted death with high area under curve. Multivariate Cox regression analysis identified plasma visfatin level as an independent predictor of overall survival. Thus, our results suggest that high preoperative plasma visfatin level is associated with prognostic factors for gastric cancer as well as may play a role as prognostic biomarker in gastric cancer survival.

Effect of simvastatin treatment on plasma visfatin levels in obese women

Aims: Obesity is one of the major concerns in the world currently, its prejudicial effect is exerted by proteins secreted by adipose tissue, among them visfatin was demonstrated to be related with BMI and cardiovascular diseases. The HMG-CoA reductase inhibitors are known to minimize the cardiovascular risk in hyperlipidemic patients and recently the discovery of various pleiotropic effects has made the statins evidencing among others anti-inflammatory effect. Our objective in this study was to determinate if simvastatin treatment may modulate visfatin levels in obese women without any other metabolic disorder.Methods: We recruited 25 obese women without any other metabolic disorder and treated with simvastatin for 6 weeks 20 mg/day.Results: The levels of plasma visfatin were similar before and after treatment (22 ± 20 versus 27 ± 14 ng/mL, p > 0.05) and correlated with BMI before treatment (p = 0.001). We also found correlations among visfatin and insulin levels (p = 0.015) and HOMA-IR (p = 0.025) only after treatment.Conclusion: These findings suggest that visfatin is not modulated by simvastatin treatment in this group but the treatment may interfere on the relation among visfatin, BMI, insulin and HOMA-IR.

Extracellular visfatin has nicotinamide phosphoribosyltransferase enzymatic activity and is neuroprotective against ischemic injury.

Visfatin, a novel adipokine, is predominantly produced by visceral adipose tissue and exists in intracellular and extracellular compartments. The intracellular form of visfatin is proved to be nicotinamide phosphoribosyltransferase (NAMPT) and exhibits neuroprotection through maintaining intracellular NAD(+) pool. However, whether extracellular form of visfatin has NAMPT activity and the effect of extracellular visfatin in cerebral ischemia are unknown. Plasma concentrations of visfatin, NAD(+) , and ATP were increased in mice upon cerebral ischemia. Cultured glia, but not neuron, was able to secrete visfatin. Oxygen-glucose deprivation (OGD) stress increased the secretion of visfatin from glia. Extracellular recombinant mouse wild-type visfatin, but not mouse H247A-mutant enzymatic-dead visfatin, had NAMPT enzymatic function in vitro. Treatment of wild-type visfatin, but not H247A-mutant enzymatic-dead visfatin, significantly attenuated detrimental effect of OGD on the cell viability and apoptosis in both cultured mouse neuron and glia. Treatment of neutralizing antibody, abolished the protective effect of extracellular visfatin on cell viability, but failed to block the antiapoptotic effect of extracellular visfatin. At last, we observed that plasma visfatin concentrations decreased in 6-month-old but not 3-month-old SHR-SP compared with that in age-matched Wistar-Kyoto rats. Inhibition of NAMPT enzymatic function of visfatin (by FK866) accelerated the occurrence of stroke in SHR-SP. Extracellular visfatin has NAMPT enzymatic activity and maybe be neuroprotective just as intracellular visfatin in cerebral ischemic injury.

Effects of 12-week high-intensity interval training on plasma visfatin concentration and insulin resistance in overweight men

The purpose of this study was to determine the effects of 12 weeks of high-intensity interval training (HIIT) on visfatin and insulin resistance (IR) in overweight adult men during a weight-loss program. Eighteen overweight men (age = 31.8 ± 9.2 years; body mass index = 28.6 ± 1.4 kg/m2) were randomly recruited into one of the two groups, namely, HIIT (3 days/week, 20 minutes/day; 85–95% peak oxygen uptake) and diet-induced weight-loss combined (DHIIT; n = 10) and diet-induced weight loss only (DIO; n = 8). The DHIIT and DIO groups undertook a 12-week weight-loss intervention using a moderate isocaloric energy-deficit diet. Both DHIIT and DIO groups demonstrated a significant reduction in body weight (p < 0.01). Total fat mass (p < 0.05) and lean body mass (p < 0.05) were decreased in the DIO group with no significant changes in abdominal fat mass, plasma insulin concentration, homeostasis model assessment-estimated IR (HOMA-IR), blood glucose level, and plasma visfatin. In the DHIIT group, total fat mass (p < 0.01), abdominal fat mass (p < 0.05), plasma insulin concentration (p < 0.05), plasma visfatin (p < 0.01), and HOMA-IR (p < 0.05) were reduced and lean body mass remained unchanged. In conclusion, adding a low-volume 20-minute HIIT (three times/week) to an energy-deficit diet not only can improve the efficiency of weight-loss program in the reduction of body fat, plasma visfatin levels, and HOMA-IR, but also has a reservation effect on lean body mass.

Plasma visfatin levels and mRNA expression of visfatin in peripheral blood mononuclear cells and peripheral blood monocyte-derived macrophages from normal weight females with polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a common reproductive endocrinology disease, however, an explicit etiology is not known. Insulin resistance (IR) appears to be central to the pathogenesis of PCOS and inflammation may be significant in the pathogenesis of IR in PCOS. The aims of the present study were to investigate the plasma visfatin level and the gene expression of visfatin in peripheral blood mononuclear cells (PBMCs) and peripheral blood monocyte-derived macrophages (PBMMs) from PCOS patients, in addition to investigating the association between PCOS and IR. A total of 21 PCOS patients and 21 control subjects were enrolled in the study; the homeostasis model assessment of insulin resistance (HOMA-IR) was considered to be a stratified method for establishing the subgroups. Fasting blood samples were collected and the levels of sex hormones, insulin, glucose, blood lipids and visfatin were measured. In addition, visfatin gene expression levels in PBMCs and PBMMs were assessed using quantitative polymerase chain reaction. The plasma visfatin and gene expression levels of visfatin in PBMCs and PBMMs were not observed to increase in the normal weight PCOS and normal weight IR patients. Furthermore, plasma visfatin levels did not correlate with the normal weight PCOS patients or the normal weight IR patients per se. Further investigation into the role of visfatin in the pathogenesis of PCOS or IR should examine macrophages in the tissues, rather than macrophages in the peripheral blood.

Beijing ambient particle exposure accelerates atherosclerosis in ApoE knockout mice by upregulating visfatin expression

Ambient particulate matter (PM) exposure has been associated with atherosclerosis. However, research on the effect of real-world exposure to ambient PM in regulating visfatin expression in an animal model is very limited. The objective is to investigate whether Beijing ambient PM exposure could accelerate atherosclerosis in ApoE knockout (ApoE(-/-)) mice by upregulating visfatin expression. Forty male ApoE(-/-) mice were exposed to untreated ambient air (PM group, n = 20) or filtered air (FA group, n = 20), 24 h/day, 7 days/week, for 2 months. During the exposure, the mass concentrations of PM2.5 and PM10 in the two groups were continuously monitored. Moreover, a receptor source apportionment model was applied to apportion sources of PM2.5. At the end of the exposure, visfatin in plasma and aorta, biomarkers of inflammation, oxidative stress and lipid metabolism in blood samples, and bronchoalveolar lavage fluid (BALF) were determined, and the plaque area of the atherosclerosis lesions was quantified. PM-exposed mice were significantly higher than FA-exposed mice in terms of plasma visfatin, OxLDL, MDA, serum TC, LDL, TNF-α as well as IL-6, TNF-α, OxLDL, and MDA in BALF, while SOD and GSH-Px activities in plasma and BALF were reduced in PM-exposed mice. Pathological analysis of the aorta demonstrated that the plaque area and visfatin protein in the PM group increased significantly compared to the FA group. Our findings indicate that ambient PM exposure could accelerate atherosclerosis, which is related to visfatin upregulation, as well as the activation of inflammation and oxidative stress.

An elevated plasma level of visfatin increases the risk of myocardial infarction

Visfatin, an adipocytokine involved in metabolic and immune disorders, plays an important role in the etiology of cardiovascular disease. Recent evidence has shown that an elevated plasma level of visfatin may increase the risk of myocardial infarction (MI), but individual published studies have shown inconclusive results. This study aimed to obtain a more precise estimate of the association between the plasma visfatin level and MI risk through a detailed meta-analysis of studies published in peer-reviewed journals. A literature search of articles published before May 1, 2013 was performed on the PubMed, Embase, Web of Science, and China BioMedicine databases. Crude standardized mean differences (SMDs) with 95% confidence intervals (CI) were calculated. Eleven case-control studies comprising 362 MI patients and 322 healthy controls were included. The meta-analysis revealed that an elevated plasma level of visfatin was associated with an increased risk of MI (SMD = 3.82, 95%CI = 2.67-4.98, P < 0.001). Further stratification based on the source of the controls showed that an elevated plasma level of visfatin was significantly associated with increased risk of MI in both hospital-based and population-based studies (SMD = 4.12, 95%CI = 2.23-6.01, P < 0.001 and SMD = 3.65, 95%CI = 2.67- 4.98, P < 0.001, respectively). No publication bias was evident in this meta-analysis. In conclusion, the current meta-analysis indicates that an elevated plasma level of visfatin increases the risk of MI. Therefore, plasma visfatin may be a promising biomarker for the diagnosis of MI.

Relationship between plasma visfatin and visceral fat thickness measured by ultrasonography in nonalcoholic fatty liver disease

Relationship between plasma visfatin and visceral fat thickness measured by ultrasonography in nonalcoholic fatty liver disease

Clinical significance of plasma visfatin level in patients with non-alcoholic fatty liver disease

Clinical significance of plasma visfatin level in patients with non-alcoholic fatty liver disease

Plasma levels of omentin-1 and visfatin in senile patients with coronary heart disease and heart failure

ObjectiveTo investigate the alteration of plasma levels of omentin-1 and visfatin in elderly patients with coronary heart disease (CHD) and heart failure. MethodsPlasma omentin-1 and visfatin levels were measured in 90 subjects (29 stable angina pectoris (SAP) cases, 30 unstable angina pectoris (UAP) cases and 31 age- and sex-matched healthy controls (age ≥ 60 years) by enzyme-linked immunosorbent assay methods. According to the New York Heart Association classification, 59 CHDs were divided into three groups: functional I class, 11 cases; functional II/III class, 36 cases; and functional IV class, 12 cases. ResultsThe plasma level of omentin-1 in CHD patients was significantly lower than that of the control group. Omentin-1in SAP group and UAP group were significantly lower compared to the control group (there was no statistical significance between UAP group and SAP group; P >0.05). The plasma level of visfatin in CHD patients was significantly higher than that of the control group. Similarly, visfatin in SAP group and UAP group were all significantly higher compared to the control group, while there was no statistical significance between UAP group, and SAP group. The plasma omentin-1 level was negatively correlated with SBP (r=-0.264, P<0.05), positively correlated with HDL-c level (r=0.271, P<0.05); the plasma visfatin level was positively correlated with TC (r=0.292,P<0.05), negatively correlated with HDL-c level (r=-0.266,P<0.05). There was a negative correlation between plasma omentin-1 and visfatin levels (r=-0.280, P<0.05). Moreover, multiple linear stepwise regression analysis showed that omentin-1 and visfatin levels might be affected by HDL-c level. Logistic regression analysis showed that visfatin could be an independent risk factor of CHD. ConclusionsDecreased levels of omentin-1 and increased levels of visfatin may be involved in the occurrence and development of CHD. Omentin-1 and visfatin, independently, may be protective and pro-inflammatory cytokines. Additionally, both omentin-1 and visfatin may be related to lipid metabolism. Visfatin may be an independent risk factor of CHD.

Central visfatin potentiates glucose-stimulated insulin secretion and β-cell mass without increasing serum visfatin levels in diabetic rats

IntroductionOur previous study revealed that plasma visfatin levels were lower in pregnant women with gestational diabetes (GDM) than non-GDM independent of prepreganacy BMI. We examined whether central visfatin modulates energy and glucose homeostasis via altering insulin resistance, insulin secretion or islet morphometry in diabetic rats. MethodsPartial pancreatectomized, type 2 diabetic, rats were interacerbroventricularly infused with visfatin (100ng/rat/day, Px-VIS), visfatin+visfatin antagonist, CHS-828 (100μg/rat/day, Px-VIS-ANT), or saline (control, Px-Saline) via osmotic pump, respectively, for 4weeks. ResultsCentral visfatin improved insulin signaling (pAkt→pFOXO-1) but not pSTAT3 in the hypothalamus. Central visfatin did not alter serum visfatin levels in diabetic rats whereas the levels were higher in non-diabetic rats than diabetic rats. Body weight at the 2nd week was lowered in the Px-VIS group due to decreased food intake in the first two weeks compared to the Px-Saline group and energy expenditure was not significantly different among the treatment groups of diabetic rats. Visfatin antagonist treatment nullified the central visfatin effect. Px-VIS increased whole body glucose disposal rates in euglycemic hyperinsulinemic clamp compared to Px-Saline and lowered hepatic glucose output, whereas Px-VIS-ANT blocked the visfatin effect on insulin resistance (P<0.05). In hyperglycemic clamp study, the area under the curve of insulin in first and second phase were significantly higher in the Px-VIS group than the Px-Saline group without modifying insulin sensitivity at the hyperglycemic state, whereas the increase in serum insulin levels was blocked in the Px-VIS-ANT group. Central visfatin also increased β-cell mass by increasing β-cell proliferation. ConclusionsCentral visfatin improved glucose homeostasis by increasing insulin secretion and insulin sensitivity at euglycemia through the hypothalamus in diabetic rats. Therefore, visfatin is a positive modulator of glucose homeostasis by delivering the hypothalamic signals into the peripheries.

The comparison of serum vaspin and visfatin concentrations in obese and normal weight women

Background and objectivesThere is evidence based studies which show that plasma level of visfatin and vaspin in patients with type 2 diabetes mellitus elevate in comparison with healthy people. But there is no consistency in plasma visfatin and vaspin concentration between studies done on obese people. For this reason, the aim of this study is to investigate the serum level concentrations of visfatin and vaspin in obese women compared to normal weight women. Materials and methodsThe participants of this study consist of 43 women aged 20–50, and 43 healthy women with normal weight as a control group. They were matched for age and physical activity. 24h food recall was used to collect dietary information from subjects. Moreover, blood sampling was taken to measure the blood levels of sugar, lipid profile, vaspin and visfatin. ResultsThe mean serum level of visfatin was not statistically different between obese and normal weight women. But, the obese women had statistically higher mean serum level of vaspin than normal women (p=0.04). We found no relations between serum levels of vaspin with serum concentration of visfatin. Also, serum levels of these two adipokines were not related to the serum concentrations of fasting glucose, total cholesterol, low-density lipoprotein cholesterol and triglyserides and high-density lipoprotein cholesterol. Also, there was a significant positive relationship between carbohydrate intake and serum visfatin level in women participating to this study (p=0.018, r=0.257). ConclusionThe results of this study demonstrated that the level of serum vaspin was significantly higher in obese women. But there were no differences in serum levels of visfatin in comparison to normal weight women. Meanwhile this study demonstrated a positive relationship between serum levels of visfatin with dietary intake of carbohydrate, but no relationship between serum level of visfatin and vaspin in women participating in this study.

Plasma visfatin, a possible prognostic marker in aneurysmal subarachnoid hemorrhage

Visfatin is linked to inflammation and associated with clinical outcomes of intracerebral hemorrhage. This study was designed to investigate whether visfatin might serve as a marker of severity and prognosis in aneurysmal subarachnoid hemorrhage. In this study, plasma visfatin levels of 172 consecutive patients and 172 sex and age-matched healthy subjects were determined using enzyme-linked immunosorbent assay. The recorded clinical outcomes included in-hospital mortality and 6-month mortality and unfavorable outcome (Glasgow Outcome Scale score of 1–3). Plasma visfatin level was substantially higher in patients than in healthy controls (92.1±20.5ng/mL vs. 12.4±3.2ng/mL; P<0.001), was significantly associated with the World Federation of Neurological Surgeons (WFNS) score (r=0.569, P<0.001) and Fisher score (r=0.657, P<0.001), was an independent predictor of in-hospital mortality [odds ratio (OR), 1.378; 95% confidence interval (CI), 1.036–1.866; P=0.002] and 6-month mortality (OR, 1.261; 95% CI, 1.018–1.745; P=0.004) and unfavorable outcome (OR, 1.207; 95% CI, 1.012–1.682; P=0.008) in multivariate logistic regression analysis and had high predictive value for in-hospital mortality [area under curve (AUC), 0.849; 95% CI, 0.787–0.899; P<0.001] and 6-month mortality (AUC, 0.868; 95% CI, 0.808–0.915; P<0.001) and unfavorable outcome (AUC, 0.859; 95% CI, 0.797–0.907; P<0.001) using receiver operating characteristic curves. AUCs of visfatin were similar to those of WFNS score and Fisher score (all P>0.05), but visfatin did not improve the predictive values of WFNS score and Fisher score (all P>0.05). Thus, visfatin may be associated with clinical severity of aneurysmal subarachnoid hemorrhage and also have prognostic value for clinical outcomes.

Association of plasma visfatin with risk of colorectal cancer: An observational study of Chinese patients

To investigate the association between plasma visfatin levels and risk of early and advanced colorectal cancer (CRC). In total, 358 CRC patients and 286 controls were enrolled. According to the T factor of the TNM system. cancer patients were divided into two subgroups: early and advanced cancer. Levels of visfatin, anthropometric and metabolic parameters, which were classified as low, medium, and high, based on the tertile distributions in the control group, were determined. The visfatin levels in patients with advanced and early cancer were higher than in controls (least significant difference test, P = 0.004 and 0.013, respectively). The patients in the highest tertile of visfatin concentration presented significantly higher odds for early and advanced CRC, adjusted for potential confounding factors (odds ratio 3.37; 95% CI, 1.93-8.37; P = 0.011; odds ratio 2.38; 95% CI: 1.82-8.35; P = 0.015, respectively). The visfatin level correlated significantly with waist:hip ratio (P < 0.05 for all) among case and control participants. Plasma visfatin levels in early and advanced CRC yielded a receiver operating characteristic curve area of 72 and 86%, respectively. The optimal sensitivity and specificity were 73% and 57% in discriminating between early CRC and normal controls while they were 76% and 68% in discriminating between advanced CRC and normal controls. An increased level of visfatin was a strong risk factor for both early and advanced CRC in Chinese patients. Plasma visfatin levels might be a potential biomarker for CRC detection.

GW24-e2520 Circulating visfatin levels and clinical significance in patients with coronary heart disease

ObjectivesThe aim of the study is to 1. observe the changes of circulating visfatin levels in patients with coronary heart disease (CHD), 2. and investigate the relationship between visfatin levels...

Admission plasma visfatin level strongly correlates with hematoma growth and early neurologic deterioration in patients with acute spontaneous basal ganglia hemorrhage

BackgroundVisfatin, a proinflammatory mediator, has been associated with poor clinical outcomes after acute brain injury. The present study is designed to investigate the potential association between plasma visfatin levels and the risk of hematoma growth (HG) and early neurologic deterioration (END) after intracerebral hemorrhage. MethodsThere were 85 patients as cases who presented with first-time hemorrhagic stroke that were assessed within 6h after the incident. The control group consisted of 85 healthy volunteers. HG was defined as hematoma enlargement >33% at 24h. END was defined as an increase of≥4 points in National Institute of Health Stroke Scale score at 24h from symptoms onset. Plasma visfatin levels were determined using enzyme immunoassay. ResultsPlasma visfatin levels were significantly higher in patients compared to controls. Plasma visfatin level emerged as an independent predictor of HG [odds ratio (OR), 1.154; 95% confidence interval (CI), 1.046–3.108; P=0.009] and END (OR, 1.195; 95% CI, 1.073–3.516; P=0.005). For predicting HG, area under curve (AUC) of plasma visfatin level (0.814; 95% CI: 0.715–0.890) was similar to that of hematoma volume (0.839; 95% CI, 0.743–0.909) (P=0.703). For predicting END, AUC of plasma visfatin level (0.828; 95% CI: 0.730–0.901) was similar to that of hematoma volume (0.863; 95% CI, 0.771–0.928) (P=0.605). Visfatin did not improve AUC of hematoma volume for predicting HG and END (both P>0.05). ConclusionPlasma visfatin level represents a novel biomarker for predicting HG and END.

Association of plasma visfatin with hepatic and systemic inflammation in nonalcoholic fatty liver disease

Background. Visfatin is a proinflammatory and insulin-mimetic adipokine contributing to whole body glucose and lipid metabolism. Studies to date are conflicting regarding the relationship between visfatin and non-alcoholic fatty liver disease (NAFLD). The aim of the present study was to evaluate the relationship of circulating visfatin with NAFLD. Material and methods. The study included 114 NAFLD patients and 60 healthy non-diabetic controls. Plasma visfatin, adiponectin, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) levels were measured by ELISA. High sensitive C-reactive protein (hsCRP) levels were measured by immunoturbidimetric fixed rate method. Insulin sensitivity determined by homeostasis model assessment (HOMA-IR) index. Results. TNF-α, IL-6 and hsCRP levels were higher and, Adiponectin levels were lower in NAFLD group when compared to healthy controls (p < 0.001, for all). However, no difference was found regarding to visfatin levels between two groups. Different histologic subgroups of NAFLD had a significantly higher TNF-α, IL-6 and hsCRP, and lower adiponectin levels than those with controls (p < 0.001, for all). On the other hand, no statistically significant difference was found regarding to visfatin levels among different histologic groups. Visfatin was found to be negatively correlated with TNF-α (r = −0.236, p = 0.011) in NAFLD group. However, no association was found between visfatin and histological findings. Conclusion. Our findings show that plasma visfatin levels are not altered in the early stages of NAFLD. However, it is inversely associated with TNF-α. These findings suggest a role for visfatin in protection against liver injury in this widespread disease.