Plasma Visfatin Research Articles

Differential Regulation of Adipokines May Influence Migratory Behavior in the White-Throated Sparrow (Zonotrichia albicollis)

White-throated sparrows increase fat deposits during pre-migratory periods and rely on these fat stores to fuel migration. Adipose tissue produces hormones and signaling factors in a rhythmic fashion and may be controlled by a clock in adipose tissue or driven by a master clock in the brain. The master clock may convey photoperiodic information from the environment to adipose tissue to facilitate pre-migratory fattening, and adipose tissue may, in turn, release adipokines to indicate the extent of fat energy stores. Here, we present evidence that a change in signal from the adipokines adiponectin and visfatin may act to indicate body condition, thereby influencing an individual's decision to commence migratory flight, or to delay until adequate fat stores are acquired. We quantified plasma adiponectin and visfatin levels across the day in captive birds held under constant photoperiod. The circadian profiles of plasma adiponectin in non-migrating birds were approximately inverse the profiles from migrating birds. Adiponectin levels were positively correlated to body fat, and body fat was inversely related to the appearance of nocturnal migratory restlessness. Visfatin levels were constant across the day and did not correlate with fat deposits; however, a reduction in plasma visfatin concentration occurred during the migratory period. The data suggest that a significant change in the biological control of adipokine expression exists between the two migratory conditions and we propose a role for adiponectin, visfatin and adipose clocks in the regulation of migratory behaviors.

Role of adipocytokines and its correlation with endocrine pancreatic function in patients with pancreatic cancer

IntroductionSome authors suggest that adipocytokines contribute to the induction of pancreatic carcinogenesis as well as the development of endocrine insufficiency. AimsWe evaluate the circulating concentrations of leptin, resistin and visfatin in patients with newly diagnosed pancreatic cancer (PC) and relationship between serum adipocytokines level and clinicopathological features of PC. Moreover the usefulness of those adipocytokines as possible biomarkers of endocrine pancreatic function in PC has been assessed. MethodsThe pilot study group consisted of 45 individuals (mean age 65.6 ± 11.5 years, BMI 21.8 ± 3.4 kg/m2) with newly diagnosed PC (within last 1–3 months) and 13 healthy individuals with age, gender and BMI matched to the study group. Among PC patients 18 (40%) had recently diagnosed diabetes. Fasting plasma leptin, resistin, visfatin concentrations were determined with ELISA (R&D Systems, Phoenix Pharmaceuticals) and insulin by RIA (DakoCytomation). ResultsPatients with PC as compared to controls had significantly lower plasma leptin (40.6 ± 21.3 vs 63.2 ± 16.3 pg/mL; p < 0,0008). In contrast PC patients showed more than six fold higher level of resistin (126.2 ± 143.2 vs 18.9 ± 7.2 ng/mL; p < 0.009) than controls. The median plasma visfatin was 2.8 ± 1.8 ng/mL, which was not significantly different from the controls (3.8 ± 1.1 ng/mL). When PC patients with and without diabetes were considered separately, plasma leptin concentrations among nondiabetic patients were slightly, but not significantly higher (44.6 ± 21.0) as compared to diabetics (34.5 ± 20.7). Moreover there was no difference between visfatin and resistin level in PC, among patients with and without diabetes. No significant differences between serum level of leptin, visfatin and resistin and age, gender, BMI, smoking status, tumor localization, distant metastases and pain has been found. ConclusionThe results of this study confirm previous findings that patients with newly diagnosed pancreatic cancer are characterized with lower level of leptin. This pilot study showed significantly higher resistin concentrations in patients with PC in comparison to healthy controls, which may be helpful in PC early diagnosis. Changes in leptin and resistin level in PC are not likely related to endocrine disorders.

RETRACTED: Evaluation of the positive effects on insulin-resistance and β-cell measurements of vildagliptin in addition to metformin in type 2 diabetic patients

We evaluated the positive effects of vildagliptin in addition to metformin on glycemic control and β-cell function in type 2 diabetic patients. One hundred and seventy-one type 2 diabetic patients were instructed to add vildaglipin 50mg twice a day or placebo to metformin for 12 months. Body mass index (BMI), glycemic control, fasting plasma insulin (FPI), HOMA-IR, HOMA-β, fasting plasma proinsulin (FPPr), proinsulin/fasting plasma insulin ratio (Pr/FPI ratio), C-peptide, glucagon, vaspin, visfatin, and omentin-1 were evaluated. Before, and after 12 months since the addition of vildagliptin, patients underwent a combined euglycemic hyperinsulinemic and hyperglycemic clamp, with subsequent arginine stimulation. Vildagliptin+metformin were more effective than placebo+metformin in reducing body weight and BMI, glycemic control, HOMA-IR, glucagon and insulin resistance measurements. Vildagliptin+metformin gave also a better increase of HOMA-β, and of all β-cell parameters after the clamp. We also recorded a significant correlation between M value increase and the decrease of vaspin, visfatin, and omentin-1 obtained with vildagliptin+metformin. Vildagliptin, in addition to metformin, proved to be effective in improving β-cell function and in reducing insulin resistance measurements.

Differential Significance of Plasma Visfatin Concentrations according to Adiposity in Children and Adolescents

Background/Aims: Visfatin is an adipocytokine predominantly expressed in visceral adipose tissue. We examined the relationship between plasma visfatin concentrations and anthropometric and metabolic parameters in children and adolescents, who are relatively less influenced by the effects of accompanying disease. Methods: We studied 135 children and adolescents (8-16 years old). Plasma glucose, insulin, lipid profile, visfatin and other adipocytokine levels were measured. CT scans were performed to evaluate the distribution of abdominal fat. We analyzed the relationship between circulating visfatin levels and anthropometric and metabolic parameters according to central adiposity (total abdominal fat by CT scan). Results: In the lower-adiposity group, plasma visfatin concentrations were significantly correlated with total abdominal fat, visceral fat, subcutaneous abdominal fat, plasma triglyceride level and homeostasis model assessment of insulin resistance (HOMA-IR). In a multiple linear regression analysis, visceral fat and triglycerides were independently associated with plasma visfatin levels. In the higher-adiposity group, plasma visfatin concentrations were not correlated with visceral fat or HOMA-IR but were significantly correlated with circulating interleukin-6 levels. Conclusion: These data suggest that the relationship between plasma visfatin concentrations and metabolic parameters differs according to central adiposity and that plasma visfatin concentrations are correlated with visceral fat and triglyceride levels, especially in children and adolescents with lower adiposity.

Acute and Chronic Effects of Biliopancreatic Diversion with Duodenal Switch Surgery on Plasma Visfatin and Apelin Levels in Patients with Severe Obesity

Visfatin is an adipokine linked to obesity and inflammation, and it has insulin-mimetic properties. Apelin is an adipokine with positive cardiac inotropic effects, and it may be related to inflammatory molecules. Variations in plasma visfatin and apelin levels following bariatric surgery remain controversial. In this study, patients who underwent a biliopancreatic diversion with duodenal switch (BPD-DS) were compared to a severely obese group (control group). Anthropometric measures and blood samples were taken before surgery, on days 1 and 5, as well as at 6 and 12months after surgery in the BDP-DS group. For the control group, the tests were performed at baseline and at 6 and 12months. Seventy subjects in the BPD-DS group and 28 in the control group were included. The expected reduction in body weight at 1 year after a BPD-DS was observed (85.9 ± 18.5 vs. 136.6 ± 27.7kg at baseline; p < 0.001). Plasma visfatin levels decreased at day 1 (16.13 ± 5.56 vs. 18.82 ± 7.36ng/mL at baseline; p = 0.001), while plasma apelin levels decreased at day 5 (0.50 ± 0.28 vs. 0.55 ± 0.33ng/mL at baseline; p = 0.040) after surgery. There were no changes at 6 and 12months compared to baseline, and no changes were observed in the control group. Our data show that 1-year weight loss induced by BPD-DS did not influence the overall plasma visfatin and apelin levels in severely obese patients.

Effects of different levels of physical inactivity on plasma visfatin in healthy normal-weight men

We tested whether physical inactivity (PI) is an independent predictor of plasma visfatin, a newly discovered adipokine likely involved in the relationship between obesity-associated low-grade inflammation and insulin resistance. PI was induced in healthy men (Body Mass Index = 23.4 ± 0.6 kg·m(-2)) by 10 days of confinement (n = 8), 1 month of detraining (n = 10), and 3 months of bed rest with (n = 7) and without exercise (n = 8). Visfatin was negatively associated with activity energy expenditure (p = 0.03). No relationship was observed with insulin sensitivity. This suggested that PI itself increases visfatin concentrations.

Elevated plasma visfatin concentrations in patients with community-acquired pneumonia

Visfatin has been associated with some inflammatory disease. This study aimed to compare plasma visfatin levels in patients with community-acquired pneumonia and healthy controls and to furthermore investigate the relationship between their concentrations and 30-day mortality in patients. Plasma visfatin concentrations were measured in 176 patients and 95 healthy controls. The admission visfatin levels were significantly increased in all patients, survivals and non-survivals with community-acquired pneumonia compared with healthy control individuals, associated with pneumonia severity index score, Acute Physiology and Chronic Health Evaluation II score, white blood cell count, and plasma C-reactive protein level, and identified as an independent predictor for 30-day mortality. Its predictive value was similar to those of pneumonia severity index score and Acute Physiology and Chronic Health Evaluation II score. However, visfatin did not statistically significantly improve the predictive values of pneumonia severity index score and Acute Physiology and Chronic Health Evaluation II score. Thus, higher plasma visfatin level correlates with disease severity and markers of system inflammation and represent a novel biomarker for predicting 30-day mortality in patients with community-acquired pneumonia.

Gestational diabetes is associated with high energy and saturated fat intakes and with low plasma visfatin and adiponectin levels independent of prepregnancy BMI

Gestational diabetes mellitus (GDM) risk factors are well established for Caucasians, but not for Asians. We hypothesized that nutrient intakes, plasma adipokines and/or gestational hormones might be linked to GDM development among pregnant Korean women. This study sought to identify new risk factors for GDM and adverse pregnancy outcomes according to body weight at prepregnancy. All subjects were pregnant women visiting the Cheil General Hospital and Women's Healthcare Center between June 2006 and March 2009. Non-GDM (n=531) and GDM (n=215) participants were divided into normal-weight and overweight groups according to prepregnancy body mass index (BMI) above or below 23 kg/m(2) at 24-28th week of gestation. At that time, glucose tolerance, insulin resistance as homeostatic model assessment for insulin resistance, insulin secretory capacity as homeostatic model assessment for β-cell function, anthropometric measurement, nutrient intakes, and plasma levels of adipokines and gestational hormones were determined. GDM women gained more weight in early pregnancy than non-GDM among normal-weight women. GDM was mainly associated with increased insulin resistance in overweight women and decreased insulin secretory capacity in normal-weight women. Plasma visfatin and adiponectin were lower and progesterone levels higher in GDM than non-GDM independent of BMI while plasma resistin levels were higher in non-GDM, but not GDM, overweight women. Energy and saturated fat intakes were higher in GDM independent of body weight, whereas taurine intakes were lower in GDM than non-GDM only in normal-weight women. Low visfatin and adiponectin and high progesterone levels in the circulation and high energy and saturated fat intakes were common risk factors for GDM and pregnancy outcome such as large for gestational age. Daily reference intakes for energy and fat during pregnancy need to be re-evaluated according to prepregnancy BMI.

Visfatin, Leptin, and TNF-α: Interrelated Adipokines in Insulin-Resistant Clinical and Subclinical Hypothyroidism

Purpose. This study is designed to evaluate the interrelationships among adipokines—visfatin, leptin, and tumor necrosis factor-α (TNF-α)— and insulin resistance (IR) in overt (n = 40) and subclinic hypothyroid (n = 25) patients and compare our findings with sex and body mass index-matched healthy controls (n = 25). Methods. Serum visfatin, leptin, and TNF-α levels were measured by enzyme-linked immunosorbent assay and C-reactive protein by immunoturbidimetry. Thyroid status (TSH, FT3, FT4) and lipid status (triglyceride, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, total cholesterol) parameters were measured. IR was determined by homeostatic model assessment (HOMA-IR) and McAuley (McA) indices. Results. HOMA-IR (p < 0.05) and McA indices (p < 0.01) revealed the presence of IR in overt hypothyroid patients. C-reactive protein, TNF-α, leptin, and visfatin levels were significantly higher (p < 0.01, p < 0.01, p < 0.001, and p < 0.001) in overt hypothyroid patients than euthyroid control group. Subclinic hypothyroid patients were observed to have significantly higher leptin and visfatin levels (p < 0.05) than euthyroid control group. In overt hypothyroid patients, we found plasma visfatin to be significantly positively correlated with HOMA-IR index (r = 0.336, p < 0.05) and body mass index (r = 0.445, p < 0.01) and negatively correlated with McA index (r = –0.574, p < 0.01). Conclusion. This study demonstrates the presence of IR in overt hypothyroid patients by HOMA and McA indices. Increased levels of visfatin, leptin, and TNF-α in overt and subclinic hypothyroid patients and the correlations among these adipokines highlighten their crucial role in the IR-associated disorders.

Prognostic significance of plasma visfatin levels in patients with ischemic stroke

Plasma visfatin concentration has been enhanced in ischemic stroke. The aim of the current investigation was to test whether determination of visfatin in plasma is associated with 6-month clinical outcomes including mortality and unfavorable outcome (modified Rankin Scale score>2) in the patients with ischemic stroke. Between July 2009 and January 2012, plasma visfatin concentrations of 186 patients and 100 healthy individuals were quantified by enzyme-linked immunosorbent assay. Plasma visfatin concentrations were higher in patients than in healthy individuals (108.5±41.1ng/mL vs. 13.8±3.9ng/mL, P<0.001). A logistic regression analysis selected plasma visfatin concentration as an independent predictor for 6-month clinical outcomes (both P<0.01). Using receiver operating characteristic curve analysis, plasma visfatin concentration was found to predict 6-month clinical outcomes with the high predictive performance. The predictive value of visfatin was in the range of National Institutes of Health Stroke Scale score (both P>0.05). Combined use of visfatin and National Institutes of Health Stroke Scale score did not improve the predictive significance (both P>0.05). Thus, visfatin may help in the prediction of long-term clinical outcomes in patients with ischemic stroke.

The Effect of Sodium Restricted Diet on Plasma Visfatin Levels in Hypertensive Patients with Visceral Obesity

Aim/Background: Experimental and clinical studies revealed contradictory data concerning the influence of renin-angiotensin-aldosterone (RAA) system activation on visfatin release. The aim of the present study was the assessment of the effect of dietary sodium restriction with RAA system activation on visfatin level in hypertensive and normotensive patients with visceral obesity. Methods: The study included 24 hypertensive patients with visceral obesity (12 women) and 22 normotensive subjects with visceral obesity (11 women) constituting the control group. Plasma renin activity, plasma insulin, aldosterone and visfatin levels were determined twice, on normal-salt diet after 6-8 h in recumbent position and the second time after 3 days of dietary sodium restriction and upright position for 2 h. Dietary compliance was controlled by 24 h natriuresis measurement. Results: Hypertensive patients had significantly higher plasma visfatin level than the control group [11.0 (8.5-13.5) vs. 6.8 (6.0-7.6) ng/ml, p=0.003]. Dietary sodium restriction and upright position caused significant increase in PRA and plasma aldosterone level in both groups. While, plasma visfatin level remained unaffected. In the combined group plasma visfatin levels correlated with BMI (r=0.398), waist circumference (r=0.391), glucose (r=0.328), insulin (r=0.663), HOMA-IR (r=0.698), triglycerides (r=0.500) and CRP (r=0.546) but not with percentage of fat mass, percentage of trunk fat, and blood pressure values. Conclusions: 1) Increased plasma visfatin concentration may play a significant role in the pathogenesis of hypertension in patients with visceral obesity. 2) RAA system activation by dietary sodium restriction and upright position has no effect on plasma visfatin levels in subjects with visceral obesity.

Plasma visfatin, associated with a genetic polymorphism −1535C > T, is correlated with C-reactive protein in Chinese Han patients with traumatic brain injury

Visfatin is a newly identified pro-inflammatory adipokine and a genetic polymorphism −1535 C>T located in the visfatin gene promoter has been suggested to be associated with the regulation of visfatin expression in some inflammatory illness. However, there were some conflicting results regarding whether this variant is functional or not. This study aimed to examine the relations of the −1535 C>T single nucleotide polymorphism (SNP) of visfatin gene to the plasma visfatin and C-reactive protein concentrations in traumatic brain injury (TBI). 318 Chinese Han patients with TBI were recruited in this study. Plasma visfatin and C-reactive protein levels were significantly different between the genotypes in the SNP-1535 C>T even after adjustment for age, sex and body mass index. The genotype C–C had the highest plasma visfatin and C-reactive protein concentrations. The plasma visfatin and C-reactive protein concentrations between the variant genotypes C–T and T–T did not differ significantly. Plasma visfatin level was significantly associated with plasma C-reactive protein level using multivariate linear regression. Thus, the SNP-1535 C>T of visfatin gene seemed to be potentially involved in the inflammatory component of TBI through a decreased production of visfatin.

Elevated plasma level of visfatin/pre-b cell colony-enhancing factor in male oral squamous cell carcinoma patients

Objectives: Visfatin, also known as nicotiamide phosphoribosyltransferase or pre-B cell colony enhancing factor, is a pro-inflammatory cytokine whose serum level is increased in various cancers. In this study, we investigated whether plasma visfatin levels were altered in patients with oral squamous cell carcinoma (OSCC). The relationship between plasma visfatin levels and the pretreatment hematologic profile was also explored. Study Design: Plasma visfatin concentrations were measured through ELISA in OSCC patients and control subjects. A total of 51 patients with OSCC and 57 age- and body mass index (BMI)-matched control subjects were studied. All study subjects were male. Results: Plasma visfatin was found to be elevated in patients with OSCC (7.0 ± 4.5 vs. 4.8 ± 1.9 ng/ml, p = 0.002). Multiple logistic regression analysis revealed visfatin as an independent association factor for OSCC, even after full adjustment of known biomarkers. Visfatin level was significantly correlated with white blood cell (WBC) count, neutrophil count, and hematocrit (all p < 0.05). In addition, WBC count, neutrophil count, and visfatin gradually increased with stage progression, and hematocrit gradually decreased with stage progression (all p < 0.05). Conclusion: Increased plasma visfatin levels were associated with OSCC, independent of risk factors, and were correlated with inflammatory biomarkers. These data suggest that visfatin may act through inflammatory reactions to play an important role in the pathogenesis of OSCC. Key words:Visfatin; oral squamous cell carcinomas; white blood cell count; neutrophil count.

High concentrations of visfatin in the peripheral blood of patients with acute basal ganglia hemorrhage are associated with poor outcome

Higher plasma visfatin concentration has been associated with clinical outcomes of traumatic brain injury. No published information exists to date about change in plasma visfatin after intracerebral hemorrhage. This study included one hundred and twenty-eight healthy controls and 128 patients with intracerebral hemorrhage. The unfavorable outcome was defined as modified Rankin Scale score >2 at 6 months. The patients had higher plasma visfatin measurements than control subjects. Plasma visfatin levels were highly correlated with National Institutes of Health Stroke Scale score and plasma C-reactive protein levels in the patients. A multivariate analysis identified plasma visfatin level as an independent predictor for 6-month mortality and unfavorable outcome. According to receiver operating characteristic curve analysis, the predictive value of the plasma visfatin concentration was similar to National Institutes of Health Stroke Scale score. In a combined logistic-regression model, visfatin improved the predictive value of National Institutes of Health Stroke Scale score for 6-month unfavorable outcome. Thus, increased plasma visfatin level is associated with 6-month clinical outcomes after intracerebral hemorrhage.

Plasma visfatin levels and gene expression in morbidly obese women with associated fatty liver disease

ObjectivesThe few studies on the physiopathological role of visfatin in morbid obesity and the related metabolic diseases have led us to examine visfatin levels and its liver gene expression in morbidly obese women with non-alcoholic fatty liver disease (NAFLD). Design and methodsWe examined the circulating levels of visfatin by ELISA in serum samples from 95 morbidly obese women (MO) (BMI>40kg/m2) who underwent bariatric surgery and 38 normal weight control women (BMI<25kg/m2). We analysed visfatin liver and adipose tissue mRNA expression by RT-PCR. We evaluated the circulating levels and gene expression of adiponectin, resistin, RBP4, TNFα, IL6 and CRP. ResultsSerum visfatin was significantly higher in MO compared with controls, and also in MO with NAFLD was significantly higher than MO with normal liver. We found that NAFLD diabetic patients presented similar serum visfatin levels than non-diabetic. Serum visfatin correlated with IL6 (r=0.496; p<0.001) and CRP levels (r=0.241; p=0.049).Liver visfatin expression was significantly higher in MO compared to controls and was also significantly higher in MO with NAFLD than in MO with normal liver. Visfatin liver expression correlated positively with resistin (r=0.436, p=0.018) and TNFα expression (r=0.328, p=0.028).Visfatin expression in adipose tissues was similar among the MO groups analysed. ConclusionSerum visfatin and its liver expression are higher in MO women with NAFLD, irrespective of the presence of diabetes. Serum visfatin and its liver expression correlate positively with pro-inflammatory factors. These findings suggest that visfatin may be a molecule related with fat inflammation in morbid obesity and fatty liver disease.

Elevated serum visfatin levels in patients with acute myocardial infarction.

Visfatin, a novel adiopocytokine, has been proven to be a proinflammatory mediator involved in the process of atherosclerosis. Visfatin has been shown to play a role in plaque destabilization as it is found abundantly in foam cell macrophages within unstable atherosclerotic plaques. The present study is designed to investigate the potential association between serum vistafin levels and the risk of acute myocardial infarction (AMI). There were 72 patients (mean age: 61.57 ± 11.40 years) as cases who presented with first-time AMI that were assessed 8 hours after the incident. The control group consisted of 83 healthy volunteers (mean age: 60.30 ± 8.32 years). Plasma visfatin levels were measured using enzyme immunoassay in both groups. Biochemical parameters were analyzed. Blood pressure, body mass index (BMI), waist circumference, diabetes, and hypertension were recorded. Serum visfatin levels were significantly higher in patients with AMI (12.77 ± 8.06 ng/ml) compared to controls (6.57 ± 2.96 ng/ml, P ≤ 0.001). We found that a visfatin level > 7.244 ng/ml (log visfatin > 0.86) had a sensitivity of 70% and a specificity of 75% for predicting AMI. We have detected high levels of visfatin in patients with AMI. It can be concluded that proinflammatory cytokines such as visfatin may play a role in the development of atherosclerosis as well as destabilization of the atherosclerotic plaque.

Change in plasma visfatin level after severe traumatic brain injury

Higher plasma visfatin concentration has been associated with ischemic stroke. Thus, we sought to investigate change in plasma visfatin level after traumatic brain injury and to evaluate its relation with disease outcome. Seventy-six healthy controls and 98 patients with acute severe traumatic brain injury were recruited. Twenty-seven patients (27.6%) died and 48 patients (49.0%) suffered from unfavorable outcome (Glasgow outcome scale score of 1–3) in 6 months. On admission, plasma visfatin level was increased in patients than in healthy controls and was highly correlated with Glasgow Coma Scale score. A multivariate analysis identified plasma visfatin level as an independent predictor for 6-month mortality and unfavorable outcome. According to receiver operating characteristic curve analysis, the predictive value of the plasma visfatin concentration was similar to Glasgow Coma Scale score's. In a combined logistic-regression model, visfatin did not improve the predictive value of Glasgow Coma Scale score. Thus, increased plasma visfatin level is associated with 6-month clinical outcomes after severe traumatic brain injury.

The significance of visfatin in patients with coronary heart disease

Objective To investigate the change of plasma visfatin in patients with coronary heart disease and its clinical significance.Methods A total of 310 patients with coronary heart disease (ACS group:n =217; SAP group:n =93) and of 90 healthy subjects with a matched age and gender were included in this study.The plasma concentration of visfatin of each subject was measured using ELISA assay,and each patient underwent selective coronary angiography examination.A total of 85 cases of patients in CHD group underwent 64-slice CT coronary imaging to evaluate the main plaque within the coronary.Results The visfatin,LDL,BMI,blood glucose levels was significantly higher in CHD group[ ( 128.18 ± 13.86)ng/ml,(3.63 ± 1.48) mmol/L,( 26.18 ± 1.82) kg/m2,(7.25 ± 2.03 ) mmol/L] than in control group [ (75.96 ± 10.27 )ng/ml,(2.64 ± 0.53 ) mmol/L,( 23.51 ± 0.89 ) kg/m2,(5.11 ± 1.53 ) mmol/L,P ＜ 0.05 ],respectively.The visfatin level in the ACS group [ ( 145.57 ± 19.95 ) ng/ml ] was significantly higher than the SAP group [ (110.79 ±7.78)ng/ml,P ＜0.05].The visfatin concentration gradually increased with the aggravation of the complexity of coronary lesion types and severity of coronary lesions( P ＜ 0.05).The plasma visfatin concentrations in Soft plaque group and the fibrous plaque group were significantly higher than calcified plaque (P ＜ 0.05).HDL-C and Gensini score of coronary lesions were negatively correlated ( r =- 0.055,P ＜0.05) ; LDL-C,Glu,and visfatin was positively correlated with coronary lesions Gensini score ( r =0.464,0.279,0.531,P ＜ 0.05 ),respectively.Conclusions The plasma visfatin level in patients with Coronary heart disease increased and affected its lipid metabolism.It may be an important inflammatory factors promoting arterial atherosclerosis occurs and development,which has a certain value to the judgment of coronary lesions and plaque stability combined with 64-slice spiral CT examination. Key words: Adipokines/blood; Coronary disease/metabolism/etiology

Study on expression of visfatin mRNA in abdominal omental adipose tissue and its relationship with blood lipid in type 2 diabetics

Objective To investigate the expression of visfatin mRNA in abdominal omental adipose tissue and its relationship with blood lipid in type 2 diabetes mellitus.Methods 161 type 2 diabetic patients were divided into two groups according to triglyceride ( TG ),high triglyceride group ( TG ≥ 1.7mmol/L) and normal triglyceride group(TG ＜ 1.7 mmol/L).The expression of visfatin mRNA in abdominal omental adipose tissue was measured with Northern Blot.Visfatin plasma concentration,fasting plasma glucose (FPG),blood lipid profiles and other biochemical indicators were also measured.Results Comparing with normal triglyceride group,the diabetic patients in high triglyceride group had significantly increased levels of visfatin plasma concentration [ ( 129.07 ± 21.35)ng/mL vs ( 101.65 ± 15.23 ) ng/mL,t =2.295,P ＜0.05]and mRNA expression in omental adipose tissue( P ＜0.05).Visfatin plasma concentration was positively correlated with TG( β =0.592,P ＜0.05 ) and FPG( β =0.763,P ＜0.01 ).Visfatin mRNA expression in omental adipose tissue had no correlation with FPG,TG and other biochemical indicators.Conclusions The plasma visfatin level in T2DM patients may be associated with triglyceride metabolism. Key words: Diabetes mellitus, type 2/complications/metabolism/blood; Hypertriglyceridemia/complications/ metabolism/blood; Omentum/metaholism; Nicotinamide phosphoribosyltransferase/metabolism/blood

NALP3 Inflammasome Activation in the Coronary Arterial Wall of Obese Mice

Inflammasomes as intracellular inflammatory machinery has been reported to switch on the inflammatory response to various danger signals. The present study hypothesized that activation of NALP3 inflammasomes turns on the endothelial inflammatory response and results in arterial endothelial dysfunction during the early stage of obesity and in response to adipokines. To test this hypothesis, we first observed increased inflammasomes activation in coronary arterial wall of obese mice, as shown by colocalization of NALP3 with apoptosis‐associated speck‐like protein (ASC) or caspase‐1 under confocal microscopy. The further studies in these obese mice found that plasma visfatin concentrations increased by 53.8% compared to normal mice. In addition, local transfection of visfatin shRNA in heart or daily injection of caspase‐1 inhibitor, WEHD (1 mg/kg/d) had no effects on visfatin level, but almost blocked obesity‐associated formation of NALP3 inflammasomes as shown by no co‐localization of NALP3 with ASC or caspase‐1. Correspondingly, IHC anlysis revealed that accumulation of T‐cells was abolished by visfatin shRNA and WEHD as shown by much less CD43 stains. In cultured mouse endothelial cells (ECs), confocal microscopy and size exclusion chromatography studies revealed that visfatin treatment significantly enhanced the NALP3 inflammasome complex formation and activation compared to control cells. Additionally visfatin treatment increased the caspase‐ 1 activity by 2.4 folds and IL‐1β production by 2.3 folds compared to control cells. ASC siRNA and WEHD substantially attenuated the visfatin‐induced caspase‐1 activity and IL‐1β production. In conclusion, the activation of NALP3 inflammasomes may be an important initiating mechanism responsible for the adipokine, visfatin to produce inflammatory response and endothelial dysfunction in coronary artery (supported by NIH grant HL057244, HL091464 and HL075316).