Plasma Visfatin Research Articles

Emerging Roles of Antiangiogenic and Angiogenic Proteins in Pathogenesis and Prediction of Preeclampsia

Hypertensive disorders are a major cause of maternal and fetal death, especially in developing nations, with the pregnancy-specific disease preeclampsia-eclampsia responsible for most of this mortality. Preeclampsia, recognized by ancient Greeks, was only sporadically investigated until late last century, current literature still labeling this disorder a “disease of theories.” Thus, not surprisingly, we have started the new millennium unable to predict or prevent preeclampsia, and management strategies remain but supportive, with pregnancy termination still the only definitive “therapy.” This may be about to change, as focused research, mainly in the past decade, has resulted in dramatic progress regarding pathogenesis of disease manifestations and risk assessment, while investigators have begun designing and testing definitive therapy.1 There are still a myriad of uncertainties and unanswered questions to address, but here we summarize the extent of 1 new and exciting chapter in preeclampsia research: the roles of angiogenic and antiangiogenic factors, to which an article in this issue by Rana and colleagues,2 contributes. A landmark report published in 2003 set the stage for all that followed.3 Dr Karumanchi’s laboratory, previously involved in renal cancer research, changed its focus to the kidney in preeclampsia. Using microarray chip technology, they probed gene expression profiles in placentas of women with preeclampsia and those with uncomplicated pregnancies. Of course many differences were noted, but one that caught the investigators’ attention was upregulation of the mRNA for the antiangiogenic protein soluble fms-like tyrosine kinase 1 (abbreviated as sFlt-1 or sVEGFR-1) in placentas from women with preeclampsia. Aware that de novo hypertension and proteinuria were 2 disturbing side effects of certain antiangiogenic compounds tested in cancer patients, these …

Job stress related to glyco‐lipid allostatic load, adiponectin and visfatin

AbstractJob stress has been associated with an increased risk for glyco‐lipid metabolic dysfunction, which can lead to coronary artery disease, diabetes and other adverse health outcomes. We undertook a cross‐sectional study to evaluate the relationship between job stress and glyco‐lipid metabolic change in healthy industrial employees in China. Volunteers (n = 504) were investigated during the routine annual health examination period between June and August 2006. Job stress was assessed by the 22‐item Job Content Questionnaire (JCQ), which included three dimensions: job control, job demand and social support. Glyco‐lipid metabolic status was determined by the glyco‐lipid allostatic load based on the allostasis paradigm and the concept of allostatic load. There were 11 parameters comprising the glyco‐lipid allostatic load: body mass index (BMI); waist to hip ratio (WHR); high‐density lipoprotein (HDL); low‐density lipoprotein (LDL); total cholesterol (TC); triglyceride (TG); glycosylated haemoglobin (HbA1C); homeostasis model assessment‐insulin resistance (HOMA‐IR); HOMA‐β‐cell function; plasma concentrations of adiponectin; and visfatin. Score points were given for values in the high‐risk quartile (0–11). Multivariate analysis of variance (MANOVA) revealed that BMI, WHR, TG, adiponectin, visfatin and glyco‐lipid allostatic load were significantly different between high and low job stress groups after being adjusted for demographic characteristics and health‐related behaviour. Plasma adiponectin levels were negatively correlated with BMI, WHR, HbA1C, TG, IR and visfatin, and positively correlated with HDL. Plasma concentration of visfatin was positively correlated with BMI, WHR, TC and IR. Multiple stepwise linear regression analysis indicated that job control was significantly related to glyco‐lipid allostatic load, plasma adiponectin concentration and plasma visfatin concentration after controlling for demographic characteristics and health‐related behaviour. In conclusion, we found association between job stress, job control and the glyco‐lipid metabolism summary score. Plasma adiponectin and visfatin concentrations related with job stress and job control. Copyright © 2007 John Wiley & Sons, Ltd.

Visfatin Response to Glucose Is Reduced in Women With Gestational Diabetes Mellitus

Abstract The insulin-mimetic adipocytokine visfatin has been associated with insulin resistance in some studies and is regulated by glucose. We hypothesized that glucose-induced changes in plasma visfatin are different in women with gestational diabetes mellitus (GDM). Plasma visfatin concentrations were studied in 10 women with GDM and 10 age-matched healthy women in pregnancy week 24-28 during a standard oral glucose tolerance test (OGTT). Women with GDM had lower systemic visfatin concentrations than controls (1.9±0.8 ng/ml vs 5.2±4.4 ng/ml, respectively, p<0.05), which were associated with fasting glucose (p<0.05). The glucose-induced increase in visfatin over baseline was smaller in GDM, with an area under the curve of 409±106 ng/ml*min versus 780±345 ng/ml*min in controls (p<0.05). Reduced glucose-induced increases in circulating visfatin may be associated with impaired glucose tolerance in women with GDM.

Increased plasma levels of visfatin/pre-B cell colony-enhancing factor in obese and overweight patients with metabolic syndrome

Visfatin [pre-B cell colony- enhancing factor (PBEF)] is a cytokine highly expressed in visceral fat that exhibits insulin-mimetic properties. However, its role in insulin-resistant states, such as in metabolic syndrome (MetS), remains largely unknown. To investigate the possible differences of plasma visfatin levels between obese and overweight subjects with and without MetS. Plasma visfatin concentrations were measured with enzyme-linked immunosorbent assay (ELISA) in 28 overweight and obese [body mass index (BMI)>28 kg/m2] subjects with Mets and 28 age- and sex-matched overweight and obese (BMI>28 kg/m2) individuals without MetS (control group). Patients with MetS exhibited significantly elevated waist circumference (WCR ) values, higher blood pressure readings, higher fasting glucose and triglyceride concentrations as well as lower levels of HDL cholesterol (HDL-C) compared with controls. Total and LDL cholesterol (LDL-C) concentrations did not differ significantly between the two groups. Plasma visfatin concentrations were significantly higher in subjects with MetS compared with controls [27 (16- 65) ng/ml vs 19 (10-47) ng/ml, p<0.05]. The same results were observed even after adjustment for age, sex and BMI. Plasma visfatin levels were positively correlated with age (r=0.32, p<0.05), WCR (r=0.31, p<0.05), triglyceride (r=0.59, p<0.01) and glucose (r=0.33, p<0.05) levels and were negatively correlated with HDL-C levels (r=-0.38, p<0.05). Multiple linear regression analysis revealed similar results. Plasma visfatin levels are increased in overweight and obese subjects with MetS compared with those individuals who do not fulfil the criteria for the diagnosis of MetS.

CORRIGENDUM: Effect of Rosiglitazone on Visfatin and Retinol-binding Protein-4 Plasma Concentrations in HIV-positive Patients

CORRIGENDUM: Effect of Rosiglitazone on Visfatin and Retinol-binding Protein-4 Plasma Concentrations in HIV-positive Patients

Reduced plasma visfatin in end-stage renal disease is associated with reduced body fat mass and elevated serum insulin

Reduced plasma visfatin in end-stage renal disease is associated with reduced body fat mass and elevated serum insulin

Association between plasma visfatin and vascular endothelial function in patients with type 2 diabetes mellitus

Visfatin is a newly identified adipocytokine that mimics insulin action. However, the pathophysiological role of visfatin in diabetic patients is not fully understood. The main purpose of this study was to investigate the association of plasma visfatin with endothelial function in patients with type 2 diabetes mellitus. In addition, the relationships of visfatin with oxidative stress, low-grade inflammation, atherosclerosis, adiponectin, plasma renin activity, and aldosterone were also explored, and the effect of pioglitazone on visfatin was examined. Visfatin levels were measured in 80 patients with type 2 diabetes mellitus and in 28 age-matched healthy subjects. Endothelial function was evaluated by using flow-mediated vasodilatation (FMD), oxidative stress was assessed by the level of urinary 8-iso-prostaglandin F 2 α , and atherosclerosis and inflammation were measured by using the intimal-medial complex thickness and the levels of high-sensitivity C-reactive protein and fibrinogen. Pioglitazone was administered for 12 weeks at a dose of 30 mg/d in a further 20 patients with type 2 diabetes mellitus. There was a significant negative correlation between the log 10-transformed (log) plasma visfatin concentration and FMD or creatinine clearance ( R = −0.2672, P = .0167; R = −0.2750, P = .0136). Log visfatin was also positively correlated with log urinary albumin excretion ( R = 0.2305, P = .0397). In addition, it was also found that visfatin had a significant negative correlation with plasma aldosterone ( R = −0.2432, P = .0297). In stepwise regression analysis, creatinine clearance, log aldosterone, FMD, and sex showed a significant association with log visfatin ( P = .0040, P = .0069, P = .0444, and P = .0487, respectively), and log 8-iso-prostaglandin F 2 α showed a tendency for an association ( P = .0515). Pioglitazone therapy did not affect the visfatin concentration in the 20 pioglitazone-treated patients with diabetes, although a significant elevation of visfatin was obtained in a subgroup of 11 female patients ( P = .0381). In conclusion, the current study showed that visfatin is negatively associated with vascular endothelial function evaluated by FMD and creatinine clearance, and positively associated with log urinary albumin excretion. Visfatin was also negatively correlated with circulating aldosterone. Pioglitazone therapy for 12 weeks did not affect the plasma visfatin concentration significantly in all diabetic patients, but a significant elevation in visfatin was obtained in women only.

Increased plasma visfatin concentrations in women with polycystic ovary syndrome

To test the hypothesis that plasma visfatin concentrations will be higher in women with polycystic ovary syndrome (PCOS) than in women without PCOS. Clinical study. University hospital. A total of 52 women were evaluated. Twenty-six had PCOS, and the remaining 26 were healthy women with regular menstrual cycles who served as control subjects. Plasma visfatin concentrations were analyzed with the use of RIA. Serum concentrations of FSH, LH, TSH, PRL, T, insulin, E(2), and visfatin. Plasma visfatin concentrations were significantly higher in the PCOS group (336.8 +/- 50.2 ng/mL) than in the healthy control group (282.4 +/- 43.3 ng/mL). Logistic regression analysis indicated a significant association between odds ratio (OR) values of PCOS and visfatin levels (OR = 2.81; 95% confidence interval [CI], 2.74-2.90), T (OR = 3.39; 95% CI, 2.85-4.16), and LH levels (OR = 3.49; 95% CI, 2.79-4.56). There was no correlation between plasma visfatin concentrations and T, insulin, and LH levels or age in either the PCOS group or the control group. We observed that plasma visfatin levels were positively correlated with body mass index in the PCOS group (r = 0.396, r(2) = 0.157) but not in the control group (r = -0.328, r(2) = 0.108). Our data show that women with PCOS exhibit higher plasma visfatin levels than control subjects of similar body mass index. Further studies are required to clarify the etiology and effects of hypervisfatinemia in women with PCOS.

Circulating Levels of Visfatin/Pre–B-Cell Colony–Enhancing Factor 1 in Relation to Genotype, GFR, Body Composition, and Survival in Patients With CKD

Visfatin, also known as pre-B-cell colony-enhancing factor 1 (PBEF-1), recently was shown to be secreted from adipocytes and have insulin-mimetic properties in mice. Because renal failure per se is associated with both increased levels of circulating peptides and marked insulin resistance, even in the absence of diabetes mellitus, we hypothesized that visfatin could be a factor linking inflammation, kidney disease, and insulin resistance in this patient group. Altogether, we studied 189 patients with chronic kidney disease (CKD), comprising 149 patients with CKD stage 5 (glomerular filtration rate [GFR] < 15 mL/min; mean, 7 +/- 2 mL/min [<0.25 mL/s; mean, 0.12 +/- 0.03 mL/s]; 61% men; mean age, 54 +/- 12 years) and 40 patients with CKD stages 3 to 4 (GFR, 15 to 60 mL/min; mean, 33 +/- 21 mL/min [0.25 to 1.00 mL/s; mean, 0.55 +/- 0.35 mL/s]; 72% men; age, 59 +/- 15 years). We compared these with 30 randomly selected population controls (mean GFR, 85 +/- 16 mL/min [1.42 +/- 0.27 mL/s]; 69% men; age, 64 +/- 11 years). Serum visfatin was measured by using commercially available enzyme-linked immunosorbent assay, and we also performed genotyping of 3 verified polymorphisms in the visfatin gene (-423A/G, -1001T/G, and -1535C/T). Body fat was estimated by using dual-energy x-ray absorptiometry. Serum visfatin levels were greater in patients with CKD stage 5 (41.3 +/- 18.0 ng/mL) than in those with CKD stages 3 to 4 (34.0 +/- 9.8 ng/mL; P < 0.01 versus CKD stage 5) or healthy controls (29.3 +/- 8.1 ng/mL; P < 0.0001). However, there were no significant differences between patients with and without diabetes, and the significant differences in circulating visfatin levels between genotypes disappeared after adjustment for differences in age, sex, GFR, and serum albumin level. In univariate analysis, visfatin level correlated with levels of GFR (rho = -0.22; P = 0.001), interleukin 6 (IL-6; rho = 0.17; P = 0.01), high-sensitivity C-reactive protein (rho = 0.14; rho < 0.05), and soluble vascular cell adhesion molecule 1 (sVCAM-1; rho = 0.39; P < 0.0001), but not total or truncal fat mass, insulin resistance, or hemoglobin A(1c) level. High plasma visfatin level predicted mortality in patients with CKD, also after adjustment for age and sex (likelihood ratio, 18.2; P < 0.0001), but not after additional correction for GFR, sVCAM-1, serum albumin, and serum IL-6 levels. Circulating levels of the cytokine visfatin/PBEF-1 are influenced by renal function, but are not associated with fat mass or surrogate markers of insulin resistance in patients with CKD. Visfatin was associated independently with level of sVCAM-1, a marker of endothelial damage.

Clinical Correlates of Circulating Visfatin Levels in a Community-Based Sample

Visfatin, a novel adipokine with insulin-mimetic characteristics, is highly expressed in visceral fat (1). Associations of circulating visfatin concentrations with diabetes and obesity have not been rigorously established, most likely due to small sample sizes of prior studies. Furthermore, relations of visfatin to other cardiovascular risk factors in the general population have not been examined systematically. Accordingly, we tested the hypothesis that plasma visfatin would be positively related to obesity, diabetes, and visceral adiposity in a community-based sample. The design and selection criteria of the Framingham Third Generation Cohort are detailed elsewhere (2). Briefly, 4,095 adults (53% women; mean age 40 years) having at least one parent in the Framingham Offspring Study cohort were recruited in 2001–2005. At their first examination, participants underwent anthropometry, medical history and physical examination, laboratory assessment of cardiovascular risk factors, and, in a subsample, imaging for coronary calcification and adiposity using multidetector computer tomography (MDCT). The present study was performed in a subsample of 374 participants (9% eligible; 53% women) in whom plasma visfatin was assayed. We randomly selected these participants using a weighted sampling scheme with oversampling of the lowest and highest sex-specific quintiles of BMI (ratio of 1.5:2:1.5 for the lowest, middle three, and upper quintiles, respectively) using the participants undergoing MDCT imaging as the sampling frame. We chose this sampling strategy for cost efficiency and optimizing the use of nonrenewable serological resources (given …

Effect of Rosiglitazone on Visfatin and Retinol-Binding Protein-4 Plasma Concentrations in HIV-Positive Patients

Thiazolidinediones (TZD) may improve insulin resistance in patients with diabetes and HIV. The novel adipocytokines visfatin and retinol-binding protein-4 (RBP-4) have been proposed to influence the development of impaired glucose tolerance. The impact of TZD on these cytokines is yet unknown. In this randomized, double-blind, placebo-controlled parallel group study, 37 lean HIV-positive subjects aged 19-50 years were treated with 8 mg/day rosiglitazone (n=20) or placebo (n=17) for 6 months. Insulin sensitivity was estimated from the homeostasis model assessment (HOMA) index. Fasting visfatin, RBP-4, leptin, and adiponectin plasma concentrations were analyzed by immunoassays. Rosiglitazone had no effect on impaired insulin sensitivity, but increased median plasma visfatin from 6.2 ng/ml (95% CI: 5.9; 6.5) to 13.7 ng/ml (12.6; 19.1) (P<0.001) and adiponectin from 3.2 ng/ml (2.2; 4.0) to 4.0 ng/ml (3.3; 8.5; P<0.001). RBP-4 was lowered from 21.0 ng/ml (19.6; 23.1) to 16.3 ng/ml (15.2; 17.0; P<0.001), and leptin concentrations were unchanged. Adipocytokine concentrations were stable in subjects receiving placebo, where a deterioration in insulin sensitivity was detectable (P<0.05). Changes in visfatin and RBP-4 were correlated in subjects receiving rosiglitazone (r=-0.64, P<0.01) but not placebo (r=0.12, P=0.15). TZD treatment affects circulating adipocytokine concentrations in subjects with HIV. Reductions in RBP-4 and increases in visfatin may contribute to the pharmacodynamic action of TZD on glucose homeostasis. Quantification of adipocytokines might be useful to assess TZD treatment effectiveness in insulin-resistant subjects with HIV.

Plasma visfatin response to combined exercise training in healthy women

Purpose: Visfatin is recently identified adipocytokine and its role in response to exercise in human is not known. In this study we have investigated whether plasma visfatin is altered by exercise training in healthy women. Methods: Fasting plasma visfatin concentrations was measured in 10 women who participated in a supervised combined exercise program (60 min/day, 60–70% HR-reserve, 400 kcal, 10RM/3set, 3 days/week) for three months. Twelve women subjects were served as controls. Body weight, body mass index, lipids, FFA, growth hormone, insulin homeostasis model assessment (HOMA-R), and fasting levels for visfatin and glucose were measured before and after the exercise program. Results: Body weight, BMI, lipids, and % body fat, and FFA were significantly decreased in exercise training group (p<.05) compared with control group. However, visfatin levels were not significantly changed after combined exercise training in both exercise group and control group. Conclusion: In this study plasma visfatin was not significantly changed by combined exercise training in healthy women. In addition, visfatin concentrations was not correlated with other variables.

Changes and Relations of Circulating Visfatin, Apelin, and Resistin Levels in Normal, Impaired Glucose Tolerance, and Type 2 Diabetic Subjects

Visfatin and apelin are two novel adipocyte- secreted hormone proposed to link obesity with insulin resistance. In this study we investigated whether plasma visfatin and apelin levels were altered in normal, impaired glucose tolerance, and type 2 diabetic subjects. We also assessed the association between plasma visfatin, or apelin and body composition, metabolic parameters, and resistin concentrations in these subjects. The visfatin levels of fasting and 2-h post-glucose load were found to be significantly decreased in diabetics compared with the controls ( P<0.05). In contrast, basal apelin levels were significantly increased in the IGT and diabetic subjects compared with the controls ( P<0.05 and P<0.01). The apelin levels of 2-h post-glucose load were significantly higher than the basal levels in every group (all P<0.05). Fasting plasma visfatin was found to correlate positively and significantly with BMI, WHR, and fasting plasma resistin, but negatively with HbA1c and 2 h OGTT glucose. Multiple regression analysis showed that WHR, HbA1c, 2 h OGTT glucose were independent related factors influencing plasma visfatin levels. Fasting plasma apelin levels correlated positively with HOMA-IR, BMI, TC, LDL-C, FBG and Fasting plasma insulin. Multiple regression analysis also showed that HOMA-IR, BMI, and TC were independent related factors influencing plasma apelin levels. The present work indicates the potential link of visfatin and apelin with the pathogenesis of insulin resistance and T2DM.

Plasma visfatin levels in young male patients with uncomplicated and newly diagnosed hypertension

Plasma visfatin levels in young male patients with uncomplicated and newly diagnosed hypertension

Human Visfatin Expression: Relationship to Insulin Sensitivity, Intramyocellular Lipids, and Inflammation

Visfatin (VF) is a recently described adipokine preferentially secreted by visceral adipose tissue (VAT) with insulin mimetic properties. The aim of this study was to examine the association of VF with insulin sensitivity, intramyocellular lipids (IMCL), and inflammation in humans. VF mRNA was examined in paired samples of VAT and abdominal sc adipose tissue (SAT) obtained from subjects undergoing surgery. Plasma VF and VF mRNA was also examined in SAT and muscle tissue, obtained by biopsy from well-characterized subjects with normal or impaired glucose tolerance, with a wide range in body mass index (BMI) and insulin sensitivity (S(I)). The study was conducted at a University Hospital and General Clinical Research Center. S(I) was measured, and fat and muscle biopsies were performed. In impaired glucose tolerance subjects, these procedures were performed before and after treatment with pioglitazone or metformin. We measured the relationship between VF and obesity, S(I), adipose tissue inflammation, IMCL, and response to insulin sensitizers. No significant difference in VF mRNA was seen between SAT and VAT depots. VAT VF mRNA associated positively with BMI, whereas SAT VF mRNA decreased with BMI. SAT VF correlated positively with S(I), and the association of SAT VF mRNA with S(I) was independent of BMI. IMCL and markers of inflammation (adipose CD68 and plasma TNFalpha) were negatively associated with SAT VF. Impaired glucose tolerance subjects treated with pioglitazone showed no change in SAT VF mRNA despite a significant increase in S(I). Plasma VF and muscle VF mRNA did not correlate with BMI or S(I) or IMCL, and there was no change in muscle VF with either pioglitazone or metformin treatments. SAT VF is highly expressed in lean, more insulin-sensitive subjects and is attenuated in subjects with high IMCL, low S(I), and high levels of inflammatory markers. VAT VF and SAT VF are regulated oppositely with BMI.

The Adipokine Visfatin is Markedly Elevated in Obese Children

The insulin-mimetic adipocytokine visfatin has been linked to adiposity and the metabolic syndrome. Cross-sectional study. Eighty-three nondiabetic obese children and 40 healthy controls. We analyzed plasma visfatin concentrations to assess whether this adipokine is associated with adiposity. Plasma visfatin concentrations were nearly 2-fold higher in obese children (mean, 1.1 ng/mL; 95% CI, 0.2-6.6) than in controls (0.6 ng/mL, 95% CI, 0.6 to 0.6; P < 0.001). No relationship was detectable between visfatin and other subject characteristics, hsCRP or the lipid profile. Visfatin may be involved in the development of metabolic derangements in obese children.

Increased Visfatin Messenger Ribonucleic Acid and Protein Levels in Adipose Tissue and Adipocytes in Women with Polycystic Ovary Syndrome: Parallel Increase in Plasma Visfatin

Polycystic ovary syndrome (PCOS) is a multifaceted metabolic disease linked with insulin resistance (IR) and obesity. Recent studies have shown that plasma levels of the insulin-mimetic adipokine visfatin increase with obesity. Currently, no data exist on the relative expression of visfatin in either plasma or adipose tissue of PCOS women. We investigated the mRNA expression of visfatin from sc and omental (om) adipose tissue and sc adipocytes in women with PCOS compared with matched normal women, as well as visfatin protein in adipose tissue; plasma visfatin was also assessed. Real-time RT-PCR and Western blotting were used to assess the relative mRNA and protein expression of visfatin. Biochemical measurements were performed. There was significant up-regulation of visfatin mRNA in both sc (P < 0.05) and om (P < 0.05) adipose tissue of PCOS women, when compared with normal controls; these findings were also reflected in isolated sc adipocytes (PCOS > controls; P < 0.05). In addition to elevated plasma visfatin levels in women with PCOS (mean +/- sd, 30.2 +/- 10.4 vs. 11.2 +/- 6.2 ng/ml; P < 0.01) when compared with normal controls, visfatin protein levels were significantly greater in both sc and om adipose tissue of PCOS women (P < 0.05 and P < 0.01, respectively). The precise reason for the up-regulation of visfatin seen in women with PCOS, a proinflammatory state, is unknown. Additional studies are needed to clarify the potential role of visfatin in the pathophysiology of PCOS.

Plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus and impaired glucose tolerance

Visfatin, a new adipokine, facilitates adipogenesis and has insulin-mimetic properties. We aimed to investigate the plasma visfatin levels in patients with newly diagnosed and untreated type 2 diabetes mellitus (T2DM) and impaired glucose tolerance (IGT), who had no obesity or hypertension. Twenty-two patients with T2DM, 18 subjects with IGT and 40 healthy controls were enrolled. Visfatin levels were measured along with the BMI, blood pressure, lipids, glucose, insulin, adiponectin and hsCRP levels, and HOMA-IR indexes. Age, sex and BMI were similar in all groups. Visfatin levels were higher in the diabetic group than the controls ( p = 0.01). There was no significant difference in the visfatin levels between the T2DM and IGT groups as well as IGT group and healthy controls. Plasma visfatin concentrations did not differ between men and women. Visfatin levels did not correlate with BMI, blood pressure, plasma adiponectin, insulin, hsCRP, glucose and lipid levels or HOMA-IR indexes in the three groups. These results indicate that hyperglycemia causes an increase in plasma visfatin levels and, as in people with T2DM but not with IGT, this increase gets more prominent as the glucose intolerance worsens.

Impact of antiretroviral therapy on visfatin and retinol‐binding protein 4 in HIV‐infected subjects

To determine circulating levels of adipocytokines, especially the recently characterized visfatin, and the fat-derived factor retinol-binding protein-4 (RBP-4) in HIV-infected subjects and their respective changes following treatment with highly active antiretroviral therapy (HAART). Fourteen HIV-positive, HAART-naïve subjects were compared with 10 HIV-negative healthy controls and reassessed after a 1-year treatment with HAART. Plasma visfatin and RBP-4 were determined by ELISA, whereas leptin and adiponectin by RIA. Body composition was measured with dual X-ray absorptiometry (DXA). Homeostasis model assessment (HOMA-IR) was assessed using insulin and glucose levels. Visfatin and RBP-4 levels in HIV-positive subjects were comparable with those of HIV-negative controls before treatment with HAART. Treatment with HAART for 12 months resulted in a 6.9-fold and 7.1-fold increase of visfatin and RBP-4 levels (+54.0 +/- 9.7 ng mL(-1), P < 0.0001 and +95.3 +/- 31.7 ng mL(-1), P < 0.01), respectively. Leptin (-2.7 +/- 1.6 ng mL(-1), P = 0.054) was unchanged and adiponectin (-2.8 +/- 0.7 microg mL(-1), P < 0.01) decreased. Changes of visfatin concentrations correlated significantly with the increases of RBP-4 (r = 0.78, P = 0.001), fat-free mass (FFM, r = 0.75, P < 0.05) and change of HOMA-IR (r = 0.64, P < 0.05). Parameters of glucose metabolism and body fat mass were unchanged during the observation period. Treatment with HAART induced a pronounced increase of plasma visfatin and RBP-4 as well as a decrease of adiponectin in HIV-infected patients on HAART. Although body weight, fat mass and parameters of glucose metabolism remained stable, the changes in the adipocytokines might herald subsequent alterations of these parameters.

Exercise Training Lowers Plasma Visfatin Concentrations in Patients with Type 1 Diabetes

Exercise training exerts beneficial effects on metabolic and vascular risk factors in patients with type 1 diabetes mellitus (T1DM). It is unknown whether training also influences concentrations of visfatin, a novel insulin-mimetic adipocytokine. In this study, we have investigated whether plasma visfatin concentrations are altered by training in patients with T1DM. Fasting plasma visfatin concentrations and metabolic parameters were measured in 18 patients with T1DM who participated in a supervised aerobic exercise program for 4 months. Three subjects discontinued training prematurely after 2 months. Samples were obtained before and during training and 8 months after the end of regular exercise. Fourteen healthy young subjects served as controls. At baseline, patients with T1DM had higher visfatin concentrations than controls (64.1 +/- 12.0 vs. 1.3 +/- 0.0 ng/ml, P < 0.01). Exercise reduced visfatin after 2 and 4 months to 27.8 +/- 2.6 (n = 18) and 17.5 +/- 3.4 ng/ml (n = 15), respectively (P < 0.001 for n = 15 subjects who participated in all visits, ANOVA). This effect was maintained 8 months after cessation of training, with visfatin concentrations of 19.7 +/- 5.0 ng/ml (n = 15). Metabolic parameters were not affected by the training program. Elevated visfatin concentrations in patients with T1DM can be lowered by regular physical exercise. It is unknown whether glucose tolerance is affected by changes in visfatin concentrations.