Visfatin Gene Research Articles

The mRNA Expression and Circulating Levels of Visfatin and Their Correlation with Coronary Artery Disease Severity and 25-Hydroxyvitamin D.

It is evident that coronary artery disease (CAD) is closely associated with abnormal glucose and lipid metabolism. Notably, dysregulation of inflammatory pathways and immune system also contribute to CAD development. Recently, it has been suggested that visfatin, a proinflammatory adipocytokine, may be involved in several inflammatory and metabolic diseases. In this study, we evaluated the serum visfatin levels and its mRNA expression in peripheral blood mononuclear cells (PBMCs) from CAD patients compared with control subjects. We also studied the correlation between visfatin gene expression and serum levels with clinical and metabolic parameters. This study was conducted on 56 male patients with CAD confirmed by angiography and 30 healthy men as controls. CAD severity was determined based on the number of vessels. Study of gene expression in PBMCs was performed using real time-PCR, and serum levels of visfatin and 25-hydroxyvitamin D were measured by ELISA. We found that serum visfatin levels and its gene expression in PBMCs were increased in patients with CAD compared with the control group (p=0.027 and p=0.016, respectively). Also, visfatin gene expression was positively correlated with visfatin levels and both these variables had a strong positive correlation with the severity of CAD. It appears that elevated mRNA expression and circulating level of visfatin might be of relevance to the pathogenesis and severity of CAD. However, further studies are necessary to better clarify the associations between visfatin and CAD.

Resveratrol attenuates visfatin and vaspin genes expression in adipose tissue of rats with type 2 diabetes.

Visfatin and vaspin are secreted by adipose tissue and play key roles in glucose homeostasis and subsequently are potential targets for diabetes treatment. Resveratrol (RVS) corrects insulin secretion and improves insulin sensitivity. We investigated the RVS effects on serum antioxidants, insulin and glucose levels, also visfatin and vaspin genes expression in adipose tissue of streptozotocin-nicotinamide (STZ-NA) induced type 2 diabetic rats. Diabetes was induced in Wistar rats (n=32) using STZ (60 mg/kg body weight) and NA (120 mg/kg body weight); rats were divided into 4 groups (n=8). Eight untreated normal rats were used as control group; four diabetic rat groups (2-5) were treated with 0, 1, 5 and 10 mg/kg body weight of RVS, respectively for 30 days. After treatment blood and adipose tissue were prepared from all animals. Serum glucose, insulin, HOMA index, total antioxidant capacity (TAC), and malondialdehyde (MDA) were measured. Visfatin and vaspin genes expression in adipose tissue were evaluated using real-time PCR. RVS reduced blood glucose significantly and increased insulin level, resulting in insulin sensitivity improvement. Furthermore RVS increased weight and TAC, while reducing serum MDA in the diabetic groups. Visfatin gene expression increased in the diabetic group, and RVS treatment reduced it. Vaspin gene expression was reduced in RVS receiving diabetic groups. The results indicated that RVS has potential hypoglycemic effect, probably by increasing insulin level and changing gene expression of visfatin and vaspin. Moreover RVS showed antioxidant effects through reduction in peroxidiation products and augmented antioxidant capacity.

Abstract 477: Adipocyte Twist-1 Deficiency Exacerbates Weight Gain, Glucose Intolerance and Adipose Tissue Inflammation in Females

Twist1 is a transcription factor abundantly expressed by adipocytes, immune and vascular cells in adipose tissue (AT) in humans and rodents. Low twist1 expression in human AT is correlated with insulin resistance and obesity. However the role of twist-1 in different cell types component of AT is not clear. The objective of this study was to determine the role of adipocyte (Adp) twist-1 in obesity and insulin resistance. Adp-specific twist1 knock out mice ( AdiponectinCreTwistflox ) (n=6) on the C57Bl6/J background were maintained on 60%kcal fat diet for 12 weeks. Compared to littermate controls (n=6), the female mutant mice, but not the males, showed a 3- and 1.5- fold increase in visceral and subcutaneous adiposity, respectively. Similarly, only the mutant females had significantly impaired glucose tolerance (P<0.05) compared to the littermate controls. Peri-gonadal AT in mutant females showed increased CD11b+F4/80+ and CD3+CD8+ numbers compared to controls, however no differences were found between the male mice. The female mutant mice had more hypertrophied Adp and displayed a 2-4-fold increase in gene expression of IFN γ, TNF α, CD3e and Jak2 compared to controls. Also, expression of the lipogenic enzymes Acaca and Acls4 were significantly reduced by 2.2-fold in the mutant females. Interestingly expression of Nampt (visfatin) gene was significantly increased in mutant females compared to both controls and mutant males. Importantly, twist1 expression in visceral Adp of obese human females (n=15) and males (n=8) at the time of bariatric surgery was significantly higher in females (p<0.01). Also, in a longitudinal cohort at ~1.2 years following surgical weight loss, twist1 expression was significantly increased in visceral AT of males (n=3) (p<0.05) but not in females (n=6) despite a similar reduction in body weight. Collectively the rodent data suggest that twist1 deficiency in Adp increases AT inflammation and exacerbates adiposity and glucose intolerance only in females and identifies visfatin as a metabolically relevant gene potentially regulated by twist1 in females. Also, obese human females may be protected by constitutively higher expression of twist1 in visceral Adp and surgical weight loss leads to increased twist1 expression in males.

HIV/antiretroviral therapy–related lipodystrophy syndrome (HALS) is associated with higher RBP4 and lower omentin in plasma

Very little information is available on the involvement of newly characterized adipokines in human immunodeficiency virus (HIV)/antiretroviral therapy (ART)-associated lipodystrophy syndrome (HALS). Our aim was to determine whether apelin, apelin receptor, omentin, RBP4, vaspin and visfatin genetic variants and plasma levels are associated with HALS. We performed a cross-sectional multicentre study that involved 558 HIV type 1–infected patients treated with a stable highly active ART regimen, 240 of which had overt HALS and 318 who did not have HALS. Epidemiologic and clinical variables were determined. Polymorphisms in the apelin, omentin, RBP4, vaspin and visfatin genes were assessed by genotyping. Plasma apelin, apelin receptor, omentin, RBP4, vaspin and visfatin levels were determined by enzyme-linked immunosorbent assay in 163 patients (81 with HALS and 82 without HALS) from whom stored plasma samples were available. Student's t test, one-way ANOVA, chi-square test, Pearson and Spearman correlations and linear regression analysis were used for statistical analyses. There were no associations between the different polymorphisms assessed and the HALS phenotype. Circulating RBP4 was significantly higher (p < 0.001) and plasma omentin was significantly lower (p 0.001) in patients with HALS compared to those without HALS; differences in plasma levels of the remaining adipokines were nonsignificant between groups. Circulating RBP4 concentration was predicted independently by the presence of HALS. Apelin and apelin receptor levels were independently predicted by body mass index. Visfatin concentration was predicted independently by the presence of acquired immunodeficiency syndrome. HALS is associated with higher RBP4 and lower omentin in plasma. These two adipokines, particularly RBP4, may be a link between HIV/ART and fat redistribution syndromes.

Adipokine gene expression in peripheral blood of adult and juvenile dermatomyositis patients and their relation to clinical parameters and disease activity measures.

ObjectiveRecently adipokines have been implicated in the regulation of immune and inflammatory responses in autoimmune disease. To investigate the role of adipokines in adult and pediatric patients with newly diagnosed dermatomyositis (DM), we analyzed peripheral blood and skeletal muscle gene expression of four adipokines: visfatin, leptin, adiponectin and resistin.MethodsPeripheral blood mononuclear cells (PBMCs) were collected for 21 adult DM, 26 juvenile DM, 5 non-disease adult controls, and 6 non-disease pediatric controls at two time points: baseline and 6 months. Muscle biopsies from 5 adult DM patients and 5 non-disease adult controls were collected at baseline. Similarly, muscle biopsies from 7 juvenile DM patients and 5 non-disease pediatric controls were collected at baseline. The gene expression levels of leptin, adiponectin, resistin, visfatin and related inflammatory cytokines, IL-6, TNF- α, and housekeeping genes GAPDH, B2M, and ACTB were generated using a custom RT2 Profiler PCR Array.ResultsVisfatin gene expression levels in peripheral blood were significantly higher in newly diagnosed adult DM cases compared to non-disease controls (P = 0.004) and these levels correlated with baseline clinical parameters such as age (r = 0.34, P = 0.020), male sex (r = −0.35, P = 0.017), prednisone use (r = −0.42, P = 0.006), and DMARD use (r = 0.35, P = 0.025). No significant association was found between change in visfatin gene expression levels and change in disease activity measures. While visfatin gene expression was significantly up-regulated in muscle tissue of juvenile DM patients (P = 0.028), in adult DM patients only a trend towards significance was observed (P = 0.08). Also, muscle gene expression levels of resistin were significantly elevated in both adult and juvenile DM patients compared respectively to non-disease adult and pediatric controls. Furthermore, an association between peripheral blood resistin gene expression and DM disease activity, including global, muscle, and extra-skeletal disease activity was also observed.ConclusionPeripheral blood visfatin gene expression and muscle resistin gene expression are significantly increased in newly diagnosed adult DM patients. Further longitudinal studies should explore the possibility of using gene expression levels of adipokines such as visfatin and resistin as novel clinical diagnostic biomarkers in DM.

The Effect of Acute Aerobic Bout on Adipose Tissue Visfatin Gene Expression in Diabetic Rats

The Effect of Acute Aerobic Bout on Adipose Tissue Visfatin Gene Expression in Diabetic Rats

Adenovirus36 infection expresses cellular APMI and Visfatin genes in overweight Uygur individuals.

ObjectiveThis study is to determine if Adenovirus type 36 (Ad36) infection is related to macrophage infiltration in the obese group and non-obese group and the related molecular mechanisms.MethodsNinety obesity patients and 95 non-obesity Uygur individuals were enrolled in this study. CD68 levels in abdominal subcutaneous and omental adipose tissues were detected by immunohistochemistry. The cytokine expression levels of adiponectin (APMI) and visfatin in serum were measured by enzyme-linked immunosorbent assay. Infection of 3T3-L1 cells with Ad36 was performed. Real-time PCR was performed to determine expression levels of APMI and Visfatin genes in the 3T3-L1 preadipocytes infected with Ad36.ResultsIn the obese individuals infected with Ad36, the expression levels of adiponectin and visfatin in serum was elevated. For the individuals infected with Ad36, the macrophage infiltration (as indicated by CD68 level) in the obese group was also significantly higher than that in the non-obese group (P < 0.05) in both abdominal subcutaneous and omental adipose tissues. The real-time PCR results indicated that APMI mRNA levels and Visfatin mRNA levels in Ad36 infected cells were significantly increased.ConclusionsAd36 infection may be a factor related with macrophage infiltration in adipose tissues of the obese patients. The APMI and Visfatin genes may be involved in the mechanism underlying the effect of Ad36 infection on the obese patients.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1849614638119816

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.

Association of genetic variability in selected regions in visfatin (NAMPT) gene with anthropometric parameters and dietary composition in obese and non-obese Central-European population

AimsVisfatin (NAMPT/PBEF) is a recently identified adipocytokine which harbors strong insulin-mimetic activity and was reported to be associated with obesity. However, nothing is known about whether visfatin is related to specific nutritional behavior which may result in obesity development. This is the first study focusing on genetic variability of the visfatin gene and its association with circulating visfatin, anthropometric parameters and dietary composition. Materials and MethodsWe analyzed a total of 11 exons and adjacent non-coding regions of the NAMPT gene in 20 extremely obese Czech individuals (mean BMI 52.2±5.0 SD) using direct sequencing and a frequency of rs2302559 was established in the validation cohort of another 605 individuals with completed 7-day food records and complex anthropometric measurements. Serum levels of visfatin, leptin and leptin-receptor were measured in all sequenced individuals and in part of the validation cohort. ResultsThree common polymorphisms were identified, two in non-coding regions (rs78411774 A/C, rs71564769 A/C) and one synonymous SNP in exon 7 (rs2302559 A/G). The rs2302559 showed significant correlation with visfatin serum level throughout the entire study cohort (p<0.001); there was a significant tendency toward higher visfatin levels in G allele carriers with GG homozygotes having the highest visfatin serum levels. Furthermore, a negative correlation was observed between visfatin and leptin serum level (p=0.01). No association between investigated SNPs and anthropometric parameters or native dietary composition was observed. ConclusionThis is the first study to demonstrate that the rs2302559 polymorphism in the PBEF gene is related to circulating levels of visfatin. As the SNP is synonymous, we hypothesize it might be linked to another SNP in the PBEF gene which controls visfatin serum levels.

FRI0039 VISFATIN/PBEF in bone remodelling of rheumatoid arthritis

ObjectivesRheumatoid arthritis (RA) is associated with increased production of adipocytokines, which are cytokine-like mediators. Increased levels of the adipokine visfatin were found in synovial fluid and tissue of RA patients....

Visfatin and its genetic variants are associated with obesity‐related morbidities and cardiometabolic risk in severely obese children

Visfatin is an adipokine, associated with obesity and possibly glucose regulation. The aim of this study was to examine the association of visfatin and its genetic variants with adiposity, cardiometabolic risk factors and obesity-related morbidities in obese children. Anthropometric measurements, dual energy X-ray absorptiometry scan, fasting blood samples and oral glucose tolerance tests were performed for 243 obese children. We screened the visfatin gene of 24 obese subjects and then performed genotyping of identified genetic variants in other 219 obese children through direct DNA sequencing. Fasting serum visfatin correlated with measures of obesity and liver enzymes and was elevated in obese children with abnormal glucose tolerance and non-alcoholic fatty liver disease. The two upstream single nucleotide polymorphisms, -3187G>A (rs11977021) and -1537C>T (rs61330082), were at complete linkage disequilibrium. The AA genotype of -3187G>A was associated with higher serum visfatin (6.17 ± 0.76 ng mL(-1) vs. 3.92 ± 0.44 ng mL(-1)) and higher triglyceride (1.39 ± 0.08 mmol L(-1) vs. 1.19 ± 0.07 mmol L(-1)) as compared with the GG genotype. There was also a significant linear increase in serum visfatin across GG to GA to AA genotype of -3187G>A, indicating possible additive effect of A allele. The dominant GA + AA genotype model of +21426G>A (rs2302559) was associated with lower serum visfatin (3.83 ± 0.56 ng mL(-1) vs. 5.13 ± 0.34 ng mL(-1)) and lower plasma glucose (4.37 ± 0.08 mmol L(-1) vs. 4.77 ± 0.12 mmol L(-1)) as compared with the GG genotype. Visfatin and its genetic variants were associated with adiposity, obesity-related morbidities and adverse cardiometabolic parameters. This supported our hypothesis that visfatin plays a significant role in the development of obesity-related morbidities and cardiometabolic risk.

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.

Effects of visfatin gene polymorphism RS4730153 on exercise-induced weight loss of obese children and adolescents of Han Chinese.

Visfatin is a recently discovered adipokine that contributes to glucose and obesity-related conditions. This study investigates Visfatin RS4730153 polymorphism from the perspectives of its relations with glucose/lipid metabolism and its influence on the effects of exercise-induced weight loss. Eighty-eight obese Han Chinese children and adolescents were randomly selected from a 2008 Shanghai Weight Loss Summer Camp and were supervised to complete a 4 week aerobic exercise training program. Significant differences were observed in before-exercise TG value and exercise-induced HOMA-β change, with the AG group having a much higher TG value than the GG group (P ≤ 0.05), and the latter exhibiting a significantly larger before-and-after exercise HOMA-β change than the former (P ≤ 0.05). However, no significant difference was observed between the two groups in before exercise indices of body shape, function and quality, nor in exercise-induced changes of body shape, function, and quality. Findings suggest that Visfatin RS4730153 homozygous GG genotype may effect adjustment of glucose and lipid metabolism in obese children and adolescents by reducing TG levels and increasing insulin sensitivity to exercise.

Glucose Intolerance and Lipid Metabolic Adaptations in Response to Intrauterine and Postnatal Calorie Restriction in Male Adult Rats

Enhanced de novo lipogenesis (DNL), an adult hepatic adaption, is seen with high carbohydrate or low-fat diets. We hypothesized that ad libitum intake after prenatal calorie restriction will result in adult-onset glucose intolerance and enhanced DNL with modified lipid metabolic gene expression profile. Stable isotopes were used in 15-month-old adult male rat offspring exposed to prenatal (IUGR), pre- and postnatal (IPGR), or postnatal (PNGR) caloric restriction vs. controls (CON). IUGR vs. CON were heavier with hepatomegaly but unchanged visceral white adipose tissue (WAT), glucose intolerant with reduced glucose-stimulated insulin secretion (GSIS), pancreatic β-cell mass, and total glucose clearance rate but unsuppressed hepatic glucose production. Liver glucose transporter (Glut) 1 and DNL increased with decreased hepatic acetyl-CoA carboxylase (ACC) and fatty acid synthase but increased WAT fatty acid transport protein-1 and peroxisomal proliferator-activated receptor-γ, resistin, and visfatin gene expression. In contrast, PNGR and IPGR were lighter, had reduced visceral WAT, and were glucose tolerant with unchanged hepatic glucose production but with increased GSIS, β-cell mass, glucose clearance rate, and WAT insulin receptor. Hepatic Glut1 and DNL were also increased in lean IPGR and PNGR with increased hepatic ACC, phosphorylated ACC, and pAMPK and reduced WAT fatty acid transport protein-1, peroxisomal proliferator-activated receptor-γ, and ACCα. We conclude the following: 1) the heavy, glucose-intolerant and insulin-resistant IUGR adult phenotype is ameliorated by postnatal caloric restriction; 2) increased DNL paralleling hepatic Glut1 is a biomarker of exposure to early caloric restriction rather than the adult metabolic status; 3) hepatic lipid enzyme expression reflects GSIS rather than DNL; and 4) WAT gene expression reflects an obesogenic vs. lean phenotype.

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.

Characterization of chicken visfatin gene: cDNA cloning, tissue distribution, and promoter analysis

Here we report the cloning and characterization of chicken visfatin (also called pre-B cell enhancing factor; PBEF, or nicotinamide phosphoribosyltransferase; Nampt) gene. Sequence analyses revealed that the coding region of visfatin is 1,482 bp in length and encodes a protein of 493 amino acids, which shares high amino acid sequence identity not only to visfatin of human (94%), rat (94%), carp (89%), and zebrafish (89%), but also to Nampt of sponge (58%) and cyanobacterium (48%). The reverse transcription PCR assay and Northern-blot analysis demonstrated that visfatin was widely expressed in all chicken tissues examined. Using a dual luciferase reporter system, we further demonstrated that the cloned 1,372-bp fragment upstream of the putative translation start site (ATG) displayed the maximal promoter activity in cultured CHO, DF-1, and HEK293 cells, whereas the removal of its 5'-region (1,075 bp) or 3'-region (297 bp) could only partially reduce its promoter activity, implying that visfatin gene transcription was likely controlled by multiple promoters near the translation start site. Taken together, results from present study will contribute to our better understanding of the expression and roles of visfatin gene in chickens.

Increased levels and adipose tissue expression of visfatin in morbidly obese women: the relationship with pro‐inflammatory cytokines

The controversial results on the physiopathological role of visfatin led us to examine both circulating visfatin levels and gene expression in visceral (VAT) and subcutaneous fat (SAT) in a homogeneous group of morbidly obese women. We analysed circulating levels of several adipo/cytokines in 133 Spanish women: 40 lean (C) [body mass index (BMI) < 25 kg/m(2) ] and 93 morbidly obese (MO) (BMI > 40 kg/m(2) ). In the MO group, we found 31 diabetic and 62 nondiabetic subjects. We obtained follow-up blood samples at 6 and 12 months after bariatric surgery from 30 MO patients. We determined the circulating levels of visfatin, adiponectin, interleukin-6 (IL6), C-reactive protein (CRP), resistin and tumour necrosis factor-α (TNFα) by ELISA, and visfatin, adiponectin, IL6, resistin and TNFα gene expression in SAT and VAT by real-time RT-PCR. Circulating visfatin levels were higher in MO women compared with lean controls (C = 1·43 ± 0·14 μg/l, MO = 3·60 ± 0·29 μg/l, P < 0·001). After bariatric surgery-induced weight loss, visfatin levels were reduced significantly over 12 months. Visfatin expression in SAT and VAT was similar, but significantly higher in MO compared to C and independent of the presence of diabetes mellitus. Circulating visfatin levels were positively related to IL6 and CRP levels. Visfatin gene expression in VAT and SAT was strongly related to IL6 and TNFα expression. In a homogeneous cohort of morbidly obese women, our findings show that visfatin has a strong relationship with pro-inflammatory factors in severe obesity.

Novel 6-bp Deletion Mutation in visfatin Gene and Its Associations with Birth Weight and Bodyweight in Chinese Cattle

Visfatin, like insulin, induces phosphorylation of signal transduction proteins that operatate downstream of the insulin receptor. The present study is focused on detecting deletion of visfatin gene and analyzing its effect on growth traits in six Chinese cattle breeds (Nangyang, Luxi, Qinchuan, Jiaxian Red, Grassland Red, and Chinese Holstein) using DNA sequencing, PCR-SSCP and PCR-RFLP methods. For the first time, a 6-bp deletion of visfatin was described and two alleles were revealed: W and D. The χ2-test analysis demonstrated that all breeds were in agreement with Hardy-Weinberg equilibrium (Pgt;0.05). The associations of the novel 6-bp deletion of visfatin gene with growth traits of Nanyang cattle at 6-, 12-, 18-, and 24-mon-old were analyzed. Birth weight, 12- and 24-mon-old cattle with genotype WW had greater birth weight and average daily gain than genotype WD (P<0.01 or P<0.05). These results suggest that the deletion may influence the birth weight and bodyweight in 12 mon-old cattle.

Visfatin and RBP4 gene expression levels in different adipose tissues and insulin resistance

Background As an endocrine organ, adipose tissue produces and secretes lots of hormones and adipokines that play important roles in metabolism and inflammation [1]. Varied adipose tissues may affect the inflammation distinctively, mainly because of the different secretion levels of the adipokines. Adipokines like visfatin and retinol binding protein-4 (RBP4) may have important roles in insulin sensitivity and glucose uptake to the cell [2,3]. Our research focuses on different tissue secretions of visfatin and RBP4 and their inflammatory properties.

Visfatin Polymorphism May Increase Tendency to Diabetic Nephropathy

Visfatin is a novel adipocytokine, which is suggested to play a role in kidney diseases. We hypothesized that diabetics with diabetic nephropathy may have a different gene profile and this study was performed to evaluate the association between visfatin gene promoter region SNPs and diabetic nephropathy. Realtime PCR was used to study SNPs (1001T/G, 423A/G, 1535C/T) of the visfatin gene promoter region in 30 type 2 diabetics with nephropathy, 30 type 2 diabetics without nephropathy, and 30 healthy volunteers who served as control. Routine biochemical parameters, serum insulin, TNF-α, urinary protein and microalbumine were tested in subjects. Insulin resistance was evaluated by the HOMA method. Non-heterozygotes for the SNPs 423 A/G and 1001 T/G had significantly less risk of having nephropathy (for each group odds ratio 0.181 with 95% confidence interval:0.048–0.674). They also had lower serum visfatin levels than subjects with AA and TT genotypes (P=0.035 and P=0.030, respectively). We could not find any relationship between genotype and gender, BMI, HOMA-IR score, HbA1c, proteinuria, serum lipid and TNF-α levels. The two SNPs, 1001 T/G and 423 A/G were in perfect linkage disequilibrium. We, therefore, suggest that visfatin gene polymorphisms may increase the tendency to diabetic nephropathy.