The Adipokine Visfatin is Markedly Elevated in Obese Children

Department of Clinical Pharmacology, Medical University of Vienna, Austria.
Journal of pediatric gastroenterology and nutrition (Impact Factor: 2.63). 11/2006; 43(4):548-9. DOI: 10.1097/01.mpg.0000235749.50820.b3
Source: PubMed


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.

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    • "Visfatin is a protein secreted by visceral adipose tissue and has insulin-like metabolic effects on glucose metabolism [8]. Studies found that serum visfatin levels are increased in individuals with abdominal obesity and correlate strongly with the amount of visceral adipose tissue in humans [9,10]. The observed increase of visfatin in obesity may be a counterregulation preventing further glucose increase. "
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    ABSTRACT: This 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. Ninety 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. In 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. Ad36 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 Slides: The virtual slide(s) for this article can be found here:
    Diagnostic Pathology 04/2014; 9(1):83. DOI:10.1186/1746-1596-9-83 · 2.60 Impact Factor
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    • "In addition, visfatin had effects on lipid homeostasis similar to that of insulin and it was also involved in adipocyte proliferation and differentiation and triglyceride (TG) metabolism (2). Based on this knowledge, circulating visfatin levels and its determinants have been investigated in several clinical studies (3,4,5,6,7,8,9,10). The aim of this study was to determine the relation between serum visfatin levels and adiposity in obese and non-obese adolescents. "
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    ABSTRACT: Visfatin, an adipokine, has insulin-mimetic effects. The main determinants of both the production and the physiologic role of visfatin are still unclear. The aim of this study is to determine the relation of serum visfatin to adiposity and glucose metabolism. 40 pubertal adolescents (20 females, 20 males; age range: 9-17 years) with exogenous obesity and 20 age- and sex-matched healthy adolescents (10 females, 10 males) were enrolled in the study. Oral glucose tolerance test (OGTT) was performed in the obese group. Serum glucose, insulin and visfatin levels were analyzed in the fasting state in the controls and at 0, 60 and 120 minutes during the OGTT in the obese group. The obese group had higher serum visfatin levels than the control group [11.6 (3.3-26) ng/mL vs. 7.5 (3.3-10.5) ng/mL, p<0.001[. Visfatin levels were correlated positively with body mass index, waist/hip ratio, insulin, and homeostasis model assessment for insulin resistance and negatively with glucose/insulin ratio in the combined group (obese subjects plus controls). Visfatin levels were essentially similar in obese subjects with and without insulin resistance (p>0.05). Serum visfatin levels did not change at 60 and 120 minutes of the OGTT compared to the baseline levels (p>0.05). Serum visfatin levels are elevated in obese adolescents and do not change with acute changes in glucose metabolism. Visfatin levels are related with adiposity and glucose metabolism parameters. However, the role and contribution of adiposity and glucose metabolism to the circulating visfatin levels in obese patients remain to be explored.
    Journal of Clinical Research in Pediatric Endocrinology 06/2012; 4(2):76-81. DOI:10.4274/jcrpe.547
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    • "The clinical studies in which plasma levels of visfatin were measured in different patient groups showed no clear correlations. Indeed, measurements of plasma visfatin levels in human beings have yielded conflicting results, with raised levels being reported in obese children [22], diabetic patients [23, 24], patients after weight loss mediated by gastroplastic surgery [25] and patients being treated with thiazolidinedione and rosiglitazone [26], whilst other studies have reported reduced levels with gestational diabetes [27], exercise in patients with type 1 diabetes [28], massive weight loss [29] and obesity [30]. "
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    ABSTRACT: Visfatin is an adipocytokine capable of mimicking the glucose-lowering effects of insulin and activating the pro-survival kinases phosphatidylinositol-3-OH kinase (PI3K)-protein kinase B (Akt) and mitogen-activated protein kinase kinase 1 and 2 (MEK1/2)-extracellular signal-regulated kinase 1 and 2 (Erk 1/2). Experimental studies have demonstrated that the activation of these kinases confers cardioprotection through the inhibition of the mitochondrial permeability transition pore (mPTP). Whether visfatin is capable of exerting direct cardioprotective effects through these mechanisms is unknown and is the subject of the current study. Anaesthetized C57BL/6 male mice were subjected to in situ 30 min. of regional myocardial ischaemia and 120 min. of reperfusion. The administration of an intravenous bolus of visfatin (5 x 10(-6) micromol) at the time of myocardial reperfusion reduced the myocardial infarct size from 46.1+/-4.1% in control hearts to 27.3+/-4.0% (n>or= 6/group, P<0.05), an effect that was blocked by the PI3K inhibitor, wortmannin, and the MEK1/2 inhibitor, U0126 (48.8+/-5.5% and 45.9+/-8.4%, respectively, versus 27.3+/-4.0% with visfatin; n>or= 6/group, P<0.05). In murine ventricular cardiomyocytes subjected to 30 min. of hypoxia followed by 30 min. of reoxygenation, visfatin (100 ng/ml), administered at the time of reoxygenation, reduced the cell death from 65.2+/-4.6% in control to 49.2+/-3.7%(n>200 cells/group, P<0.05), an effect that was abrogated by wortmannin and U0126 (68.1+/-5.2% and 59.7+/-6.2%, respectively; n>200 cells/group, P>0.05). Finally, the treatment of murine ventricular cardiomyocytes with visfatin (100 ng/ml) delayed the opening of the mPTP induced by oxidative stress from 81.2+/-4 sec. in control to 120+/-7 sec. (n>20 cells/group, P<0.05) in a PI3K- and MEK1/2-dependent manner. We report that the adipocytokine, visfatin, is capable of reducing myocardial injury when administered at the time of myocardial reperfusion in both the in situ murine heart and the isolated murine cardiomyocytes. The mechanism appears to involve the PI3K and MEK1/2 pathways and the mPTP.
    Journal of Cellular and Molecular Medicine 04/2008; 12(4):1395-403. DOI:10.1111/j.1582-4934.2008.00332.x · 4.01 Impact Factor
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