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.
"Several studies have demonstrated elevated visfatin levels both in obese adults (Auguet et al., 2013; Jin et al., 2008; Manco et al., 2007; Pagano et al., 2006; Terra et al., 2012; Wen et al., 2012) and children (Davutoglu et al., 2009; Dogru et al., 2007; Pagano et al., 2006; Revollo et al., 2004; Sandeep et al., 2007) as well as in patients with diabetes mellitus (Chen et al., 2006; Dogru et al., 2007; Pagano et al., 2006; Revollo et al., 2004; Sandeep et al., 2007), suggesting a possible link to insulin and glucose homeostasis. Further investigations found visfatin to be closely correlated with white adipose tissue (WAT) accumulation (Curat et al., 2006; Jia et al., 2004). "
"However, it is unknown whether the increased visfatin/Nampt concentrations in blood or tissues are related to insulin resistance. In the current study, diabetic and prediabetic subjects had higher blood visfatin/Nampt concentrations than nondiabetic subjects, which is consistent with other studies [13–16, 28, 29]. This is the first study to measure visfatin/Nampt protein concentrations in liver, muscle, and three adipose depots and correlate their concentrations with insulin resistance. "
[Show abstract][Hide abstract] ABSTRACT: Visfatin/Nampt, vaspin, and retinol binding protein-4 (RBP-4) play an important role in insulin resistance. The objectives of this study were to measure visfatin/Nampt, vaspin, and RBP-4 concentrations in blood, liver, muscle, subcutaneous, omental, and mesenteric adipose tissues in morbidly obese subjects and investigate their relationship to insulin resistance. Blood and tissue samples were collected from 38 morbidly obese subjects during Roux-en-Y surgery. Insulin resistance biomarkers were measured using standard kits. Visfatin/Nampt, vaspin, and RBP-4 gene expression levels in tissues were measured using real-time PCR. Their protein concentrations in blood and tissues were measured using ELISA kits. Diabetic subjects had significantly higher homeostasis model of assessment-insulin resistance and age and lower blood HDL-cholesterol concentrations than nondiabetic and prediabetic subjects. Diabetic and prediabetic subjects had significantly higher blood concentrations of visfatin/Nampt and vaspin than nondiabetic subjects. Liver RBP-4 concentrations were positively associated with blood glucose concentrations. Blood insulin resistance biomarker levels were positively associated with visfatin/Nampt concentrations in omental adipose tissue and liver, and vaspin concentrations in mesenteric adipose tissue. In conclusion, the correlations of visfatin/Nampt, vaspin, and RBP-4 with insulin resistance are tissue dependent.
"One study compared plasma visfatin levels between type 2 diabetes subjects and non-diabetic healthy subjects and found that type 2 diabetes subjects had higher serum visfatin levels than non-diabetic healthy subjects (Sandeep et al., 2007b). However, this positive correlation between serum visfatin levels and diabetes status was no longer significant after adjusting for anthropometrics such as BMI and waist circumference (Dogru et al., 2007; Alghasham and Barakat, 2008; Retnakaran et al., 2008). In contrast, other studies reported that serum visfatin levels were significantly associated with obesity even after adjusting for age, sex, and diabetes (Fukuhara et al., 2005; Sandeep et al., 2007b). "
[Show abstract][Hide abstract] ABSTRACT: Over a third of the US population is obese and at high risk for developing type 2 diabetes, insulin resistance, and other metabolic disorders. Obesity is considered a chronic low-grade inflammatory condition that is primarily attributed to expansion and inflammation of adipose tissues. Indeed, adipocytes produce and secrete numerous proinflammatory and anti-inflammatory cytokines known as adipokines. When the balance of these adipokines is shifted toward higher production of proinflammatory factors, local inflammation within adipose tissues and subsequently systemic inflammation occur. These adipokines including leptin, visfatin, resistin, apelin, vaspin, and retinol binding protein-4 can regulate inflammatory responses and contribute to the pathogenesis of diabetes. These effects are mediated by key inflammatory signaling molecules including activated serine kinases such as c-Jun N-terminal kinase and serine kinases inhibitor κB kinase and insulin signaling molecules including insulin receptor substrates, protein kinase B (PKB, also known as Akt), and nuclear factor kappa B. Bariatric surgery can decrease body weight and improve insulin resistance in morbidly obese subjects. However, despite reports suggesting reduced inflammation and weight-independent effects of bariatric surgery on glucose metabolism, mechanisms behind such improvements are not yet well understood. This review article focuses on some of these novel adipokines and discusses their changes after bariatric surgery and their relationship to insulin resistance, fat mass, inflammation, and glucose homeostasis.
Frontiers in Endocrinology 06/2013; 4:69. DOI:10.3389/fendo.2013.00069
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