Human Active RBP4 ELISA Kit

Objective: To assess the association and prognostic value of adipokines (adipocyte-secreted peptide hormones) in renal cell carcinoma (RCC). Materials and methods: Plasma samples from 54 RCC patients and 25 age-matched healthy controls were analyzed for levels of adipokines (adiponectin, leptin, retinol-binding protein 4 [RBP4], and nicotinamide phosphoribosyltransferase [NAMPT]). Baseline characteristics and adipokine levels were compared between patients and controls. The effect of adipokine levels on RCC severity was also investigated. Results: Medians (patients/controls) were body mass index: 24.6/23.5 kg/m(2), serum glucose: 111/93 mg/dl, and high-density lipoprotein: 43/53 mg/dl, and significantly differed between the 2 groups. Median levels (patients/controls) of adipokines were adiponectin: 4.36/8.84 ug/ml, leptin: 2.91/2.92 ng/ml, RBP4: 30.27/16.17 ug/ml and NAMPT: 2.26/2.06 ng/ml; adiponectin, RBP4 and NAMPT (but not leptin) were independently associated with RCC in logistic regression models, and only serum NAMPT was significantly associated with RCC severity (T stage). Conclusions: Lower plasma levels of adiponectin, and higher levels of RBP4 and NAMPT, are strongly correlated with RCC, indicating that these adipokines could be used as biomarkers for RCC. (c) 2016 Elsevier Inc. All rights reserved.

Retinol-binding protein-4 (RBP4) is elevated in serum and adipose tissue (AT) in obesity-induced insulin resistance and correlates inversely with insulin-stimulated glucose disposal. But its role in insulin-mediated suppression of lipolysis, free fatty acids (FFA), and endogenous glucose production (EGP) in humans is unknown. RBP4 mRNA or protein levels were higher in liver, subcutaneous adipose tissue (SAT), and visceral adipose tissue (VAT) in morbidly obese subjects undergoing Roux-en-Y gastric bypass surgery compared to lean controls undergoing elective laparoscopic cholecystectomy. RBP4 mRNA expression in SAT correlated with the expression of several macrophage and other inflammation markers. Serum RBP4 levels correlated inversely with glucose disposal and insulin-mediated suppression of lipolysis, FFA, and EGP. Mechanistically, RBP4 treatment of human adipocytes in vitro directly stimulated basal lipolysis. Treatment of adipocytes with conditioned media from RBP4-activated macrophages markedly increased basal lipolysis and impaired insulin-mediated lipolysis suppression. RBP4 treatment of macrophages increased TNF alpha production. These data suggest that elevated serum or adipose tissue RBP4 levels in morbidly obese subjects may cause hepatic and systemic insulin resistance by stimulating basal lipolysis and by activating macrophages in adipose tissue, resulting in release of pro-inflammatory cytokines that impair lipolysis suppression. While we have demonstrated this mechanism in human adipocytes in vitro, and correlations from our flux studies in humans strongly support this, further studies are needed to determine whether this mechanism explains RBP4-induced insulin resistance in humans.