4.7 Article

Retinol binding protein 4 concentrations are influenced by renal function in patients with type 2 diabetes mellitus

Journal

METABOLISM-CLINICAL AND EXPERIMENTAL
Volume 57, Issue 10, Pages 1340-1344

Publisher

W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.metabol.2008.03.013

Keywords

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Funding

  1. Japanese Ministry of Education, Science and Culture
  2. Research Grants for Intractable Diseases
  3. Japanese Ministry of Health and Welfare
  4. Smoking Research Foundation
  5. Venture Business Laboratory in Oita University

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Retinol binding protein 4 (RBP-4), a newly discovered adipocytokinc, has been involved in glucose and lipid metabolism. We assess the impacts of renal function on plasma RBP-4 levels in patients with type 2 diabetes mellitus with a wide range of nephropathy. Plasma RBP-4 levels were measured using the enzyme immunoassay method in 38 type 2 diabetes mellitus patients with nephropathy and were compared with those in 20 patients with normoalbuminuria. The levels of plasma RBP-4 were increased by 1.4- and 3.3-fold in patients with renal disease with macroalbuminuria (P = .04) and end-stage renal disease (plasma creatinine level >2.0 mg/dL) (P < .0001) compared with those in patients with normal renal function. In addition, RBP-4 levels were correlated with the creatinine level and 24-hour creatinine clearance (Ccr) on simple and multiple regression analyses in all patients. Furthermore, in patients having Ccr of more than 60 mL/min, RBP-4 levels were correlated with the homeostasis model assessment (HOMA)-r index and triglyceride (TGL) both on simple and multiple regression analyses. Interestingly, in patients having Ccr of less than 60 mL/min, RBP-4 levels were not correlated with the HOMA-r index and TGL on simple regression analysis. The RBP-4 concentrations are influenced by renal function in type 2 diabetes mellitus patients. In addition, RBP-4 levels were correlated with HOMA-r and TGL in diabetic subjects without end-stage renal disease. (C) 2008 Elsevier Inc. All rights reserved.

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