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Journal of Diabetes Research
Volume 2013, Article ID 143515, 5 pages
http://dx.doi.org/10.1155/2013/143515
Clinical Study

Impact of Serum Retinol-Binding Protein 4 Levels on Regulation of Remnant-Like Particles Triglyceride in Type 2 Diabetes Mellitus

1Department of Internal Medicine, Graduate School of Medical Science, Kanazawa University, 13-1 Takaramachi, Kanazawa 920-8640, Japan
2Department of General Medicine, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku 920-0293, Japan

Received 25 December 2012; Accepted 12 February 2013

Academic Editor: Aristidis Veves

Copyright © 2013 Naoto Yamaaki et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Background. Although retinol-binding protein 4 (RBP4) associates with insulin resistance and remnant-like particles triglyceride (RLP-TG) elevated in the insulin resistant state, few data exist regarding the relationship between RBP4 and RLP-TG. Subjects and Methods. The study included 92 Japanese type 2 diabetic mellitus (T2DM) male patients (age years, body mass index (BMI)  kg/m2, waist circumference (WC)  cm, and HbA1c (NGSP) %). Patients on medications affecting insulin sensitivity, including fibrates, biguanides, and thiazolidinedione, were excluded. Visceral fat area (VFA) and subcutaneous fat area (SFA) were measured by computed tomography. Results. RBP4 levels showed a significant positive correlation with RLP-TG ( and ), TG ( and ), RLP-TG/TG ( and ), and age ( and ), although there was no significant correlation with VFA, SFA, adiponectin levels, or homeostasis model of assessment insulin resistance (HOMA-R). Multiple regression analysis revealed that RBP4 was an independent determinant of RLP-TG ( ) but was not a determinant of TG. Conclusions. RBP4 correlates positively with serum RLP-TG independent of fat accumulation in T2DM. RBP4 may regulate remnant metabolism independent of glycemic control in T2DM.