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

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 t...

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Bibliographic Details
Main Authors: Naoto Yamaaki, Kunimasa Yagi, Junji Kobayashi, Atsushi Nohara, Naoko Ito, Akimichi Asano, Kaoru Nakano, Jianhui Liu, Takuya Okamoto, Yukiko Mori, Azusa Ohbatake, Satoko Okazaki, Yoshiyu Takeda, Masakazu Yamagishi
Format: Article
Language:English
Published: Hindawi Limited 2013-01-01
Series:Journal of Diabetes Research
Online Access:http://dx.doi.org/10.1155/2013/143515
Description
Summary: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.
ISSN:2314-6745
2314-6753