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Journal of Diabetes Research
Volume 2017 (2017), Article ID 6549242, 8 pages
https://doi.org/10.1155/2017/6549242
Research Article

The Association between Monocyte Surface CD163 and Insulin Resistance in Patients with Type 2 Diabetes

1Metabolism, Endocrinology, and Molecular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan
2Department of Premier Preventive Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan
3Department of Vascular Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan

Correspondence should be addressed to Koka Motoyama; pj.ca.uc-akaso.dem@6779931m

Received 30 June 2017; Accepted 22 November 2017; Published 28 December 2017

Academic Editor: Sandeep Singh

Copyright © 2017 Reina Kawarabayashi 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

Aim. To investigate the association between monocyte CD163 and insulin resistance in patients with type 2 diabetes. Methods. One hundred sixty-six patients with type 2 diabetes without inflammatory or chronic kidney disease were recruited. The monocyte CD163 levels were measured by flow cytometry and soluble CD163 (sCD163) by ELISA. Insulin resistance was evaluated by the index of the homeostasis model assessment (HOMA-R). Results. The median sCD163 and monocyte CD163 expression levels were 582.9 (472.4–720.0) ng/ml and 6061 (4486–7876) mean fluorescent intensity (MFI), respectively. In a simple regression analysis, monocyte CD163 was inversely correlated with log [HOMA-R] (, ), and sCD163 was positively correlated with log [HOMA-R] (, ). In multiple regression analyses, monocyte CD163 was an independent contributor to log [HOMA-R] (, ) even after adjustment of various clinical factors for HOMA-R (, ), whereas sCD163 was not. Conclusions. Monocyte surface CD163 expression levels were more significantly associated with insulin resistance than sCD163 in patients with type 2 diabetes, suggesting a novel pathophysiological role of CD163.