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

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          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] ( r = –0.257, p = 0.010), and sCD163 was positively correlated with log [HOMA-R] ( r = 0.198, p = 0.042). In multiple regression analyses, monocyte CD163 was an independent contributor to log [HOMA-R] ( β = –0.220, p = 0.020) even after adjustment of various clinical factors for HOMA-R ( R 2 = 0.281, p = 0.001), 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.

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          Most cited references25

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          Macrophage subsets in atherosclerosis.

          Giulia Chinetti-Gbaguidi, Sophie Colin, Bart Staels (2015)
          Macrophage accumulation within the vascular wall is a hallmark of atherosclerosis. In atherosclerotic lesions, macrophages respond to various environmental stimuli, such as modified lipids, cytokines, and senescent erythrocytes, which can modify their functional phenotypes. The results of studies on human atherosclerotic plaques demonstrate that the relative proportions of macrophage subsets within a plaque might be a better indicator of plaque phenotype and stability than the total number of macrophages. Understanding the function of specific macrophage subsets and their contribution to the composition and growth of atherosclerotic plaques would aid the identification of novel strategies to delay or halt the development of the disease and its associated pathophysiological consequences. However, most studies aimed at characterizing the phenotypes of human macrophages are performed in vitro and, therefore, their functional relevance to human pathology remains uncertain. In this Review, the diverse range of macrophage phenotypes in atherosclerotic lesions and their potential roles in both plaque progression and stability are discussed, with an emphasis on human pathology.
          Article 0 comments Cited 236 times – based on 0 reviews     Review now
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            Regulation of scavenger receptor CD163 expression in human monocytes and macrophages by pro- and antiinflammatory stimuli.

            C Buechler, M. Ritter, E Orsó … (2000)
            CD163, also referred to as M130, a member of the scavenger receptor cysteine-rich family (SRCR) is exclusively expressed on cells of the monocyte lineage. In freshly isolated monocytes the CD14bright CD16+ monocyte subset revealed the highest expression of CD163 among all monocyte subsets. CD163 mRNA and protein expression is up-regulated during macrophage colony-stimulating factor (M-CSF)-dependent phagocytic differentiation of human blood monocytes. In contrast, monocytic cells treated with GM-CSF and interleukin-4 (IL-4) for dendritic differentiation down-regulate this antigen. CD163 expression is also suppressed by proinflammatory mediators like lipopolysaccharide (LPS), interferon-gamma (IFN-gamma), and tumor necrosis factor alpha, whereas IL-6 and the antiinflammatory cytokine interleukin-10 (IL-10) strongly up-regulate CD163 mRNA in monocytes and macrophages. The effects of the immunosuppressants dexamethasone, cyclosporin A (CA), and cortisol differ in their capacity to influence CD163 mRNA levels. Our results demonstrate that CD163 expression in monocytes/macrophages is regulated by proinflammatory and antiinflammatory mediators. This expression pattern implies a functional role of CD 163 in the antiinflammatory response of monocytes.
            Article 0 comments Cited 191 times – based on 0 reviews     Review now
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              The assessment of insulin resistance in man.

              Brent D. Matthews, Nneka Wallace (2002)
              Insulin resistance exists when a normal concentration of insulin produces a less than normal biological response. The ability to measure insulin resistance is important in order to understand the aetiopathology of Type 2 diabetes, to examine the epidemiology and to assess the effects of intervention. We assess and compare methods of measurement and have undertaken a literature review from 1966 to 2001. Quantitative estimates of insulin resistance can be obtained using model assessments, clamps or insulin infusion sensitivity tests. There is considerable variation in the complexity and labour intensity of the various methods. The most well-established methods are the euglycaemic clamp, minimal model assessment and homeostatic model assessment (HOMA). No single test is appropriate under all circumstances. There are a number of well-established tests used to measure insulin resistance: the choice of method depends on the size and type of study to be undertaken. Although the so-called 'gold-standard' test, the euglycaemic clamp, is useful for intensive physiological studies on small numbers of subjects, a simpler tool such as HOMA is more appropriate for large epidemiological studies. It is important to be aware that most techniques measure stimulated insulin resistance whereas HOMA gives an estimate of basal insulin resistance. Caution should be exercised when making comparisons between studies due to variations in infusion protocols, sampling procedures and hormone assays used in different studies.
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                Author and article information

                Contributors
                Koka Motoyama:
                ORCID: http://orcid.org/0000-0002-8737-5774
                Journal
                Journal ID (nlm-ta): J Diabetes Res
                Journal ID (iso-abbrev): J Diabetes Res
                Journal ID (publisher-id): JDR
                Title: Journal of Diabetes Research
                Publisher: Hindawi
                ISSN (Print): 2314-6745
                ISSN (Electronic): 2314-6753
                Publication date (Print): 2017
                Publication date (Electronic): 28 December 2017
                Volume: 2017
                Electronic Location Identifier: 6549242
                Affiliations
                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
                Author notes

                Academic Editor: Sandeep Singh

                Author information
                http://orcid.org/0000-0002-8737-5774
                http://orcid.org/0000-0002-2329-8191
                http://orcid.org/0000-0002-0099-1161
                Article
                DOI: 10.1155/2017/6549242
                PMC ID: 5763167
                SO-VID: 809c562d-46ec-4345-9e9f-5949cfe13b50
                Copyright © Copyright © 2017 Reina Kawarabayashi et al.
                License:

                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.

                History
                Date received : 30 June 2017
                Date accepted : 22 November 2017
                Funding
                Funded by: Japan Society for the Promotion of Science
                Award ID: 15K08925
                Categories
                Subject: Research Article

                Data availability:

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