Research Article Relationship of Soluble RAGE with Insulin Resistance and Beta Cell Function during Development of Type 2 Diabetes Mellitus Subrata Kumar Biswas, 1 Sabreena Mohtarin, 1 Sonchita Rani Mudi, 2 Taznuva Anwar, 1 Laila Anjuman Banu, 3 Sheikh Md. Khorshed Alam, 1 Md. Fariduddin, 4 and M. Iqbal Arslan 1 1 Department of Biochemistry, Bangabandhu Sheikh Mujib Medical University (BSMMU), Shahbag, Dhaka 1000, Bangladesh 2 Department of Biochemistry and Cell Biology, Bangladesh Institute of Research and Rehabilitation in Diabetes, Endocrine and Metabolic Disorders (BIRDEM), 122 Kazi Nazrul Islam Avenue, Shahbag, Dhaka 1000, Bangladesh 3 Department of Anatomy, Bangabandhu Sheikh Mujib Medical University (BSMMU), Shahbag, Dhaka 1000, Bangladesh 4 Department of Endocrinology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Shahbag, Dhaka 1000, Bangladesh Correspondence should be addressed to Subrata Kumar Biswas; su.biswas@yahoo.com Received 14 April 2015; Accepted 12 May 2015 Academic Editor: Roberto Mallone Copyright © 2015 Subrata Kumar Biswas et al. his 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. his study examined whether circulating levels of soluble receptor for advanced glycation end products (sRAGE) alter in prediabetes and correlate with insulin resistance (IR) and beta cell function in prediabetes and newly diagnosed type 2 diabetes mellitus (T2DM). Subjects without previous history of diabetes were recruited and grouped as control, prediabetes, and newly diagnosed T2DM. he control subjects ( = 40) and people with prediabetes ( = 52) and diabetes ( = 66) were similar in terms of age, sex, BMI, systolic and diastolic BP, and fasting insulin level. HOMA-IR was found signiicantly higher in people with diabetes than control subjects ( < 0.001) and people with prediabetes ( = 0.005); and HOMA-%B was found signiicantly deteriorated in people with diabetes ( < 0.001) compared to control subjects and people with prediabetes. However, serum sRAGE levels did not show any signiicant alteration in people with prediabetes compared to control subjects. Moreover, univariate and multivariate analyses did not identify any signiicant correlation and statistical association of sRAGE with HOMA-IR and HOMA-%B in people with prediabetes and newly diagnosed T2DM. Our data suggest that serum sRAGE levels do not alter in people with prediabetes compared to control subjects and do not correlate or associate with IR and beta cell function during development of T2DM. 1. Introduction he receptor for advanced glycation end products (RAGE) is a cell surface receptor of immunoglobulin superfamily. RAGE activation through ligand binding can induce chronic inlammation and oxidative stress, and it has been linked with diseases like diabetic complications, cardiovascular and neurodegenerative diseases, and cancer [1]. A soluble form of RAGE (sRAGE), which is a splice variant of full-length RAGE or a shedding/cleavage product of membrane-bound RAGE, has been found circulating in the plasma [2, 3]. he sRAGE can bind and sequester RAGE ligands and thereby can reduce RAGE activation. herefore, the sRAGE is generally considered as protective against diseases originating from RAGE activation [13]. RAGE-ligand interaction was previously claimed to be involved in the pathogenesis of autoimmune diabetes, and treatment with sRAGE was shown to efectively prevent transfer of diabetes into NOD/scid mice that receive spleen cells from a diabetic NOD donor [4]. Subsequently, blockade of high-mobility group box 1, a RAGE ligand, was shown to inhibit insulitis progression and diabetes development in NOD mice [5]. A minor role of genetic variation in RAGE was also suggested to be associated with insulin resistance (IR) in a human population [6]. However, recent studies have suggested that low levels of circulating sRAGE may be involved in the development of diabetes mellitus [79]. A declining level of sRAGE at the time of seroconversion to autoantibody positivity has been suspected to be a predictor of type 1 diabetes [7, 8], and an independent association has Hindawi Publishing Corporation Journal of Diabetes Research Volume 2015, Article ID 150325, 6 pages http://dx.doi.org/10.1155/2015/150325