Himmetoglu et al. Int Arch Endocrinol Clin Res 2017, 3:011 Volume 3 | Issue 1 ISSN: 2572-407X Open Access International Archives of Endocrinology Clinical Research DOI: 10.23937/2572-407X.1510011 Citaon: Himmetoglu S, Yuksel S, Damcı T, Ilkova H, Dincer Y (2017) Serum Level of Cytokeran-18/ M30 Angen is Increased in the Cases with Impaired Glucose Tolerance. Int Arch Endocrinol Clin Res 3:011. doi.org/10.23937/2572-407X.1510011 Received: September 18, 2017: Accepted: November 20, 2017: Published: November 22, 2017 Copyright: © 2017 Himmetoglu S, et al. This is an open-access arcle distributed under the terms of the Creave Commons Aribuon License, which permits unrestricted use, distribuon, and reproducon in any medium, provided the original author and source are credited. • Page 1 of 5 • Himmetoglu et al. Int Arch Endocrinol Clin Res 2017, 3:011 Serum Level of Cytokeran-18/M30 Angen is Increased in the Cases with Impaired Glucose Tolerance Solen Himmetoglu 1 , Selin Yuksel 2 , Taner Damcı 3 , Hasan Ilkova 3 and Yildiz Dincer 2* 1 Department of Medical Biochemistry, T.C. Biruni University Medical Faculty, Turkey 2 Department of Medical Biochemistry, Istanbul University, Turkey 3 Department of Endocrinology, Istanbul University, Turkey *Corresponding author: Yildiz Dincer, Department of Medical Biochemistry, Istanbul University, Cerrahpasa Medical Faculty, Dere Sok. Umut Ap. No: 11/44 Sahrayicedit, Erenkoy, Istanbul, Turkey, Tel: 90-212-4143000/23004, E-mail: yldz.dincer@gmail.com Abstract Background: Beta cell death by apoptosis is an important mechanism in beta cell dysfunction and development of diabetes. Inhibition of apoptosis may be helpful approach in the prevention of diabetes. In this context, non-invasive, specific markers are needed to detect apoptosis in predia- betic stage. In the present study serum levels of cytokera- tin-18/M30 antigen, a surrogate marker of apoptosis were investigated in cases with type 2 diabetes and Impaired Glucose Tolerance (IGT). Materials and methods: A total of 44 patients with type 2 diabetes, 27 cases with IGT, and 27 control cases were involved in the study. Serum levels of cytokeratin-18/M30 antigen were determined by ELISA kit in the blood samples taken after an overnight fast. Results: Serum level of cytokeratin-18/M30 antigen was found to be higher in the IGT group than those in the control group (P < 0.05). Serum level of cytokeratin-18/M30 antigen was also higher in the type 2 diabetes group in comparison to those in the control group, but this increase was not sta- tistically significant. In the type 2 diabetes group, a positive correlation was determined between cytokeratin-18/M30 antigen and fasting glucose (r: 0.430; P < 0.005); cytokera- tin-18/M30 antigen level was negatively correlated with ratio of c-peptide/fasting glucose (r: -0.506; P < 0.05). Conclusion: Serum cytokeratin-18/M30 antigen level is increased in the cases with IGT. This would imply that it may be a useful marker in the detection of apoptosis in prediabetic stage. However, the origin of increased cyto- keratin-18/M30 antigen is not clear. This increase may also reflect apoptosis of inflamed fatty liver cells that is linked the pathogenesis of type 2 diabetes. Keywords Type 2 diabetes, Impaired glucose tolerance, Apoptosis, Cytokeratin-18/ M30 antigen Introducon Insulin resistance is an early event in development of type 2 diabetes. In order to balance insulin resistance, pancreac β-cells enhance producon and secreon of insulin. Chronic hyperglycemia and prolonged tempo- rary postprandial hyperglycemia causes further deteri- oraon in β-cell funcon [1]. Apoptosis, programmed cell death, is a normal process that occurs during mor- phogenesis, but it also contributes to some pathological processes. Pancreac beta cells can undergo apoptosis in vivo. Beta cell death by apoptosis was clearly demon- strated by Scaglia, et al. in 1995 for the first me [2]. Over me, invesgaons revealed the mechanisms in- volved in β-cell apoptosis and responsible smuli in this event [3-5]. Apoptoc cell death occurs via extrinsic and intrin- sic pathways. Extrinsic pathway is iniated by binding of death ligands to cell surface receptors. The intrinsic pathway is acvated by DNA damage, and results in cytochrome c release from mitochondria. Acvaon of both pathways results in a downstream acvaon of a group of proteases, called as procaspases, in the cytoplasm. Acvated caspases lead to acvaon of en- donucleases, which in turn causes DNA fragmentaon RESEARCH ARTICLE Check for updates