Abstract
Introduction: Diabetic nephropathy (DN) is one of the major microvascular complications of diabetes mellitus. Patients with diabetic nephropathy are at a higher risk of morbidity and mortality than those without nephropathy. In this case, early diagnosis and prevention of DM are crucial. SIRT1, which is among the seven members of sirtuins, is recognized as an important element in the pathogenesis of type 2 diabetes, therefore it has several actions in the diabetic nephropathy that will be further discussed in this study. This study will analyse the relationship between SIRT1 gene polymorphism and serum sirt1 in the pathogenesis of diabetic nephropathy. Aim of the study: evaluation of the association of Silent Information Regulator1 (SIRT1) gene polymorphism and serum SIRT1 protein with type 2 diabetic patients and their role in the pathogenesis of diabetic nephropathy. Subjects and Methods: This study was carried out on 120 subjects with matched age and sex. They were divided into 3 groups: (Group 1: 40 diabetic nephropathy patients, Group 2: 40 diabetic patients without diabetic nephropathy, Group 3: 40 healthy control subjects ) to discuss the association of sirt1 gene polymorphism and the pathogenesis of diabetic nephropathy. Results: The mean levels of the serum SIRT1 protein was significantly increasing in the diabetic nephropathy group than the diabetics without diabetic nephropathy and the controls, while it was not significant between the diabetics without DN and the control group. Conclusion: Basedon this study, SIRT1 gene polymorphism is a significant factor in the development and progression of DN.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: International Journal of Scientific Research and Management
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.