Abstract
Type 1 diabetes (T1D) results from the immune-mediated destruction of insulin-secreting β-cells that reside in the pancreatic Islets of Langerhans. Genetic susceptibility is necessary but not sufficient for the development of autoimmune diabetes, indicating a key role for risk modification by environmental factors. Epigenetic mechanisms could mediate the effect of specific environmental factors and could therefore explain, at least in part, non-genetic susceptibility to Type 1 diabetes. Exposure to variable nutrition or infection in early life, including in utero experiences can modify T1D susceptibility, which may occur via epigenetic means. T1D is characterized by autoimmune destruction of pancreatic insulin-secreting β-cells and their aberrant development and function of β-cells; these pathogenic mechanisms are also subject to epigenetic regulation. Furthermore, the diabetic state, characterized by fluctuations in insulin and glucose, can influence genomic methylation profiles and gene expression, which can potentially impact susceptibility to co-morbidities of T1D. This chapter identifies potential epigenetic mechanisms that may modify T1D risk and describes study designs that can be implemented to determine the role played by epigenetics in disease pathogenesis.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: 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.
