Abstract
Type 1 diabetes (T1D) is an autoimmune condition where the body’s immune cells destroy their insulin-producing pancreatic beta cells leading to dysregulated glycaemia. Individuals with T1D control their blood glucose through exogenous insulin replacement therapy, often using multiple daily injections or pumps. However, failure to accurately mimic intrinsic glucose regulation results in glucose fluctuations and long-term complications impacting key organs such as the heart, kidneys, and/or the eyes. It is well established that genetic and environmental factors contribute to the initiation and progression of T1D, but recent studies show that epigenetic modifications are also important. Here, we discuss key epigenetic modifications associated with T1D pathogenesis and discuss how recent research is finding ways to harness epigenetic mechanisms to prevent, reverse, or manage T1D.
Highlights
The hallmark of type 1 diabetes (T1D) is T cell-mediated autoimmune destruction of pancreatic beta cells, leading to insulin deficiency, elevated blood glucose concentrations, and life-long need for exogenous insulin therapy
In conjunction with the advent of precision medicine, studies elucidating the relationship between individual genetic variants and specific epigenetic alterations/epigenetic patterns will provide a pathway for developing effective diagnostic approaches and innovative therapeutic strategies for T1D
We have described some of the latest discoveries in the field of epigenetics of T1D: how interactions between epigenetic modifications and genetic variants can induce T1D pathogenesis, how altering metabolite concentrations could erase or generate various epigenetic markers and vice versa, how metabolism and chromatin modifications are interconnected, how these processes could significantly influence disease etiology and progression, and how skewing epigenetics can be the key for T1D therapy
Summary
The hallmark of type 1 diabetes (T1D) is T cell-mediated autoimmune destruction of pancreatic beta cells, leading to insulin deficiency, elevated blood glucose concentrations, and life-long need for exogenous insulin therapy. Other studies showed that in siblings sharing an HLA haplotype, it is rather the age at diabetes onset in their sibling that determines their risk of developing the condition, and not the shared HLA type itself [12]. It is the possession of high-risk genes that decide whether or not an individual progress to the clinical presentation of T1D and whether, when, and to what extent those genes are expressed. We discuss recent initiatives targeting epigenetic mechanisms involved in T1D, namely, DNA methylation, histone (post-translational) modifications, and non-coding RNA-mediated gene silencing (for a comprehensive discussion of these mechanisms see references [13,14]), as well as highlighting future avenues for productive therapeutic research
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