Epigenetics: deciphering how environmental factors may modify autoimmune type 1 diabetes

Epigenetics: deciphering how environmental factors may modify autoimmune type 1 diabetes Type 1 diabetes (T1D) is an autoimmune disease that has increased two- to threefold over the past half century by as yet unknown means. It is generally accepted that T1D is the result of gene–environment interactions, but such rapid increases in incidence are not explained by Mendelian inheritance. There have been numerous advances in our knowledge of the pathogenesis of T1D. Indeed, there has been a large number of genes identified that contribute to risk for this disease and several environmental factors have been proposed. The complexity of such interactions is yet to be understood for any major chronic disease. Epigenetic regulation is one way to explain the rapid increase in incidence and could be a central mechanism by which environmental factors influence development of diabetes. However, there is remarkably little known about the contribution of epigenetics to T1D pathogenesis. Here we speculate on various candidate processes and molecules of the immune and endocrine systems that could modify risk for T1D through epigenetic regulation. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Mammalian Genome Springer Journals

Epigenetics: deciphering how environmental factors may modify autoimmune type 1 diabetes

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Publisher
Springer-Verlag
Copyright
Copyright © 2009 by Springer Science+Business Media, LLC
Subject
Life Sciences; Zoology ; Anatomy ; Cell Biology
ISSN
0938-8990
eISSN
1432-1777
D.O.I.
10.1007/s00335-009-9213-6
Publisher site
See Article on Publisher Site

Abstract

Type 1 diabetes (T1D) is an autoimmune disease that has increased two- to threefold over the past half century by as yet unknown means. It is generally accepted that T1D is the result of gene–environment interactions, but such rapid increases in incidence are not explained by Mendelian inheritance. There have been numerous advances in our knowledge of the pathogenesis of T1D. Indeed, there has been a large number of genes identified that contribute to risk for this disease and several environmental factors have been proposed. The complexity of such interactions is yet to be understood for any major chronic disease. Epigenetic regulation is one way to explain the rapid increase in incidence and could be a central mechanism by which environmental factors influence development of diabetes. However, there is remarkably little known about the contribution of epigenetics to T1D pathogenesis. Here we speculate on various candidate processes and molecules of the immune and endocrine systems that could modify risk for T1D through epigenetic regulation.

Journal

Mammalian GenomeSpringer Journals

Published: Aug 22, 2009

References

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