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| Content Provider | Springer Nature Link |
|---|---|
| Author | MacFarlane, Amanda J. Strom, Alexander Scott, Fraser W. |
| Copyright Year | 2009 |
| 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. |
| Starting Page | 624 |
| Ending Page | 632 |
| Page Count | 9 |
| File Format | |
| ISSN | 09388990 |
| Journal | Mammalian Genome |
| Volume Number | 20 |
| Issue Number | 9-10 |
| e-ISSN | 14321777 |
| Language | English |
| Publisher | Springer-Verlag |
| Publisher Date | 2009-08-22 |
| Publisher Place | New York |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Zoology Anatomy Cell Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics |
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