Genetic Influence for Late-In-Life T1D Examined

DNA gene editing
DNA gene editing
High-risk genotypes represent 6.4% of the included study population, but accounted for 61% of all cases of T1D.
This article is part of Endocrinology Advisor’s coverage of the 53rd European Association for the Study of Diabetes (EASD) Annual Meeting taking place in Lisbon, Portugal. Check back regularly for more news on the latest clinical research in bone health from EASD 2017.

Homozygous genetic alleles may increase type 1 diabetes (T1D) risk in those diagnosed with late-in-life diabetes, according to research presented at the 53rd European Association for the Study of Diabetes (EASD) Annual Meeting, held September 11-15 in Lisbon, Portugal.

Researchers from Exeter University in Exeter, UK, used data stored in the UK Biobank to assess diabetes development in 120,192 people. People in the highest human leukocyte antigen (HLA) groups (DR3/DR3, DR3/DR4, and DR4/DR4 alleles) were examined.

Among the high-risk HLA groups, there were “marked differences” noted in participants’ likelihood of T1D developing: 1.2%, 4.2%, and 3.5% in the DR3/DR3, DR3/DR4, and DR4/DR4 groups, respectively. Mean age at T1D diagnosis was 17, 28, and 38 years (P <.001) in each HLA group, respectively, with the majority (71%) of T1D cases associated with DR4/DR4 diagnosed in patients age 30 or older.

“Population analysis has shown for the first time that DR4/DR4 specifically predisposes to T1D over 30 years of age and carriers of this genotype have the highest risk for development of late-onset T1D,” the researchers concluded. “This result is consistent with heterogenity in age of diagnosis reflecting heterogenity in immune mechanisms in T1D.”

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Thomas NJM, Jones SE, Weedon M, Oram R, Hattersley A. New insights into HLA in type 1 diabetes from population analysis: DR4 homozygosity specifically predisposes to type 1 diabetes after 30 years. Presented at: 53rd European Association for the Study of Diabetes Annual Meeting; September 11-15, 2017; Lisbon, Portugal. Abstract 49.