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Insulin VNTR I/III genotype is associated with autoantibodies against glutamic acid decarboxylase in newly diagnosed type 1 diabetes
Author(s) -
Rajasalu T.,
Haller K.,
Salur L.,
Kisand K.,
Tillmann V.,
Schlosser M.,
Uibo R.
Publication year - 2007
Publication title -
diabetes/metabolism research and reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.307
H-Index - 110
eISSN - 1520-7560
pISSN - 1520-7552
DOI - 10.1002/dmrr.745
Subject(s) - autoantibody , genotype , type 1 diabetes , human leukocyte antigen , allele , logistic regression , immunology , variable number tandem repeat , medicine , autoimmunity , diabetes mellitus , glutamate decarboxylase , insulin , endocrinology , biology , genetics , antigen , antibody , gene , enzyme , biochemistry
Background In type 1 diabetes (T1D), the influence of age at diagnosis and of the IDDM1 and IDDM2 genetic susceptibility loci on the profile of β‐cell autoantibodies has been demonstrated. We studied these associations in a group of 92 patients (children, adolescents and adults, aged 2–62 years) with newly diagnosed T1D. Methods The prevalence of the HLA‐DQB1 *02 and *0302 alleles and of the classes of variable number of tandem repeats (VNTR) of the insulin gene ( INS ), and of β‐cell autoantibodies (GADA, IA‐2A, ICA and IAA) was determined. Statistical analysis was performed using linear and logistic regression models. Results The presence of IAA, IA‐2A and ICA, but not of GADA, was negatively associated with age at diagnosis. Younger patients were more likely to have multiple autoantibodies. There was a tendency of a higher prevalence of IAA in patients with the HLA‐DQB1 *02/0302 genotype or with the DQB1 *0302 allele compared to patients lacking these markers. As a novel observation, the INS VNTR I/III genotype was significantly associated with the presence of GADA (OR = 4.79; p = 0.018). Conclusion The association between the INS VNTR I/III genotype and GADA may suggest that in patients with T1D lacking the INS VNTR I/I genotype, the effect of other susceptibility factors prevails, which promotes the development of autoimmunity to β‐cell antigens other than insulin. Copyright © 2007 John Wiley & Sons, Ltd.