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The role of an iNOS polymorphism at the post-diagnosis diabetes development in children with Type 1 diabetes

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Objective: A missense polymorphism (rs2297518) of the inducible nitric oxide synthase (iNOS) gene causing a serine to leucine substitution at amino acic position 608 has previously been associated to the development of type 1 diabetes (T1DM). Activation of iNOS is a main effector pathway in cytokine mediated beta-cell destruction. Here, we evaluate whether rs2297518 associates to interleukin-1β (IL-1β) levels, metabolic control and development of autoantibodies 12 months post-diagnosis. Materials and Methods: The International Hvidoere cohort includes 275 children from 18 paediatric centers. The rs2297518 was tested in 256 participants and analyzed for its association to serum IL-1β levels, concentration of autoantibodies and residual beta-cell function as assessed by stimulated C-peptide, HbA1c and calculated insulin dose adjusted HbA1c (IDAA1c) at 1, 6 and 12 months post-diagnosis. Results: At 1 month IL-1β was detected more frequently in CC-genotype individuals as compared to CT and TT individuals, 24/168 vs. 3/75 and 0/9, respectively (p=0.03). This effect was not present at 6 and 12 months post-diagnosis. The iNOS polymorphism was not associated to diabetic ketoacidosis status at diagnosis, stimulated C-peptide, measured HbA1c levels or the calculated IDAA1c at any time point during the first 12 months post-diagnosis. Conclusion: The rs2297518 polymorphism of the iNOS gene may be involved in circulating IL-1β levels after diagnosis. However, this polymorphism does not seem to influence the metabolic outcome the first 12 months after diagnosis.
TidsskriftJournal of Endocrinology and Diabetes Research
Udgave nummer2
Antal sider6
StatusUdgivet - 2016

ID: 49899852