Plasma ascorbic acid (vitamin C) and the risk of islet autoimmunity and type 1 diabetes mellitus: The Environmental Determinants of Diabetes in the Young (TEDDY) Study

This abstract has open access
Abstract Summary

Background

Vitamin C might protect beta cells from oxidative damage and thus prevent islet autoimmunity (IA) and type 1 diabetes mellitus (T1DM). We studied the association of plasma vitamin C concentration with the risk of developing T1DM related outcomes and examined whether missense single nucleotide polymorphisms (SNP) in vitamin C transport genes modifies the association.

Methods

TEDDY (The Environmental Determinants of Diabetes in the Young) is a longitudinal cohort study of children at high genetic risk for T1DM (n=8 676) born between 2004-2010 in the U.S., Finland, Sweden, and Germany. Plasma vitamin C was measured at the age 6 and 12 months and annually up to 6 year of age. The SNPs in sodium L-ascorbic acid cotransport SLC23A1 gene (rs33972313) and dehydro-L-ascorbic ascorbic acid transport genes SLC2A1 (rs1105297, rs3754223) and SLC2A2 (rs5400) were genotyped using ImmunoChip custom array. Primary outcomes were persistent confirmed IA defined by repeated positivity for at least 1 of the 3 islet autoantibodies (IAA, GADA, IA-2A) or T1DM. Secondary outcomes were IAA or GADA as the only first appearing autoantibody. A nested case-control study included 350 IA cases with 974 controls and 102 T1DM cases with 288 controls matched for family history of T1DM, clinical center, and sex.

Results

Childhood mean plasma vitamin C concentration was inversely associated with the risk of IA (OR 0.96; 95% Cl, 0.92-1.00), T1DM (OR 0.91; 95% Cl, 0.84-0.99) and IAA first (OR 0.94; 95% Cl, 0.88-0.99). The SLC2A2 SNP rs5400 was associated with increased risk of T1DM (OR 1.67; 95% Cl, 1.07-2.61). None of the transport genes SNPs modified the association between vitamin C status and IA or T1DM.

Conclusion

Higher plasma vitamin C status might protect against IA, T1DM and primary insulin autoimmunity in children genetically susceptible to T1DM. The SLC2A2 gene might influence T1DM development.

Submission ID :
IDS29134
Submission Type
Abstract Topics
University of Tampere, Faculty of Social Sciences/Health, University of Tampere, Tampere, Finland
University of South Florida
National Instute for Health and Welfare
Department of Epidemiology, Colorado School of Public Health, University of Colorado Denver, Aurora, Colorado, United States
University of South Florida, USA
Barbara Davis Center
Institute of Diabetes Research, Helmholtz Zentrum München, German Research Center for Environmental Health, Munich-Neuherberg, Germany
Lund University, Lund (Sweden)
University of Turku
Pacific Northwest Diabetes Research Institute, USA
Center for Public Health Genomics, University of Virginia, Charlottesville, Virginia, United States
Institute of Diabetes Research, Helmholtz Zentrum München and Forschergruppe Diabetes, Klinikum rechts der Isar, Technische Universität München and Forschergruppe Diabetes e.V., Munich, Germany
Department of Clinical Sciences, Lund University/CRC, Skåne University Hospital, Malmö, Sweden
Health Informatics Institute, University of South Florida
Department of Public Health Solutions, National Institute for Health and Welfare, Helsinki, Finland
Health Informatics Institute, University of South Florida
Department of Public Health Solutions, National Institute for Health and Welfare, Helsinki, Finland

Abstracts With Same Type

Submission ID
Submission Title
Submission Topic
Submission Type
Primary Author
2 visits

KEY DATES

Event dates:
Thursday 25 October - Monday 29 October 2018

Abstract submission deadline:
Monday 14 May 2018

Abstract notification:
July 2018

Early registration deadline:
Monday 3 September 2018

Registration deadline:
Monday 15 October 2018

Contact
British Society for Immunology
+44 (0)20 3019 5901
congress@immunology.org