Importance of Zinc Transporter 8 Autoantibody in the Diagnosis of Type 1 Diabetes in Latin Americans
Carregando...
Citações na Scopus
22
Tipo de produção
article
Data de publicação
2017
Título da Revista
ISSN da Revista
Título do Volume
Editora
NATURE PUBLISHING GROUP
Autores
Citação
SCIENTIFIC REPORTS, v.7, article ID 207, 7p, 2017
Resumo
There is a scarcity of data of zinc transporter-8 autoantibody (ZnT8A) on mixed populations such as Brazilian. Therefore, we evaluated the relevance of ZnT8A for type 1 diabetes (T1D) diagnosis and the role of ZnT8 coding gene (SLC30A8) in T1D predisposition. Patients with T1D (n=629; diabetes duration = 11 (6-16) years) and 651 controls were genotyped for SLC30A8 rs16889462 and rs2466295 variants (BeadXpress platform). ZnT8 triple antibody was measured by ELISA; glutamic acid decarboxylase (GAD65A) and protein tyrosine phosphatase (IA-2A) autoantibodies by radioimmunoassay. Results: Znt8A was detected in 68.7% of recent-onset T1D patients and 48.9% of the entire patient cohort, similar to GAD65A (68.3% and 47.2%) and IA-2A (64.8% and 42.4%) positivities respectively. ZnT8A was the only antibody in 8.4% of patients. Znt8A and IA2A frequencies and titers were independent of gender and ethnicity, whereas GAD65A titers were greater in females. The diabetes duration-dependent decline in ZnT8A frequency was similar to GAD65A and IA-2A. The SLC30A8 rs2466293 AG + GG genotypes were associated with T1D risk in non-European descents (56.2% x 42.9%; p=0.018), and the GG genotype with higher ZnT8A titers in recent-onset T1D: 834.5 IU/mL (711.3-2190.0) x 281 IU/mL (10.7-726.8); p=0.027. Conclusion ZnT8A detection increases T1D diagnosis rate even in mixed populations. SLC30A8 rs2466293 was associated with T1D predisposition in non-European descents.
Palavras-chave
Referências
- Achenbach P, 2009, DIABETOLOGIA, V52, P1881, DOI 10.1007/s00125-009-1438-0
- American Diabetes Association Classification and diagnosis of diabetes, 2015, DIABETES CARE S1, V38, pS8, DOI 10.2337/DC15-S005
- Andersson C, 2011, AUTOIMMUNITY, V44, P394, DOI 10.3109/08916934.2010.540604
- Andersson C., 2011, PEDIAT DIABETES, V14, P97
- Billings LK, 2014, J CLIN ENDOCR METAB, V99, pE926, DOI 10.1210/jc.2013-2378
- Mattana TCC, 2014, MEDIAT INFLAMM, DOI 10.1155/2014/694948
- de Souza ACCB, 2015, HEALTH QUAL LIFE OUT, V13, DOI 10.1186/s12955-015-0396-0
- Delli AJ, 2012, DIABETES, V61, P2556, DOI 10.2337/db11-1659
- Eisenbarth G. S., 2015, TYPE 1 DIABETES CELL
- Goda N, 2015, BMC MED GENET, V16, DOI 10.1186/s12881-015-0219-5
- Gohlke Henning, 2008, Rev Diabet Stud, V5, P25, DOI 10.1900/RDS.2008.5.25
- Herold KC, 2009, CLIN IMMUNOL, V132, P166, DOI 10.1016/j.clim.2009.04.007
- Huang QO, 2010, EUR J CLIN PHARMACOL, V66, P1207, DOI 10.1007/s00228-010-0882-6
- Kawasaki E, 2011, CLIN IMMUNOL, V138, P146, DOI 10.1016/j.clim.2010.10.007
- Miller S. A., 1998, NUCLEIC ACIDS RES, V16, P215, DOI 10.1093/NAR/16.3.1215
- Naserke HE, 1998, J IMMUNOL, V161, P6963
- Nielsen LB, 2011, AUTOIMMUNITY, V44, P616, DOI 10.3109/08916934.2011.576724
- Pena SDJ, 2011, PLOS ONE, V6, DOI 10.1371/journal.pone.0017063
- Raj SM, 2009, DIABETOLOGIA, V52, P2109, DOI 10.1007/s00125-009-1391-y
- Salonen KM, 2013, DIABETES-METAB RES, V29, P646, DOI 10.1002/dmrr.2440
- Sladek R, 2007, NATURE, V445, P881, DOI 10.1038/nature05616
- Vaziri-Sani F, 2011, J IMMUNOL METHODS, V371, P25, DOI 10.1016/j.jim.2011.06.011
- Vaziri-Sani F, 2010, AUTOIMMUNITY, V43, P598, DOI 10.3109/08916930903555927
- Wenzlau JM, 2010, J CLIN ENDOCR METAB, V95, P4712, DOI 10.1210/jc.2010-0169
- Wenzlau JM, 2008, DIABETES, V57, P2693, DOI 10.2337/db08-0522
- Wenzlau JM, 2007, P NATL ACAD SCI USA, V104, P17040, DOI 10.1073/pnas.0705894104
- Wenzlau JM, 2015, DIABETES CARE, V38, pS14, DOI 10.2337/dcs15-2004
- Wenzlau JM, 2008, ANN NY ACAD SCI, V1150, P256, DOI 10.1196/annals.1447.029
- Wijesekara N, 2010, DIABETOLOGIA, V53, P1656, DOI 10.1007/s00125-010-1733-9
- Yang L, 2010, DIABETES-METAB RES, V26, P579, DOI 10.1002/dmrr.1128
- Zhang Y, 2015, DIABETES-METAB RES, V31, P790, DOI 10.1002/dmrr.2670