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Childhood height growth rate association with the risk of islet autoimmunity and development of type 1 diabetes |
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| Author: | Li, Zhiguo1; Veijola, Riitta2; Koski, Eileen1; |
| Organizations: |
1Center for Computational Health, IBM T.J. Watson Research Center, Yorktown Heights, 10598 NY, and Cambridge, 02142 MA, USA 2Department of Pediatrics, PEDEGO Research Unit, University of Oulu, 90014 Oulu, and Oulu University Hospital, 90029 Oulu, Finland 3JDRF, New York, 10281 NY, USA
4Barbara Davis Center for Diabetes, University of Colorado, Denver, 80440 CO, USA
5Department of Virology, Faculty of Medicine and Health Technology, Tampere University, and Fimlab Laboratories, Pirkanmaa Hospital District, 33520 Tampere, Finland 6Institute of Diabetes Research, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764 Munich-Neuherberg, Germany 7Forschergruppe Diabetes e.V. at Helmholtz Zentrum, München, German Research Center for Environmental Health, 85764 Munich-Neuherberg, Germany 8Forschergruppe Diabetes, Technical University Munich, at Klinikum rechts der Isar, 80934 Munich, Germany 9Pacific Northwest Research Institute, Seattle, 98122 WA, USA 10Department of Clinical Sciences, Lund University Diabetes Center, 21428 Malmö, Sweden 11Department of Pediatrics, Kristianstad Hospital, 29133 Kristianstad, Sweden 12Institute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, and Centre for Population Health Research, University of Turku, and Department of Pediatrics, Turku University Hospital, 20520 Turku, Finland |
| Format: | article |
| Version: | published version |
| Access: | open |
| Online Access: | PDF Full Text (PDF, 8.4 MB) |
| Persistent link: | http://urn.fi/urn:nbn:fi-fe2023061656017 |
| Language: | English |
| Published: |
Endocrine society,
2022
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| Publish Date: | 2023-06-16 |
| Description: |
AbstractContext: Rapid growth has been suggested to promote islet autoimmunity and progression to type 1 diabetes (T1D). Childhood growth has not been analyzed separately from the infant growth period in most previous studies, but it may have distinct features due to differences between the stages of development. Objective: We aimed to analyze the association of childhood growth with development of islet autoimmunity and progression to T1D diagnosis in children 1 to 8 years of age. Methods: Longitudinal data of childhood growth and development of islet autoimmunity and T1D were analyzed in a prospective cohort study including 10 145 children from Finland, Germany, Sweden, and the United States, 1-8 years of age with at least 3 height and weight measurements and at least 1 measurement of islet autoantibodies. The primary outcome was the appearance of islet autoimmunity and progression from islet autoimmunity to T1D. Results: Rapid increase in height (cm/year) was associated with increased risk of seroconversion to glutamic acid decarboxylase autoantibody, insulin autoantibody, or insulinoma-like antigen-2 autoantibody (hazard ratio [HR] = 1.26 [95% CI = 1.05, 1.51] for 1-3 years of age and HR = 1.48 [95% CI = 1.28, 1.73] for <3 years of age). Furthermore, height rate was positively associated with development of T1D (HR = 1.80 [95% CI = 1.15, 2.81]) in the analyses from seroconversion with insulin autoantibody to diabetes Conclusion: Rapid height growth rate in childhood is associated with increased risk of islet autoimmunity and progression to T1D. Further work is needed to investigate the biological mechanism that may explain this association. see all
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| Series: |
Journal of clinical endocrinology & metabolism |
| ISSN: | 0021-972X |
| ISSN-E: | 1945-7197 |
| ISSN-L: | 0021-972X |
| Volume: | 107 |
| Issue: | 6 |
| Pages: | 1520 - 1528 |
| DOI: | 10.1210/clinem/dgac121 |
| OADOI: | https://oadoi.org/10.1210/clinem/dgac121 |
| Type of Publication: |
A1 Journal article – refereed |
| Field of Science: |
3123 Gynaecology and paediatrics 3121 General medicine, internal medicine and other clinical medicine |
| Subjects: | |
| Funding: |
This work was supported by funding from JDRF (IBM: 1-RSC-2017-368-I-X, 1-IND-2019-717-I-X), (DAISY: 1-SRA2019-722-I-X, 1-RSC-2017-517-I-X, 5-ECR-2017-388- A-N), (DiPiS: 1-SRA-2019-720-I-X, 1-RSC-2017-526-I-X), (DIPP: 1-RSC-2018-555-I-X), (DEW-IT: 1-SRA-2019-719- I-X, 1-RSC-2017-516-I-X) as well as National Institutes of Health (NIH) (DAISY: DK032493, DK032083, DK104351; DiPiS: DK26190 and the Center for Disease Control (CDC) (DEW-IT: UR6/CCU017247). The DIPP study was funded by JDRF (grants 1-SRA-2016- 342-M-R, 1-SRA-2019-732-M-B); European Union (grant BMH4-CT98-3314); Novo Nordisk Foundation; Academy of Finland (Decision No 292538 and Centre of Excellence in Molecular Systems Immunology and Physiology Research 2012-2017, Decision No. 250114); Special Research Funds for University Hospitals in Finland; Diabetes Research Foundation, Finland; and Sigrid Juselius Foundation, Finland. The BABYDIAB study was funded by the German Federal Ministry of Education and Research to the German Center for Diabetes Research. The DiPiS study was funded by Swedish Research Council (grant no. 14064), Swedish Childhood Diabetes Foundation, Swedish Diabetes Association, Nordisk Insulin Fund, SUS funds, Lion Club International, district 101-S, The Royal Physiographic Society, Skåne County Council Foundation for Research and Development, and LUDC-IRC/EXODIAB funding from the Swedish foundation for strategic research (Dnr IRC15-0067) and Swedish Research Council (Dnr 2009-1039). Additional funding for DEW-IT was provided by the Hussman Foundation and by the Washington State Life Science Discovery Fund. |
| Dataset Reference: |
The data that support the findings of this study are not publicly available because they were used under license for the current study only. Data are, however, available upon reasonable request with permission from the originating sites, whose representatives are William Hagopian (DEW-IT), Markus Lundgren (DiPiS), Marian Rewers (DAISY), Riitta Veijola (DIPP), and Anette Ziegler (BABYDIAB). Zhiguo Li is responsible for the accuracy of the data analysis. The resources used included open-source software; however, the specific code is subject to proprietary constraints but can be made available upon reasonable request to the corresponding author. |
| Copyright information: |
© The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. |
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https://creativecommons.org/licenses/by/4.0/ |