The Influence of Pubertal Development on Autoantibody Appearance and Progression to Type 1 Diabetes in the TEDDY Study
Warncke, Katharina; Tamura, Roy; Schatz, Desmond A; Veijola, Riitta; Steck, Andrea K; Akolkar, Beena; Hagopian, William; Krischer, Jeffrey P; Lernmark, Åke; Rewers, Marian J; Toppari, Jorma; McIndoe, Richard; Ziegler, Anette-G; Vehik, Kendra; Haller, Michael J; Elding Larsson, Helena (2024-05-24)
Oxford University Press
24.05.2024
Katharina Warncke, Roy Tamura, Desmond A Schatz, Riitta Veijola, Andrea K Steck, Beena Akolkar, William Hagopian, Jeffrey P Krischer, Åke Lernmark, Marian J Rewers, Jorma Toppari, Richard McIndoe, Anette-G Ziegler, Kendra Vehik, Michael J Haller, Helena Elding Larsson, The Influence of Pubertal Development on Autoantibody Appearance and Progression to Type 1 Diabetes in the TEDDY Study, Journal of the Endocrine Society, Volume 8, Issue 7, July 2024, bvae103, https://doi.org/10.1210/jendso/bvae103
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© The Author(s) 2024. 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. See the journal About page for add- itional terms.
https://creativecommons.org/licenses/by/4.0/
© The Author(s) 2024. 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. See the journal About page for add- itional terms.
https://creativecommons.org/licenses/by/4.0/
Julkaisun pysyvä osoite on
https://urn.fi/URN:NBN:fi:oulu-202406144571
https://urn.fi/URN:NBN:fi:oulu-202406144571
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Abstract
Context:
The 2 peaks of type 1 diabetes incidence occur during early childhood and puberty.
Objective:
We sought to better understand the relationship between puberty, islet autoimmunity, and type 1 diabetes.
Methods:
The relationships between puberty, islet autoimmunity, and progression to type 1 diabetes were investigated prospectively in children followed in The Environmental Determinants of Diabetes in the Young (TEDDY) study. Onset of puberty was determined by subject self-assessment of Tanner stages. Associations between speed of pubertal progression, pubertal growth, weight gain, homeostasis model assessment of insulin resistance (HOMA-IR), islet autoimmunity, and progression to type 1 diabetes were assessed. The influence of individual factors was analyzed using Cox proportional hazard ratios.
Results:
Out of 5677 children who were still in the study at age 8 years, 95% reported at least 1 Tanner Stage score and were included in the study. Children at puberty (Tanner Stage ≥2) had a lower risk (HR 0.65, 95% CI 0.45-0.93; P = .019) for incident autoimmunity than prepubertal children (Tanner Stage 1). An increase of body mass index Z-score was associated with a higher risk (HR 2.88, 95% CI 1.61-5.15; P < .001) of incident insulin autoantibodies. In children with multiple autoantibodies, neither HOMA-IR nor rate of progression to Tanner Stage 4 were associated with progression to type 1 diabetes.
Conclusion:
Rapid weight gain during puberty is associated with development of islet autoimmunity. Puberty itself had no significant influence on the appearance of autoantibodies or type 1 diabetes. Further studies are needed to better understand the underlying mechanisms.
Context:
The 2 peaks of type 1 diabetes incidence occur during early childhood and puberty.
Objective:
We sought to better understand the relationship between puberty, islet autoimmunity, and type 1 diabetes.
Methods:
The relationships between puberty, islet autoimmunity, and progression to type 1 diabetes were investigated prospectively in children followed in The Environmental Determinants of Diabetes in the Young (TEDDY) study. Onset of puberty was determined by subject self-assessment of Tanner stages. Associations between speed of pubertal progression, pubertal growth, weight gain, homeostasis model assessment of insulin resistance (HOMA-IR), islet autoimmunity, and progression to type 1 diabetes were assessed. The influence of individual factors was analyzed using Cox proportional hazard ratios.
Results:
Out of 5677 children who were still in the study at age 8 years, 95% reported at least 1 Tanner Stage score and were included in the study. Children at puberty (Tanner Stage ≥2) had a lower risk (HR 0.65, 95% CI 0.45-0.93; P = .019) for incident autoimmunity than prepubertal children (Tanner Stage 1). An increase of body mass index Z-score was associated with a higher risk (HR 2.88, 95% CI 1.61-5.15; P < .001) of incident insulin autoantibodies. In children with multiple autoantibodies, neither HOMA-IR nor rate of progression to Tanner Stage 4 were associated with progression to type 1 diabetes.
Conclusion:
Rapid weight gain during puberty is associated with development of islet autoimmunity. Puberty itself had no significant influence on the appearance of autoantibodies or type 1 diabetes. Further studies are needed to better understand the underlying mechanisms.
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