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
Journal of the Endocrine Society, Volume 8, Issue 7, July 2024, bvae103
https://doi.org/10.1210/jendso/bvae103
The 2 peaks of type 1 diabetes incidence occur during early childhood and puberty.
We sought to better understand the relationship between puberty, islet autoimmunity, and type 1 diabetes.
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.
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.
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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