The Influence of Pubertal Development on Autoantibody Appearance and Progression to Type 1 Diabetes in the TEDDY Study
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 ty...
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| Vydáno v: | Journal of the Endocrine Society Ročník 8; číslo 7; s. bvae103 |
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| Hlavní autoři: | , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
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Oxford University Press
01.07.2024
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| ISSN: | 2472-1972, 2472-1972 |
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| Abstract | 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. |
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| AbstractList | 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 selfassessment 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 [greater than or equal to] 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. Key Words: diabetes, p-cell, insulin resistance, type 1 diabetes Abbreviations: BMI, body mass index; GADA, glutamic acid decarboxylase; HLA, human leukocyte antigen; HOMA-IR, homeostasis model assessment of insulin resistance; mIAA, islet antibodies to insulin; TEDDY, The Environmental Determinants of Diabetes in the Young. 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. 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; = .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; < .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. The 2 peaks of type 1 diabetes incidence occur during early childhood and puberty.ContextThe 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.ObjectiveWe 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.MethodsThe 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.ResultsOut 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.ConclusionRapid 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. |
| Audience | Academic |
| Author | Veijola, Riitta McIndoe, Richard Ziegler, Anette-G Schatz, Desmond A Elding Larsson, Helena Warncke, Katharina Toppari, Jorma Hagopian, William Krischer, Jeffrey P Rewers, Marian J Tamura, Roy Akolkar, Beena Vehik, Kendra Haller, Michael J Lernmark, Åke Steck, Andrea K |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38867880$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society. 2024 The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society. COPYRIGHT 2024 Oxford University Press The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| CorporateAuthor | Lunds universitet Profile areas and other strong research environments Department of Clinical Sciences, Malmö Lund University Celiac Disease and Diabetes Unit Strategiska forskningsområden (SFO) EXODIAB: Excellence of Diabetes Research in Sweden Faculty of Medicine Celiaki och diabetes Strategic research areas (SRA) Medicinska fakulteten Profilområden och andra starka forskningsmiljöer Pediatrisk endokrinologi Institutionen för kliniska vetenskaper, Malmö Paediatric Endocrinology |
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| Keywords | type 1 diabetes β-cell diabetes insulin resistance |
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The 2 peaks of type 1 diabetes incidence occur during early childhood and puberty.
Objective
We sought to better understand the relationship... The 2 peaks of type 1 diabetes incidence occur during early childhood and puberty. We sought to better understand the relationship between puberty, islet... Context: The 2 peaks of type 1 diabetes incidence occur during early childhood and puberty. Objective: We sought to better understand the relationship between... Context The 2 peaks of type 1 diabetes incidence occur during early childhood and puberty. Objective We sought to better understand the relationship between... The 2 peaks of type 1 diabetes incidence occur during early childhood and puberty.ContextThe 2 peaks of type 1 diabetes incidence occur during early childhood... CONTEXT: The 2 peaks of type 1 diabetes incidence occur during early childhood and puberty. OBJECTIVE: We sought to better understand the relationship between... |
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| SubjectTerms | Autoantibodies Clinical Clinical Medicine Development and progression Diabetes Endocrinology and Diabetes Endokrinologi och diabetes Health aspects Islands of Langerhans Klinisk medicin Medical and Health Sciences Medicin och hälsovetenskap Pediatric research Physiological aspects Puberty Type 1 diabetes |
| Title | The Influence of Pubertal Development on Autoantibody Appearance and Progression to Type 1 Diabetes in the TEDDY Study |
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