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
Hlavní autoři: 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
Médium: Journal Article
Jazyk:angličtina
Vydáno: US 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.
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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CitedBy_id crossref_primary_10_1038_s41574_024_01045_0
crossref_primary_10_2337_dc24_2886
Cites_doi 10.2337/diacare.23.10.1516
10.1210/jc.2013-4455
10.1002/dmrr.2438
10.1007/s001250050514
10.2337/dc07-0103
10.1038/ijo.2011.122
10.1196/annals.1375.049
10.1542/peds.2014-0793
10.1007/s00125-004-1507-3
10.2337/dc21-0422
10.1007/s00125-012-2523-3
10.1111/pedi.12066
10.1111/dme.13295
10.1371/journal.pone.0260137
10.1093/biomet/80.1.27
10.2337/dc17-0238
10.1007/s00125-012-2472-x
10.1007/s10654-023-01002-7
10.2337/dc06-2389
10.1111/j.1399-5448.2007.00269.x
10.2307/2531910
10.1007/s001250100548
10.1196/annals.1447.062
10.2337/db17-0261
10.1016/j.immuni.2010.03.018
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Copyright The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society. 2024
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COPYRIGHT 2024 Oxford University Press
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Profile areas and other strong research environments
Department of Clinical Sciences, Malmö
Lund University
Celiac Disease and Diabetes Unit
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Faculty of Medicine
Celiaki och diabetes
Strategic research areas (SRA)
Medicinska fakulteten
Profilområden och andra starka forskningsmiljöer
Pediatrisk endokrinologi
Institutionen för kliniska vetenskaper, Malmö
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Issue 7
Keywords type 1 diabetes
β-cell
diabetes
insulin resistance
Language English
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M.J.H. and H.E.L. contributed equally to the article as joint last authors.
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References Raab (2024070105125491100_bvae103-B10) 2013; 29
Carlsson (2024070105125491100_bvae103-B27) 2012; 36
Rewers (2024070105125491100_bvae103-B5) 1996; 39
Firth (2024070105125491100_bvae103-B20) 1993; 80
Krischer (2024070105125491100_bvae103-B24) 2017; 40
Lakatos (2024070105125491100_bvae103-B22) 1988; 44
Onda (2024070105125491100_bvae103-B4) 2017; 34
De Sanctis (2024070105125491100_bvae103-B17) 2016; 14
Parikka (2024070105125491100_bvae103-B1) 2012; 55
Wilkin (2024070105125491100_bvae103-B11) 2001; 44
Rollof (2024070105125491100_bvae103-B18) 2012; 25
Fourlanos (2024070105125491100_bvae103-B7) 2004; 47
Jaruratanasirikul (2024070105125491100_bvae103-B16) 2015; 28
Elding Larsson (2024070105125491100_bvae103-B29) 2014; 15
Krischer (2024070105125491100_bvae103-B19) 2017; 66
Xu (2024070105125491100_bvae103-B8) 2007; 30
Jacobsen (2024070105125491100_bvae103-B28) 2022; 45
Rasmussen (2024070105125491100_bvae103-B15) 2015; 135
TEDDY Study Group (2024070105125491100_bvae103-B13) 2007; 8
Kelly (2024070105125491100_bvae103-B21) 2014; 99
Bingley (2024070105125491100_bvae103-B9) 2008; 31
Hagopian (2024070105125491100_bvae103-B12) 2006; 1079
Syrjälä (2024070105125491100_bvae103-B26) 2021; 16
Ziegler (2024070105125491100_bvae103-B2) 2012; 55
Cantor (2024070105125491100_bvae103-B23) 2003
Peltonen (2024070105125491100_bvae103-B25) 2023; 38
Karvonen (2024070105125491100_bvae103-B3) 2000; 23
Ziegler (2024070105125491100_bvae103-B6) 2010; 32
TEDDY Study Group (2024070105125491100_bvae103-B14) 2008; 1150
References_xml – volume: 28
  start-page: 367
  issue: 3–4
  year: 2015
  ident: 2024070105125491100_bvae103-B16
  article-title: Reliability of pubertal maturation self-assessment in a school-based survey
  publication-title: J Pediatr Endocrinol Metab
– volume: 23
  start-page: 1516
  issue: 10
  year: 2000
  ident: 2024070105125491100_bvae103-B3
  article-title: Incidence of childhood type 1 diabetes worldwide. Diabetes Mondiale (DiaMond) project group
  publication-title: Diabetes Care
  doi: 10.2337/diacare.23.10.1516
– volume: 14
  start-page: 27
  issue: 1
  year: 2016
  ident: 2024070105125491100_bvae103-B17
  article-title: Methods for rating sexual development in girls
  publication-title: Pediatr Endocrinol Rev
– volume: 99
  start-page: 2104
  issue: 6
  year: 2014
  ident: 2024070105125491100_bvae103-B21
  article-title: Age-based reference ranges for annual height velocity in US children
  publication-title: J Clin Endocrinol Metab
  doi: 10.1210/jc.2013-4455
– volume: 29
  start-page: 631
  issue: 8
  year: 2013
  ident: 2024070105125491100_bvae103-B10
  article-title: Continuous rise of insulin resistance before and after the onset of puberty in children at increased risk for type 1 diabetes—a cross-sectional analysis
  publication-title: Diabetes Metab Res Rev
  doi: 10.1002/dmrr.2438
– volume: 39
  start-page: 807
  issue: 7
  year: 1996
  ident: 2024070105125491100_bvae103-B5
  article-title: Newborn screening for HLA markers associated with IDDM: diabetes autoimmunity study in the young (DAISY)
  publication-title: Diabetologia
  doi: 10.1007/s001250050514
– volume: 31
  start-page: 146
  issue: 1
  year: 2008
  ident: 2024070105125491100_bvae103-B9
  article-title: Insulin resistance and progression to type 1 diabetes in the European Nicotinamide Diabetes Intervention Trial (ENDIT)
  publication-title: Diabetes Care
  doi: 10.2337/dc07-0103
– volume: 36
  start-page: 718
  issue: 5
  year: 2012
  ident: 2024070105125491100_bvae103-B27
  article-title: Low risk HLA-DQ and increased body mass index in newly diagnosed type 1 diabetes children in the better diabetes diagnosis study in Sweden
  publication-title: Int J Obes (Lond)
  doi: 10.1038/ijo.2011.122
– volume: 1079
  start-page: 320
  year: 2006
  ident: 2024070105125491100_bvae103-B12
  article-title: TEDDY--The environmental determinants of diabetes in the young: an observational clinical trial
  publication-title: Ann N Y Acad Sci
  doi: 10.1196/annals.1375.049
– volume: 135
  start-page: 86
  issue: 1
  year: 2015
  ident: 2024070105125491100_bvae103-B15
  article-title: Validity of self-assessment of pubertal maturation
  publication-title: Pediatrics
  doi: 10.1542/peds.2014-0793
– volume: 47
  start-page: 1661
  issue: 10
  year: 2004
  ident: 2024070105125491100_bvae103-B7
  article-title: Insulin resistance is a risk factor for progression to type 1 diabetes
  publication-title: Diabetologia
  doi: 10.1007/s00125-004-1507-3
– volume: 25
  start-page: 125
  issue: 1–2
  year: 2012
  ident: 2024070105125491100_bvae103-B18
  article-title: Evaluation of self-assessment of pubertal maturation in boys and girls using drawings and orchidometer
  publication-title: J Pediatr Endocrinol Metab
– volume: 45
  start-page: 624
  issue: 3
  year: 2022
  ident: 2024070105125491100_bvae103-B28
  article-title: Heterogeneity of DKA incidence and age-specific clinical characteristics in children diagnosed with type 1 diabetes in the TEDDY study
  publication-title: Diabetes Care
  doi: 10.2337/dc21-0422
– volume: 55
  start-page: 1926
  issue: 7
  year: 2012
  ident: 2024070105125491100_bvae103-B1
  article-title: Early seroconversion and rapidly increasing autoautoantibody concentrations predict prepubertal manifestation of type 1 diabetes in children at genetic risk
  publication-title: Diabetologia
  doi: 10.1007/s00125-012-2523-3
– volume-title: SAS Survival Analysis Techniques for Medical Research
  year: 2003
  ident: 2024070105125491100_bvae103-B23
– volume: 15
  start-page: 118
  issue: 2
  year: 2014
  ident: 2024070105125491100_bvae103-B29
  article-title: Children followed in the TEDDY study are diagnosed with type 1 diabetes at an early stage of disease
  publication-title: Pediatr Diabetes
  doi: 10.1111/pedi.12066
– volume: 34
  start-page: 909
  issue: 7
  year: 2017
  ident: 2024070105125491100_bvae103-B4
  article-title: Incidence and prevalence of childhood-onset Type 1 diabetes in Japan: the T1D study
  publication-title: Diabet Med
  doi: 10.1111/dme.13295
– volume: 16
  start-page: e0260137
  issue: 11
  year: 2021
  ident: 2024070105125491100_bvae103-B26
  article-title: Determining the timing of pubertal onset via a multicohort analysis of growth
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0260137
– volume: 80
  start-page: 27
  year: 1993
  ident: 2024070105125491100_bvae103-B20
  article-title: Bias reduction of maximum likelihood estimates
  publication-title: Biometrika
  doi: 10.1093/biomet/80.1.27
– volume: 40
  start-page: 1194
  issue: 9
  year: 2017
  ident: 2024070105125491100_bvae103-B24
  article-title: Genetic and environmental interactions modify the risk of diabetes-related autoimmunity by 6 years of age: the TEDDY study
  publication-title: Diabetes Care
  doi: 10.2337/dc17-0238
– volume: 55
  start-page: 1937
  issue: 7
  year: 2012
  ident: 2024070105125491100_bvae103-B2
  article-title: Age-related islet autoautoantibody incidence in offspring of patients with type 1 diabetes
  publication-title: Diabetologia
  doi: 10.1007/s00125-012-2472-x
– volume: 38
  start-page: 689
  issue: 6
  year: 2023
  ident: 2024070105125491100_bvae103-B25
  article-title: What is the role of puberty in the development of islet autoimmunity and progression to type 1 diabetes?
  publication-title: Eur J Epidemiol
  doi: 10.1007/s10654-023-01002-7
– volume: 30
  start-page: 2314
  issue: 9
  year: 2007
  ident: 2024070105125491100_bvae103-B8
  article-title: Role of insulin resistance in predicting progression to type 1 diabetes
  publication-title: Diabetes Care
  doi: 10.2337/dc06-2389
– volume: 8
  start-page: 286
  year: 2007
  ident: 2024070105125491100_bvae103-B13
  article-title: The environmental determinants of diabetes in the young (TEDDY) study: study design
  publication-title: Pediatr Diabetes
  doi: 10.1111/j.1399-5448.2007.00269.x
– volume: 44
  start-page: 229
  year: 1988
  ident: 2024070105125491100_bvae103-B22
  article-title: Sample sizes based on the log rank statistic in Complex clinical trials
  publication-title: Biometrics
  doi: 10.2307/2531910
– volume: 44
  start-page: 914
  issue: 7
  year: 2001
  ident: 2024070105125491100_bvae103-B11
  article-title: The accelerator hypothesis: weight gain as the missing link between Type I and Type II diabetes
  publication-title: Diabetologia
  doi: 10.1007/s001250100548
– volume: 1150
  start-page: 1
  year: 2008
  ident: 2024070105125491100_bvae103-B14
  article-title: The environmental determinants of diabetes in the young (TEDDY) study
  publication-title: Ann N Y Acad Sci
  doi: 10.1196/annals.1447.062
– volume: 66
  start-page: 3122
  issue: 12
  year: 2017
  ident: 2024070105125491100_bvae103-B19
  article-title: The influence of type 1 diabetes genetic susceptibility regions, age, sex, and family history on the progression from multiple autoantibodies to type 1 diabetes: a TEDDY study report
  publication-title: Diabetes
  doi: 10.2337/db17-0261
– volume: 32
  start-page: 468
  issue: 4
  year: 2010
  ident: 2024070105125491100_bvae103-B6
  article-title: Prediction and pathogenesis in type 1 diabetes
  publication-title: Immunity
  doi: 10.1016/j.immuni.2010.03.018
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Snippet Abstract Context 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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