PDF(Pubmed)
Abstract：
UNASSIGNED: The 2 peaks of type 1 diabetes incidence occur during early childhood and puberty.
UNASSIGNED: We sought to better understand the relationship between puberty, islet autoimmunity, and type 1 diabetes.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: We sought to better understand the relationship between puberty, islet autoimmunity, and type 1 diabetes.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
摘要：
■1型糖尿病发病率的2个高峰发生在儿童早期和青春期。
■我们试图更好地理解青春期之间的关系，胰岛自身免疫,1型糖尿病。
■青春期，胰岛自身免疫,在青年糖尿病的环境决定因素（TEDDY）研究中，对儿童的1型糖尿病进展进行了前瞻性调查。青春期的开始是由Tanner阶段的受试者自我评估确定的。青春期进展速度之间的关联，青春期生长，体重增加,胰岛素抵抗的稳态模型评估（HOMA-IR），胰岛自身免疫,并评估了1型糖尿病的进展。使用Cox比例风险比分析个体因素的影响。
■在5677名8岁仍在研究的儿童中，95%报告至少1个Tanner阶段得分并纳入研究。与青春期前儿童（Tanner阶段1）相比，青春期儿童（Tanner阶段≥2）发生自身免疫事件的风险较低（HR0.65，95％CI0.45-0.93；P=.019）。体重指数Z评分的增加与胰岛素自身抗体的发生率较高（HR2.88，95％CI1.61-5.15；P<.001）相关。在患有多种自身抗体的儿童中，HOMA-IR和Tanner第4阶段的进展速度均与1型糖尿病的进展无关.
■青春期体重的快速增加与胰岛自身免疫的发展有关。青春期本身对自身抗体或1型糖尿病的出现没有显着影响。需要进一步的研究来更好地了解潜在的机制。
■我们试图更好地理解青春期之间的关系，胰岛自身免疫,1型糖尿病。
■青春期，胰岛自身免疫,在青年糖尿病的环境决定因素（TEDDY）研究中，对儿童的1型糖尿病进展进行了前瞻性调查。青春期的开始是由Tanner阶段的受试者自我评估确定的。青春期进展速度之间的关联，青春期生长，体重增加,胰岛素抵抗的稳态模型评估（HOMA-IR），胰岛自身免疫,并评估了1型糖尿病的进展。使用Cox比例风险比分析个体因素的影响。
■在5677名8岁仍在研究的儿童中，95%报告至少1个Tanner阶段得分并纳入研究。与青春期前儿童（Tanner阶段1）相比，青春期儿童（Tanner阶段≥2）发生自身免疫事件的风险较低（HR0.65，95％CI0.45-0.93；P=.019）。体重指数Z评分的增加与胰岛素自身抗体的发生率较高（HR2.88，95％CI1.61-5.15；P<.001）相关。在患有多种自身抗体的儿童中，HOMA-IR和Tanner第4阶段的进展速度均与1型糖尿病的进展无关.
■青春期体重的快速增加与胰岛自身免疫的发展有关。青春期本身对自身抗体或1型糖尿病的出现没有显着影响。需要进一步的研究来更好地了解潜在的机制。
