Published estimates of the incidence of type 1 diabetes (T1D) in children in the last decade varies between 2% and 4% per annum. If this trend continued, the disease incidence would double in the next 20 years. The risk of developing T1D is determined by a complex interaction between multiple genes (mainly human leukocyte antigens) and environmental factors. Notwithstanding that genetic susceptibility represents a relevant element in T1D risk, genetics alone cannot explain the increase in incidence. Various environmental factors have been suggested as potential triggers for T1D, including several viruses and the hygiene hypothesis; however, none of these seems to explain the large increase in T1D incidence observed over the last decades. Several studies have demonstrated that the prevalence of childhood/adolescence overweight and obesity has risen during the past 30 years in T1D. Currently, at diagnosis, the majority of patients with T1D have normal or elevated body weight and ~50% of patients with longstanding T1D are either overweight or obese. The growing prevalence of obesity in childhood and adolescence offers a plausible explanation for the increase in T1D incidence observed in recent decades. Possible mechanisms of the enhancement of β‐cell autoimmunity by obesity include: a) insulin resistance‐induced β‐cell secretory demand triggering autoimmunity through cytokine release, neo‐epitope antigen formation and increase in β‐cell apoptosis, and b) obesity‐induced low‐grade inflammation with pro‐inflammatory cytokines secreted by locally infiltrating macrophages, which contribute to the presentation by islet cells of autoantigens generally not accessible to T cells. Further studies are needed to clarify whether the control of body weight can prevent or delay the current and continuing rise in T1D incidence.

中文翻译：

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肥胖对1型糖尿病发病率增加的影响。

在过去十年中，儿童对1型糖尿病（T1D）发病率的公开估计每年介于2％和4％之间。如果这种趋势继续下去，该疾病的发病率将在未来20年内翻一番。发生T1D的风险由多个基因（主要是人白细胞抗原）与环境因素之间的复杂相互作用决定。尽管遗传易感性是T1D风险的一个相关因素，但仅遗传学不能解释发病率的增加。各种环境因素被认为是T1D的潜在诱因，包括几种病毒和卫生假说。但是，这些似乎都不能解释过去几十年来观察到的T1D发病率的大幅上升。几项研究表明，在过去的30年中，T1D中儿童/青少年超重和肥胖的患病率上升。目前，在诊断时，大多数T1D患者的体重正常或升高，而约50％的长期T1D患者则是超重或肥胖。肥胖症在儿童期和青春期的流行程度不断上升，为近几十年来观察到的T1D发病率增加提供了合理的解释。肥胖增强β细胞自身免疫的可能机制包括：a）胰岛素抵抗诱导的β细胞分泌需求通过细胞因子释放，新表位抗原形成和β细胞凋亡增加触发自身免疫，以及b）肥胖诱导具有局部浸润巨噬细胞分泌的促炎性细胞因子的低度炎症，它们有助于胰岛细胞呈现自身抗原，这些抗原通常是T细胞无法接近的。需要进一步研究以阐明控制体重是否可以预防或延迟当前和持续的T1D发病率上升。