Phlips J-C, Radermecker R P
Service de Diabétologie, Nutrition et Maladies métaboliques, CHU de Liège, Belgique.
Rev Med Liege. 2012 May-Jun;67(5-6):319-25.
Type 1 diabetes is an autoimmune disease that results in a progressive (complete in most cases) destruction of insulin-secreting beta cells from Langerhans islets. Even if the autoimmune process becomes to be well known, no one is yet sure what specifically prompts the autoimmune response that destroys the body's ability to produce insulin. Etiology of this complex disease combines a genetic predisposition and still (almost) unknown environmental factors that trigger autoimmuninty specifically targeting beta cells. Genetic HLA predispositions are clearly identified. However, only few people with apparent genetic predisposition to type 1 diabetes actually end up getting the disease. Moreover, the remarkable increase of type 1 diabetes prevalence observed in numerous countries can not be explained by genetics. Because genetic factors can't predict alone the development of type 1 diabetes, environmental factors must be involved such as viral infections, toxins from food, cow milk during childhood (instead of breast feeding) or vitamin D deficiency. This paper aims at describing the role of the genetic predisposition and the environmental hypothesis which can be involved in the development of type 1 diabetes. We will conclude by briefly describing clinical trials targeting either the immune response or the potentially toxic environment.
1型糖尿病是一种自身免疫性疾病，会导致胰岛中分泌胰岛素的β细胞逐渐（在大多数情况下是完全）被破坏。即使自身免疫过程已为人熟知，但仍无人确切知晓究竟是什么具体引发了破坏人体产生胰岛素能力的自身免疫反应。这种复杂疾病的病因既有遗传易感性，又有（几乎）仍不明确的环境因素，这些环境因素会引发专门针对β细胞的自身免疫。遗传的HLA易感性已被明确识别。然而，仅有少数明显具有1型糖尿病遗传易感性的人最终会患上这种疾病。此外，许多国家观察到的1型糖尿病患病率的显著上升无法用遗传学来解释。由于遗传因素无法单独预测1型糖尿病的发病，所以必定涉及环境因素，如病毒感染、食物毒素、儿童期食用牛奶（而非母乳喂养）或维生素D缺乏。本文旨在描述遗传易感性的作用以及可能与1型糖尿病发病相关的环境假说。我们将通过简要描述针对免疫反应或潜在有毒环境的临床试验来得出结论。
