Lien vers Pubmed [PMID] – 20519570
Dis Model Mech 2010 Jul-Aug;3(7-8):426-9
Type 1 diabetes (T1D) is a major disease affecting primarily young children with an incidence in Western societies of around 0.3% by 20 years of age. Although both genetic and environmental factors contribute to the disease aetiology, the precise nature of both the genetic and environmental contribution to human disease onset and progression remains poorly defined. Despite showing some differences from human T1D, rodent models for T1D (Leiter and von Herrath, 2004; von Herrath and Nepom, 2009) and, in particular the nonobese diabetic (NOD) mouse (Atkinson and Leiter, 1999; Kikutani and Makino, 1992), have provided important insights into the disease process, even if they have not yet allowed definitive identification of many of the genetic factors involved in the process. The recent isolation of germline-competent embryonic stem (ES) cells from the NOD mouse strain, and from the rat, will greatly facilitate the functional analysis of T1D in the mouse, and open up the possibility of improved exploitation of rat T1D models. This important technological breakthrough has the potential to remove bottlenecks from the identification of T1D genes, allowing the underlying metabolic pathways to be established and facilitating evaluation of the eventual role of the human homologues in the disease process. The current status and perspectives for an improved mechanistic understanding of the disease process will be addressed.