Regulation of autoimmunity in NODRhebmice that represent increase of mTOR-dependent pancreatic βーcells and acceleration of autoimmune destruction.

肠促胰岛素（人GLP-1类似物）联合或不联合CFA可改善新糖尿病NOD小鼠的糖尿病，但不能改善新糖尿病NODR小鼠（R3系）的糖尿病，后者可加速糖尿病进展。新的糖尿病NODRheb小鼠没有表现出Treg被诱导进入胰岛，也没有胰岛再生。此外，在围产期，NODRheb小鼠比NOD小鼠表现出更多的糖尿病发病率和更多的分娩减少。NODRheb小鼠在分娩后也显示出比NOD小鼠更快的糖尿病进展。

Administration of incretin (human GLP-1 analog) with or withoutCFA improved diabetes in newly diabetic NOD mice, but not in newly diabetic NODRhebmice (R3 lines), which accelerate diabetes progression. Newly diabetic NODRhebmice represented no induction of Treg into pancreatic islets and no islet regeneration. In addition, NODRhebmice showed more increased diabetes onset than NOD mice during the perinatal period and more decreased delivery. NODRhebmice also showed more accelerated diabetes progression than NOD mice after delivery.