Occurrence of pretype I diabetes (pre-IDDM) and type II diabetes (NIDDM) in BC1 [(NOD x Mus spretus) F1 x NOD] mice

Type I human diabetes (IDDM), the BB rat, and the NOD mouse appear to result from autoimmune B-cell destruction in a setting of genetic predisposition.1,2 The NOD/Shi mouse was established in 1980 at the Shionogi Aburahi Laboratories.3 The NOD mouse develops IDDM secondary to B-cell destruction by infiltrating immune cells (insulitis) (Fig. 1; Table 1). Insulitis appears as early as 5 wk of age. To develop overt diabetes, at least 90% of the total islets need to be damaged by infiltrating immune cells. The immune cells invade islets and are often seen adjacent to the ducts and blood vessels. The incidence of insulitis is 90% in NOD/Shi females and 70% in NOD/Shi males at 9 wk of age, and 100% in both sexes at 5 months of age. The incidence and degree of insulitis increase with age, resulting in a lack of intrinsic insulin secretion, hyperglycemia, loss of body weight, and ketosis, as seen in human IDDM. The NOD/Shi mouse develops diabetes usually by 7 months of age.