Absence of H-2 genetic influence on streptozotocin-induced diabetes in mice.
Five daily injections of streptozotocin (40 mg/kg) produced a delayed but progressively increasing level of hyperglycaemia in long term studies with male Naval Medical Research Institute mice and C3D2F1 (DBA 2 J male x C3H/Tif female) F1 hybrid mice. The development of hyperglycaemia was paralleled by decreased amounts of pancreatic immunoreactive insulin as well as degranulation and necrosis of pancreatic B cells. Insulitis was found from days 9-25 after the first injection of streptozotocin. Compared with the F1 hybrid strain the parental inbred strains DBA 2 J and C3H/Tif demonstrated a certain resistance to streptozotocin. Development of hyperglycaemia did not differ in four congenic resistant lines of mice on the C57 BL/10 genetic background, indicating the major histocompatibility complex genes are not likely to determine susceptibility to streptozotocin-induced islet B cell damage.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000235:genetics* / Q000473:pathology; D004198:Disease Susceptibility; D005260:Female; D006183:H-2 Antigens / Q000032:analysis*; D007328:Insulin / Q000097:blood; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics; D010179:Pancreas / Q000473:pathology; D013311:Streptozocin
D001786:Blood Glucose; D006183:H-2 Antigens; D007328:Insulin; D013311:Streptozocin