renal/urinary system phenotype

• increased urine glucose level
  (MGI Ref ID J:26618)

endocrine/exocrine gland phenotype

• insulitis
  • N2 mice after a subsequent backcross to NOD show islet disruption with lymphocytic infiltration as early as 4 weeks while non-transgenic H2^g7 homozygous or heterozygous littermates show varying degrees of insulitis by ~6 weeks
  (MGI Ref ID J:26618)
  • H2^g7 homozygous transgenic mice show islet disruption with lymphocytic (T and B cell) infiltration, similar to diabetic NOD controls
  (MGI Ref ID J:26618)

homeostasis/metabolism phenotype

• increased urine glucose level
  (MGI Ref ID J:26618)

• increased circulating glucose level
  • transgenic mice exhibit blood glucose in excess of 13.9 mmol (250 mg/dl)
  (MGI Ref ID J:26618)

immune system phenotype

• insulitis
  • N2 mice after a subsequent backcross to NOD show islet disruption with lymphocytic infiltration as early as 4 weeks while non-transgenic H2^g7 homozygous or heterozygous littermates show varying degrees of insulitis by ~6 weeks
  (MGI Ref ID J:26618)
  • H2^g7 homozygous transgenic mice show islet disruption with lymphocytic (T and B cell) infiltration, similar to diabetic NOD controls
  (MGI Ref ID J:26618)

• increased susceptibility to autoimmune diabetes
  • 2/17 transgenic mice from the first cross to NOD develop diabetes between 10 and 14 weeks, compared to no diabetes in (NOD x C57BL/6)F1 non-transgenic controls
  (MGI Ref ID J:26618)
  • red to no non-transgenic H2^g7 homozygous littermates, or NOD controls which only start to exhibit diabetes at 12 weeks
  (MGI Ref ID J:26618)
  • after a further backcross to NOD, diabetes onset is accelerated relative to transgenic mice from the initial cross to NOD with some developing diabetes at 4 weeks; by 12 weeks, 46.2% of transgenic mice homozygous for H2^g7 develop diabetes compared to no non-transgenic H2^g7 homozygous littermates, or NOD controls which only start to exhibit diabetes at 12 weeks
  (MGI Ref ID J:26618)