endocrine/exocrine glands
• H2g7 homozygous transgenic mice show islet disruption with lymphocytic (T and B cell) infiltration, similar to diabetic NOD controls
• N2 mice after a subsequent backcross to NOD show islet disruption with lymphocytic infiltration as early as 4 weeks while non-transgenic H2g7 homozygous or heterozygous littermates show varying degrees of insulitis by ~6 weeks
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immune system
• H2g7 homozygous transgenic mice show islet disruption with lymphocytic (T and B cell) infiltration, similar to diabetic NOD controls
• N2 mice after a subsequent backcross to NOD show islet disruption with lymphocytic infiltration as early as 4 weeks while non-transgenic H2g7 homozygous or heterozygous littermates show varying degrees of insulitis by ~6 weeks
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• 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
• 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 H2g7 develop diabetes compared to no non-transgenic H2g7 homozygous littermates, or NOD controls which only start to exhibit diabetes at 12 weeks
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renal/urinary system
homeostasis/metabolism
• transgenic mice exhibit blood glucose in excess of 13.9 mmol (250 mg/dl)
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
type 1 diabetes mellitus | DOID:9744 |
OMIM:222100 |
J:26618 |