Mouse Genome Informatics
cx
    Ins2Akita/Ins2Akita
Itga1tm1Gdnr/Itga1tm1Gdnr

C.Cg-Ins2Akita Itga1tm1Gdnr
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
       
mortality/aging
• about 40% of mutants fail to thrive and have to be euthanized before 6 months of age

cardiovascular system
• mice show a a greater decrease in CD31 positive structures in the glomeruli than in single Ins2Akita homozygotes, indicating collapse of the glomerular tufts

growth/size/body
• decreased body weight at 4 and 6 months of age compared to wild-type mice or single Itgal1tm1Gdnr homozygotes

homeostasis/metabolism
• develop a similar level of hyperglycemia as in single Ins2Akita homozygotes
• 16-fold increase in albumin-to-creatine ratio at 4 months of age

renal/urinary system
• 16-fold increase in albumin-to-creatine ratio at 4 months of age
• glomerular basement membrane thickening is more severe than in single Ins2Akita homozygotes
• increase in glomerular collagen IV deposition at 6 months of age is more abundant than in single Ins2Akita homozygotes
• mice show a a greater decrease in CD31 positive structures in the glomeruli than in single Ins2Akita homozygotes, indicating collapse of the glomerular tufts
• excessive fibrillar collagen deposition in diffuse and nodular mesangial lesions
• increase in mesangial matrix expansion at 4 and 6 months of age is greater than in single Ins2Akita homozygotes
• diffuse and nodular mesangial sclerosis
• small increase in collagen I in the tubulointerstitial compartment of the kidney
• however tubulointerstitial fibrosis is not observed
• glomerular filtration rate is increased at 4 months of age to a similar level as in single Ins2Akita homozygotes
• by 6 months of age, glomerular filtration rate is decreased compared to controls, with an overall 50% decline compared to at 4 months

Mouse Models of Human Disease
OMIM IDRef(s)
Diabetes Mellitus, Insulin-Dependent; IDDM 222100 J:198186