| Official Name |
FVB(Cg)-Tg(Ins2-CALM1)26Ove Tg(Cryaa-TAg)1Ove/PneJ |
| Description |
Transgenic mice contain a construct in which a chicken
calmodulin minigene (CALM1) is driven by the rat insulin II
promoter (Ins2). In addition, these mice express a truncated
SV40 T antigen (TAg) controlled by a lens specific alpha A
crystallin (Cryaa) promoter. The transgenes have been shown
to co-segregate. Publications show that FVB-Ove26 transgenic
mice are viable, display small eyes with cataracts and are
hyperglycemic within 24 hours of age. S1 Nuclease protection
assays indicate expression of calmodulin in the pancreas of
40-60 day old transgenic mice. Immunofluorescence analysis
indicates increased levels of camodulin only in pancreatic
beta cells. Digital image scanning indicated the
concentration of camodulin in transgenic beta cells is
5-fold higher than in wild type controls. Pancreatic insulin
was 28% of control levels by 15 days of age. Insulin mRNA
levels were also reduced in the transgenic animals.
Transgenic mice experience hypoalbuminemia, elevated blood
pressure, impaired cardiomyocytes and late stage diabetic
nephropathy (Zheng et al. 2004). Although transgenic mice
are hyperglycemic within 24 hours of age, they are able to
survive over a year without insulin treatment. Phenotyping
of this stock at The Jackson Laboratory confirmed the
published values for diabetes-related phenotypes, but failed
to confirm diabetic nephropathy at the 6 month study
endpoint. Similarly, glomerular filtration rates were not
decreased versus non-transgenic controls at a 9-month
sampling.
|