| Description |
The congenic FVB-db strain differs from that previously
published on other genetic backgrounds in that it presents a
marked obesity/diabetes phenotype intermediate between the
severe uncompensated hyperglycemia observed in C57BLKS/J and
DBA2/J backgrounds and the mild, compensated syndrome
reported on the C57BL/6J and 129/J backgrounds. The
literature reports that obese FVB-db mice of both sexes show
long-term hyperglycemia primarily due to severe insulin
resistance. The hyperglycemia in the fed state persists
despite continued extreme hyperinsulinemia correlated with a
marked pancreatic cell hypertrophy and hyperplasia. These
phenotypes have been replicated in the stock at The Jackson
Laboratory. However, the diabetic nephropathy
(glomerulosclerosis) reported in the literature was not
evident in the stock imported to JAX at the age evaluated
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| Phenotype Description |
The phenotype of this congenic "FVB-db" strain varies from
that previously published on other genetic backgrounds.
Specifically, obese FVB-db mice show long-term hyperglycemia
that is primarily due to severe insulin resistance. The
hyperglycemia in the fed state persists despite escalating
insulin secretion and a massive increase in pancreatic
beta-cell mass. Obese FVB-db mice show evidence of mesangial
matrix expansion, a hallmark of diabetic nephropathy.
Whereas the original C57BLKS/J-db mice are hyperglycemic due
to the development of hypoinsulinemia and loss of beta-cell
mass, the hyperglycemia of FVB-db appears to be due to
severe insulin resistance with continual increases in
insulin secretory capacity from beta-cell mass expansion. As
the phenotype varies by genetic background, these mutant
mice, along with db mutants on other genetic backgrounds
(see Stock No. 000642, 000697, 000699, 000700, and 000707),
may be useful for diabetes research, including the
dissection of genetic control of beta-cell responses to
hyperglycemia and insulin resistance/sensitivity.
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