NameInsr
OrganismMus musculus
Aging PhenotypeLife-span extension
Allele TypeDeletion
StrainUnknown
DescriptionAdipocyte-specific disruption of the insulin receptor results in a 15-18% increase in mean, median, and maximum life-span (Bluher et al., 2003). Life-span extension is observed in both male and female fat-specific insulin receptor knock-out (FIRKO) animals.
Gene FunctionInsulin receptor
Other PhenotypesFIRKO mice consume the same amount of food on a per animal basis as control mice, but have 15-25% lower body mass and 50-70% reduced fat mass (Bluher et al., 2003).

Mutation of the insulin receptor extends life span up to 85% in female flies (Tatar et al., 2001). In mice, disruption of InsR in all tissues results in neo-natal lethality (Joshi et al., 1996).

HomologsC.e. daf-2
D.m. InR, sev
R.n. Ig1r, Insr
M.m. Ig1r
H.s. IGF1R, INSR
Primary ReferenceBluher, M., Kahn, B. B., and Kahn, R. C. (2003). Extended longevity in mice lacking the insulin receptor in adipose tissue. Science 299, 572-74.
Other ReferencesJoshi, R. L., Lamothe, B., Cordonnier, N., Mesbah, K., Monthioux, E., Jami, J., and Bucchini, D. (1996). Targeted disruption of the insulin receptor gene in the mouse results in neonatal lethality. Embo J 15, 1542-7. [Abstract]
Tatar, M., Kopelman, A., Epstein, D., Tu, M. P., Yin, C. M., and Garofalo, R. S. (2001). A mutant Drosophila insulin receptor homolog that extends life-span and impairs neuroendocrine function. Science 292, 107-10. [Abstract]
Relevant LinksLocusLink: http://www.ncbi.nih.gov/LocusLink/LocRpt.cgi?l=16337
Keywordsinsulin, signalling, fat, obesity, mouse, metabolism, glucose