Recent studies of positive IGF-1 influence on lifespan showed that it is highly involved into the regulation of individual's longevity and response to oxidative stress.
One more study just confirms recent results*.
Studies in invertebrates have led to the identification of a number of genes that regulate lifespan, some of which encode components of the insulin or insulin-like signalling pathways.
Examples include the related tyrosine kinase receptors InR (Drosophila melanogaster) and DAF-2 (Caenorhabditis elegans) that are homologues of the mammalian insulin-like growth factor type 1 receptor (IGF-1R).
To investigate whether IGF-1R also controls longevity in mammals, scientists have inactivated the IGF-1R gene in mice (Igf1r).
In this study heterozygous knockout mice were used, because null mutants are not viable, and it was concluded that Igf1r+/- mice lived on average 26% longer than their wild-type littermates (P < 0.02).
Female Igf1r+/- mice lived 33% longer than wild-type females (P < 0.001), whereas the equivalent male mice showed an increase in lifespan of 16%, which is not statistically significant.
Long-lived Igf1r+/- mice didn't develop dwarfism, their energy metabolism was normal, and their nutrient uptake, physical activity, fertility and reproduction were unaffected.
The Igf1r+/- mice displayed greater resistance to oxidative stress, a known determinant of ageing.
Such results indicated that the IGF-1 receptor may be a central regulator of mammalian lifespan.