Insulin-like growth factor 1 (IGF-1) is one of the better studied components of metabolic pathways and mechanisms linked to longevity. Despite the many researchers and numerous years of work involved metabolism is so complex that there is still a very long way to go yet before the research community can establish complete understanding of what is actually going on in long-lived mutant mice with different levels of IGF-1. The cost and very slow pace of progress in the face of this complexity is one of the reasons why trying to slow aging by altering metabolism is a terrible choice of strategy for human life extension - we should instead focus on what we do understand well, which is how to repair the low-level cellular damage that causes aging, and keep the metabolism we have already.
Here is an example of continuing work on IGF-1 in mice, a confirmation of extended life, which is the sort of thing that keeps the grant funds coming for further efforts to figure out what is going on under the hood:
Reduced signaling through the IGF type 1 (IGF-1) receptor increases life span in multiple invertebrate organisms. Studies on mammalian longevity suggest that reducing levels of IGF-1 may also increase life span. However, the data are conflicting and complicated by the physiology of the mammalian neuroendocrine system.
We have performed life-span analysis on mice homozygous for an insertion in the Igf1 gene. These mice produce reduced levels of IGF-1 and display a phenotype consistent with a significant decrease in IGF-1. Life-span analysis was carried out at three independent locations. Although the life-span data varied between sites, the maximum life span of the IGF-1-deficient mice was significantly increased and age-specific mortality rates were reduced in the IGF-1-deficient mice; however, mean life span did not differ except at one site, where mean life span was increased in female IGF-1-deficient animals. Early life mortality was noted in one cohort of IGF-1-deficient mice.
The results are consistent with a significant role for IGF-1 in the modulation of life span but contrast with the published life-span data for the hypopituitary Ames and Snell dwarf mice and growth hormone receptor null mice, indicating that a reduction in IGF-1 alone is insufficient to increase both mean and maximal life span in mice.