One of the most studied areas of metabolism and its interaction with aging involves the activities of, and relationships between, IGF-1, insulin, growth hormone, and their cell surface receptors, all of which are among the mechanisms strongly influenced by calorie restriction. Genetic engineering to disable growth hormone or its receptor produces dwarf mice that live 60% longer, and IGF-1 can be similarly manipulated to produce a less exceptional life extension. It is worth noting that the equivalent growth hormone loss of function mutants in our species do not live 60% longer, though they may be modestly more resistant to age-related disease. Short-lived species have evolved a far greater plasticity of life span in response to calorie restriction or interventions that directly manipulate the related cellular mechanisms. Development of therapies based upon these findings seem unlikely to produce sufficiently sizable effects on human health to justify the investment, given the range of better alternatives on the table.
Diminished growth hormone (GH) and insulin/insulin-like growth factor-1 (IGF-1) signaling extends lifespan in many laboratory models. Likewise, several dwarf models, including Ames, Snell and growth hormone receptor knockout (GHRKO)
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