Abstract
In the laboratory mouse, there are three spontaneous mutations and one gene knockout that induce primary deficits in endocrine signaling and prolong life. Increased life expectancy appears to be due to delayed aging in at least three of these four mutants. Ames dwarf (Prop1df) and Snell dwarf (Pitl dw) mice have primary deficiency of growth hormone (GH), prolactin and thyrotropin, little (GHRHRlit) mice have GH releasing hormone resistance, and GHR-KO mice are GH resistant. Reduced GH secretion or action leads, in each case, to the expected precipitous decline in peripheral levels of insulin-like growth factor-1 (IGF-1), the key mediator of GH actions. The role of reduced IGF-1 signaling in mediating the effects of these four “longevity genes” in the mouse is consistent with the findings in Caenorhabditis elegans and Drosophila melanogaster. However, the formal proof of a cause-effect relationship between reduced IGF-1 levels and delayed aging remains to be obtained, and the mechanisms of IGF-1 action on aging remain to be identified.
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