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      Extending the lifespan of long-lived mice.

      Nature

      Animals, Dwarfism, genetics, Energy Intake, Female, Homeodomain Proteins, physiology, Longevity, Male, Mice, Mice, Mutant Strains, Transcription Factors

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          Most cited references 6

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          daf-2, an insulin receptor-like gene that regulates longevity and diapause in Caenorhabditis elegans.

          A C. elegans neurosecretory signaling system regulates whether animals enter the reproductive life cycle or arrest development at the long-lived dauer diapause stage. daf-2, a key gene in the genetic pathway that mediates this endocrine signaling, encodes an insulin receptor family member. Decreases in DAF-2 signaling induce metabolic and developmental changes, as in mammalian metabolic control by the insulin receptor. Decreased DAF-2 signaling also causes an increase in life-span. Life-span regulation by insulin-like metabolic control is analogous to mammalian longevity enhancement induced by caloric restriction, suggesting a general link between metabolism, diapause, and longevity.
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            Extension of life-span by loss of CHICO, a Drosophila insulin receptor substrate protein.

            The Drosophila melanogaster gene chico encodes an insulin receptor substrate that functions in an insulin/insulin-like growth factor (IGF) signaling pathway. In the nematode Caenorhabditis elegans, insulin/IGF signaling regulates adult longevity. We found that mutation of chico extends fruit fly median life-span by up to 48% in homozygotes and 36% in heterozygotes. Extension of life-span was not a result of impaired oogenesis in chico females, nor was it consistently correlated with increased stress resistance. The dwarf phenotype of chico homozygotes was also unnecessary for extension of life-span. The role of insulin/IGF signaling in regulating animal aging is therefore evolutionarily conserved.
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              Assessment of growth parameters and life span of GHR/BP gene-disrupted mice.

              GH has many biological roles, including promotion of growth. Most, if not all, of its roles are achieved through interaction with its receptor. We chose to study the effects of loss of GH signaling on growth and aging in a mouse model for Laron Syndrome (LS) in which the GHR/BP gene has been disrupted. We observed that mice homozygous for the disruption (-/-) were significantly smaller than normal wild-type (+/+) mice as well as mice heterozygous for the disruption, even at 1.5 yr of age. IGF-I levels were also significantly lower in the -/- mice and remained low as the mice aged. IGFBP-3 levels were severely reduced in the -/- mice, whereas IGFBP-1, -2, and -4 levels remained unchanged. Finally, the -/- mice lived significantly longer than +/+ and +/- mice. The latter result contradicts the anti-aging GH data and suggests the need for further analysis of GH and aging.
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                Author and article information

                Journal
                11719795
                10.1038/35106646

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