Mice producing reduced levels of insulin-like growth factor type 1 display an increase in maximum, but not mean, life span

Antonello Lorenzini, Adam B. Salmon, Chad Lerner, Claudio Torres, Yuji Ikeno, Susan Motch, Roger McCarter, Christian Sell

Producción científica: Articlerevisión exhaustiva

38 Citas (Scopus)

Resumen

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.

Idioma originalEnglish (US)
Páginas (desde-hasta)410-419
Número de páginas10
PublicaciónJournals of Gerontology - Series A Biological Sciences and Medical Sciences
Volumen69
N.º4
DOI
EstadoPublished - abr 1 2014

ASJC Scopus subject areas

  • General Medicine

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