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Extended Longevity in Mice Lacking the Insulin Receptor in Adipose Tissue
Abstract
Caloric restriction has been shown to increase longevity in organisms ranging from yeast to mammals. In some organisms, this has been associated with a decreased fat mass and alterations in insulin/insulin-like growth factor 1 (IGF-1) pathways. To further explore these associations with enhanced longevity, we studied mice with a fat-specific insulin receptor knockout (FIRKO). These animals have reduced fat mass and are protected against age-related obesity and its subsequent metabolic abnormalities, although their food intake is normal. Both male and female FIRKO mice were found to have an increase in mean life-span of ∼134 days (18%), with parallel increases in median and maximum life-spans. Thus, a reduction of fat mass without caloric restriction can be associated with increased longevity in mice, possibly through effects on insulin signaling.
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“Studies with genetically modified mice, as well as by means of ectopic treatments, have proved that it is possible to ameliorate various age-related parameters (the so-called ‘health-span’), which is often accompanied by an increase of life-span (Bluher et al, 2003; Conboy et al, 2005; Flurkey et al, 2001; Harrison et al, 2009; Holzenberger et al, 2003; Tomas-Loba et al, 2008).”
From Telomerase gene therapy in adult and old mice delays aging and increases longevity without increasing cancer (2012) · cites this paper as Bluher et al, 2003
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“pose as a determinant of longevity and are consistent with the FIRKO mice in which insulin receptor deletion in fat decreased fat mass and caused increased longevity (Bluher et al., 2003; Kloting & Bluher, 2005).”
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Metadata
- Authors
- Blüher, M., Kahn, B. B., & Kahn, C. R.
- Venue
- Science
- Published
- 2003-01-24
- Volume
- 299
- Issue
- 5606
- Pages
- 572-574
- ISSN
- 0036-8075
- 1095-9203
- Cited by
- 1,155
- References
- 2
- Language
- en
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