| First Author | Tocchetti A | Year | 2010 |
| Journal | PLoS One | Volume | 5 |
| Issue | 3 | Pages | e9468 |
| PubMed ID | 20209148 | Mgi Jnum | J:158694 |
| Mgi Id | MGI:4439441 | Doi | 10.1371/journal.pone.0009468 |
| Citation | Tocchetti A, et al. (2010) Loss of the actin remodeler Eps8 causes intestinal defects and improved metabolic status in mice. PLoS One 5(3):e9468 |
| abstractText | BACKGROUND: In a variety of organisms, including mammals, caloric restriction improves metabolic status and lowers the incidence of chronic-degenerative diseases, ultimately leading to increased lifespan. METHODOLOGY/PRINCIPAL FINDINGS: Here we show that knockout mice for Eps8, a regulator of actin dynamics, display reduced body weight, partial resistance to age- or diet-induced obesity, and overall improved metabolic status. Alteration in the liver gene expression profile, in behavior and metabolism point to a calorie restriction-like phenotype in Eps8 knockout mice. Additionally, and consistent with a calorie restricted metabolism, Eps8 knockout mice show increased lifespan. The metabolic alterations in Eps8 knockout mice correlated with a significant reduction in intestinal fat absorption presumably caused by a 25% reduction in intestinal microvilli length. CONCLUSIONS/SIGNIFICANCE: Our findings implicate actin dynamics as a novel variable in the determination of longevity. Additionally, our observations suggest that subtle differences in energy balance can, over time, significantly affect bodyweight and metabolic status in mice. |
