Logo Logo
Help
Contact
Switch Language to German

Tocchetti, Arianna; Soppo, Charlotte Blanche Ekalle; Zani, Fabio; Bianchi, Fabrizio; Gagliani, Maria Cristina; Pozzi, Benedetta; Rozman, Jan; Elvert, Ralf; Ehrhardt, Nicole; Rathkolb, Birgit; Moerth, Corinna; Horsch, Marion; Fuchs, Helmut; Gailus-Durner, Valérie; Beckers, Johannes; Klingenspor, Martin; Wolf, Eckhard; Hrabé de Angelis, Martin; Scanziani, Eugenio; Tacchetti, Carlo; Scita, Giorgio; Di Fiore, Pier Paolo and Offenhäuser, Nina (2010): Loss of the actin remodeler Eps8 causes intestinal defects and improved metabolic status in mice.
In: PLOS ONE 5(3), e9468 [PDF, 2MB]

[thumbnail of fetchObject.pdf]
Preview
Download (2MB)

Abstract

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. 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. 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.

Actions (login required)

View Item View Item