Loss of the Actin Remodeler Eps8 Causes Intestinal Defects and Improved Metabolic Status in Mice

نویسندگان

  • Arianna Tocchetti
  • Charlotte Blanche Ekalle Soppo
  • Fabio Zani
  • Fabrizio Bianchi
  • Maria Cristina Gagliani
  • Benedetta Pozzi
  • Jan Rozman
  • Ralf Elvert
  • Nicole Ehrhardt
  • Birgit Rathkolb
  • Corinna Moerth
  • Marion Horsch
  • Helmut Fuchs
  • Valérie Gailus-Durner
  • Johannes Beckers
  • Martin Klingenspor
  • Eckhard Wolf
  • Martin Hrabé de Angelis
  • Eugenio Scanziani
  • Carlo Tacchetti
  • Giorgio Scita
  • Pier Paolo Di Fiore
  • Nina Offenhäuser
چکیده

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.

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عنوان ژورنال:

دوره 5  شماره 

صفحات  -

تاریخ انتشار 2010