Loss of the actin remodeler Eps8 causes intestinal defects and improved metabolic status in mice

PLoS One. 2010 Mar 2;5(3):e9468. doi: 10.1371/journal.pone.0009468.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Actins / metabolism*
  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / physiology*
  • Animals
  • Body Weight
  • Caco-2 Cells
  • Caloric Restriction
  • Cytoskeletal Proteins / genetics
  • Cytoskeletal Proteins / physiology*
  • Energy Metabolism
  • Female
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Humans
  • Intestinal Mucosa / metabolism*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Microvilli / metabolism

Substances

  • Actins
  • Adaptor Proteins, Signal Transducing
  • Cytoskeletal Proteins
  • Eps8 protein, mouse