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Tocchetti, A.* ; Soppo, C.B.E.* ; Zani, F.* ; Bianchi, F.* ; Gagliani, M.C.* ; Pozzi, B.* ; Rozman, J. ; Elvert, R. ; Ehrhardt, N. ; Rathkolb, B. ; Mörth, C. ; Horsch, M. ; Fuchs, H. ; Gailus-Durner, V. ; Beckers, J. ; Klingenspor, M.* ; Wolf, E.* ; Hrabě de Angelis, M. ; Scanziani, E.* ; Tacchetti, C.* ; Scita, G.* ; di Fiore, P.P.* ; Offenhäuser, N.*

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

PLoS ONE 5:e9468 (2010)
Verlagsversion Volltext DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Mechanisms linking obesity; Adipose-tissue; Microarray data; Cardiovascular-Disease; Calorie restriction; Dietary restriction; Body-temperature; Insulin-receptor; Brush-border; Life-span
ISSN (print) / ISBN 1932-6203
Zeitschrift PLoS ONE
Quellenangaben Band: 5, Heft: 3, Seiten: , Artikelnummer: e9468 Supplement: ,
Verlag Public Library of Science (PLoS)
Verlagsort Lawrence, Kan.
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Experimental Genetics (IEG)