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Lassi, M. ; Tomar, A. ; Comas-Armangue, G. ; Vogtmann, R.* ; Dijkstra, D.J.* ; Corujo, D.* ; Gerlini, R. ; Darr, J. ; Scheid, F. ; Rozman, J. ; Aguilar-Pimentel, J.A. ; Koren, O.* ; Buschbeck, M.* ; Fuchs, H. ; Marschall, S. ; Gailus-Durner, V. ; Hrabě de Angelis, M. ; Plösch, T.* ; Gellhaus, A.* ; Teperino, R.

Disruption of paternal circadian rhythm affects metabolic health in male offspring via nongerm cell factors.

Sci. Adv. 7:eabg6424 (2021)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Circadian rhythm synchronizes each body function with the environment and regulates physiology. Disruption of normal circadian rhythm alters organismal physiology and increases disease risk. Recent epidemiological data and studies in model organisms have shown that maternal circadian disruption is important for offspring health and adult phenotypes. Less is known about the role of paternal circadian rhythm for offspring health. Here, we disrupted circadian rhythm in male mice by night-restricted feeding and showed that paternal circadian disruption at conception is important for offspring feeding behavior, metabolic health, and oscillatory transcription. Mechanistically, our data suggest that the effect of paternal circadian disruption is not transferred to the offspring via the germ cells but initiated by corticosterone-based parental communication at conception and programmed during in utero development through a state of fetal growth restriction. These findings indicate paternal circadian health at conception as a newly identified determinant of offspring phenotypes.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Fetal-growth; Sex-differences; Glucocorticoids; Clocks; Mouse; Restriction; Obesity; Responses; Hormones; Stress
ISSN (print) / ISBN 2375-2548
e-ISSN 2375-2548
Zeitschrift Science Advances
Quellenangaben Band: 7, Heft: 22, Seiten: , Artikelnummer: eabg6424 Supplement: ,
Verlag American Association for the Advancement of Science (AAAS)
Verlagsort Washington, DC [u.a.]
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Experimental Genetics (IEG)
Förderungen German Center for Diabetes Research (DZD)
Fritz Thyssen Stiftung
Helmholtz Research Center Munich
Helmholtz Association
German Diabetes Research Center
FEDER/Ministerio de Ciencia e Innovacion-Agencia Estatal de Investigacion
Mercator Research Center Ruhr (MERCUR)
German Research Foundation (DFG)
Programm zur internen Forschungsforderung Essen (IFORES)
German Federal Ministry of Education and Research
German Diabetes Research Center (DZD NEXT grant)