Effect of prenatal glucocorticoids and thyroid hormones on developmental plasticity of mitochondrial aerobic metabolism, growth and survival: an experimental test in wild great tits.

Parus major Avian development Cellular metabolism Corticosterone Prenatal programming Thyroid hormones

Journal

The Journal of experimental biology
ISSN: 1477-9145
Titre abrégé: J Exp Biol
Pays: England
ID NLM: 0243705

Informations de publication

Date de publication:
01 05 2022
Historique:
received: 31 08 2021
accepted: 11 04 2022
pubmed: 15 4 2022
medline: 12 5 2022
entrez: 14 4 2022
Statut: ppublish

Résumé

Developmental plasticity is partly mediated by transgenerational effects, including those mediated by the maternal endocrine system. Glucocorticoid and thyroid hormones may play central roles in developmental programming through their action on metabolism and growth. However, the mechanisms by which they affect growth and development remain understudied. One hypothesis is that maternal hormones directly affect the production and availability of energy-carrying molecules (e.g. ATP) by their action on mitochondrial function. To test this hypothesis, we experimentally increased glucocorticoid and thyroid hormones in wild great tit eggs (Parus major) to investigate their impact on offspring mitochondrial aerobic metabolism (measured in blood cells), and subsequent growth and survival. We show that prenatal glucocorticoid supplementation affected offspring cellular aerobic metabolism by decreasing mitochondrial density, maximal mitochondrial respiration and oxidative phosphorylation, while increasing the proportion of the maximum capacity being used under endogenous conditions. Prenatal glucocorticoid supplementation only had mild effects on offspring body mass, size and condition during the rearing period, but led to a sex-specific (females only) decrease in body mass a few months after fledging. Contrary to our expectations, thyroid hormone supplementation did not affect offspring growth or mitochondrial metabolism. Recapture probability as juveniles or adults was not significantly affected by prenatal hormonal treatment. Our results demonstrate that prenatal glucocorticoids can affect post-natal mitochondrial density and aerobic metabolism. The weak effects on growth and apparent survival suggest that nestlings were mostly able to compensate for the transient decrease in mitochondrial aerobic metabolism induced by prenatal glucocorticoids.

Identifiants

pubmed: 35420125
pii: 275345
doi: 10.1242/jeb.243414
pmc: PMC10216743
pii:
doi:

Substances chimiques

Glucocorticoids 0
Thyroid Hormones 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Horizon 2020 Framework Programme
ID : 894963
Organisme : Academy of Finland
ID : 286278
Organisme : Turku Collegium for Science and Medicine
Organisme : Opetushallitus
Organisme : Maupertuis
Organisme : Ella and Georg Ehrnrooth Foundation
Organisme : Societas Pro Flora Fauna Fennica

Informations de copyright

© 2022. Published by The Company of Biologists Ltd.

Déclaration de conflit d'intérêts

Competing interests The authors declare no competing or financial interests.

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Auteurs

Nina Cossin-Sevrin (N)

Department of Biology, University of Turku, FI-20014 Turku, Finland.
Université de Strasbourg, Centre National de la Recherche Scientifique, Institut Pluridisciplinaire Hubert Curien, UMR 7178, 67087 Strasbourg, France.

Bin-Yan Hsu (BY)

Department of Biology, University of Turku, FI-20014 Turku, Finland.

Coline Marciau (C)

Department of Biology, University of Turku, FI-20014 Turku, Finland.
Institute for Marine and Antarctic Studies, University of Tasmania, Battery Point, TAS 7004, Australia.

Vincent A Viblanc (VA)

Université de Strasbourg, Centre National de la Recherche Scientifique, Institut Pluridisciplinaire Hubert Curien, UMR 7178, 67087 Strasbourg, France.

Suvi Ruuskanen (S)

Department of Biological and Environmental Sciences, University of Jyväskylä, FI-40014 Jyväskylä, Finland.

Antoine Stier (A)

Department of Biology, University of Turku, FI-20014 Turku, Finland.
Université Claude Bernard Lyon 1, CNRS, ENTPE, UMR 5023 LEHNA, F-69622 Villeurbanne, France.

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Classifications MeSH