A1 Journal article (refereed)
Developmental plasticity of mitochondrial aerobic metabolism, growth and survival by prenatal glucocorticoids and thyroid hormones : an experimental test in wild great tits (2022)


Cossin-Sevrin, N., Hsu, B.-Y., Marciau, C., Viblanc, V. A., Ruuskanen, S., & Stier, A. (2022). Developmental plasticity of mitochondrial aerobic metabolism, growth and survival by prenatal glucocorticoids and thyroid hormones : an experimental test in wild great tits. Journal of Experimental Biology, 225(9), Article jeb243414. https://doi.org/10.1242/jeb.243414


JYU authors or editors


Publication details

All authors or editorsCossin-Sevrin, Nina; Hsu, Bin-Yan; Marciau, Coline; Viblanc, Vincent A.; Ruuskanen, Suvi; Stier, Antoine

Journal or seriesJournal of Experimental Biology

ISSN0022-0949

eISSN1477-9145

Publication year2022

Publication date14/04/2022

Volume225

Issue number9

Article numberjeb243414

PublisherThe Company of Biologists

Publication countryUnited Kingdom

Publication languageEnglish

DOIhttps://doi.org/10.1242/jeb.243414

Publication open accessNot open

Publication channel open access

Publication is parallel published (JYX)https://jyx.jyu.fi/handle/123456789/83383


Abstract

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 hormones supplementation did not affect offspring growth or mitochondrial metabolism. Recapture probabilities as juveniles or adults were not significantly affected by prenatal hormonal treatments. 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.


Keywordsmetabolismcell respirationhormonal factorscorticosteronedevelopmental biologycell physiologybirdsgreat tit

Free keywordscellular metabolism; corticosterone; prenatal programming; avian development; thyroid hormones; Parus major


Contributing organizations


Ministry reportingYes

Reporting Year2022

JUFO rating2


Last updated on 2024-03-04 at 17:15