Pichaud 2013 J Exp Biol: Difference between revisions
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|abstract=Reproduction imposes significant costs and is characterized by an increased energy demand. As a consequence, individuals adjust their cellular structure and function in response to this physiological constraint. Because mitochondria are central to energy production, changes in their functional properties are likely to occur during reproduction. Such changes could cause adjustments in reactive oxygen species (ROS) production and consequently in oxidative stress levels. In this study, we investigated several mechanisms involved in energy production, including mitochondrial respiration at different steps of the electron transport system (ET-pathway) and related the results to citrate synthase activity in the liver of non-reproductive and reproductive (two and eight pups) female house mice at peak lactation. Whereas we did not find differences between females having different litter sizes, liver mitochondria of reproductive females showed lower ET activity and an increase in mitochondrial density when compared with the non-reproductive females. Although it is possible that these changes were due to combined processes involved in reproduction and not to the relative investment in lactation, we propose that the mitochondrial adjustment in liver might help to spare substrates and therefore energy for milk production in the mammary gland. Moreover, our results suggest that these changes lead to an increase in ROS production that subsequently upregulates antioxidant defence activity and decreases oxidative stress. | |abstract=Reproduction imposes significant costs and is characterized by an increased energy demand. As a consequence, individuals adjust their cellular structure and function in response to this physiological constraint. Because mitochondria are central to energy production, changes in their functional properties are likely to occur during reproduction. Such changes could cause adjustments in reactive oxygen species (ROS) production and consequently in oxidative stress levels. In this study, we investigated several mechanisms involved in energy production, including mitochondrial respiration at different steps of the electron transport system (ET-pathway) and related the results to citrate synthase activity in the liver of non-reproductive and reproductive (two and eight pups) female house mice at peak lactation. Whereas we did not find differences between females having different litter sizes, liver mitochondria of reproductive females showed lower ET activity and an increase in mitochondrial density when compared with the non-reproductive females. Although it is possible that these changes were due to combined processes involved in reproduction and not to the relative investment in lactation, we propose that the mitochondrial adjustment in liver might help to spare substrates and therefore energy for milk production in the mammary gland. Moreover, our results suggest that these changes lead to an increase in ROS production that subsequently upregulates antioxidant defence activity and decreases oxidative stress. | ||
|keywords=Citrate synthase, Liver, Metabolism, Mitochondrial respiration, Reproduction | |keywords=Citrate synthase, Liver, Metabolism, Mitochondrial respiration, Reproduction | ||
|mipnetlab=AU Sydney Ballard JW, CA Rimouski Blier PU | |mipnetlab=AU Sydney Ballard JW, CA Rimouski Blier PU, CA Moncton Pichaud N | ||
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{{Labeling | {{Labeling | ||
Latest revision as of 11:04, 23 June 2022
| Has title::Pichaud N, Garratt M, Ballard JWO, Brooks RC (2013) Physiological adaptations to reproduction II. Mitochondrial adjustments in livers of lactating mice. J Exp Biol 216:2889-95. |
» [[Has info::PMID: 23619407 Open Access]]
Was written by::Pichaud N, Was written by::Garratt M, Was written by::Ballard JWO, Was written by::Brooks RC (Was published in year::2013) Was published in journal::J Exp Biol
Abstract: [[has abstract::Reproduction imposes significant costs and is characterized by an increased energy demand. As a consequence, individuals adjust their cellular structure and function in response to this physiological constraint. Because mitochondria are central to energy production, changes in their functional properties are likely to occur during reproduction. Such changes could cause adjustments in reactive oxygen species (ROS) production and consequently in oxidative stress levels. In this study, we investigated several mechanisms involved in energy production, including mitochondrial respiration at different steps of the electron transport system (ET-pathway) and related the results to citrate synthase activity in the liver of non-reproductive and reproductive (two and eight pups) female house mice at peak lactation. Whereas we did not find differences between females having different litter sizes, liver mitochondria of reproductive females showed lower ET activity and an increase in mitochondrial density when compared with the non-reproductive females. Although it is possible that these changes were due to combined processes involved in reproduction and not to the relative investment in lactation, we propose that the mitochondrial adjustment in liver might help to spare substrates and therefore energy for milk production in the mammary gland. Moreover, our results suggest that these changes lead to an increase in ROS production that subsequently upregulates antioxidant defence activity and decreases oxidative stress.]] • Keywords: has publicationkeywords::Citrate synthase, has publicationkeywords::Liver, has publicationkeywords::Metabolism, has publicationkeywords::Mitochondrial respiration, has publicationkeywords::Reproduction
• O2k-Network Lab: Was published by MiPNetLab::AU Sydney Ballard JW, Was published by MiPNetLab::CA Rimouski Blier PU, Was published by MiPNetLab::CA Moncton Pichaud N
Labels: MiParea: MiP area::Respiration, MiP area::mt-Biogenesis;mt-density
Organism: Organism::Mouse
Tissue;cell: tissue and cell::Liver
Preparation: Preparation::Permeabilized tissue
Coupling state: Coupling states::LEAK, Coupling states::OXPHOS, Coupling states::ET
Pathway: Pathways::N, Pathways::S, Pathways::NS, Pathways::ROX
HRR: Instrument and method::Oxygraph-2k
