Abstract
Fetal programming of adult disease is an area of research that has gained considerable attention. Epidemiological studies suggest that adverse intrauterine environment in fetal life is associated with a higher incidence of hypertension and coronary disease. Several mechanisms could contribute to these diseases and be regulated in a tissue-specific manner. The Na+–K+-ATPase, a membrane-bound enzyme, maintains the Na+ and K+ gradients across the plasma membrane of animal cells and therefore provides a mechanism for cell function regulation. Furthermore, in an in vitro model of cardiac hypertrophy, a decrease in the activity of the tricarboxylic acid (TCA) cycle enzyme, aconitase, was observed. We have shown that in our model of fetal programming, these two enzymes were regulated differently in heart and kidney of adult females.
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Acknowledgments
We are grateful to Drs. Blandine Comte and James Armitage for their expert advice. This work was supported by grants from Fonds de la Recherche en Santé du Québec and Conseil de Recherches en Sciences Naturelles et Génie du Canada.
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© 2009 Humana Press, a part of Springer Science+Business Media, LLC
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Gaudet, R., Brochu, M. (2009). Renal and Cardiac Na+–K+-ATPase and Aconitase in a Rat Model of Fetal Programming. In: Vaillancourt, C., Lafond, J. (eds) Human Embryogenesis. Methods in Molecular Biology, vol 550. Humana Press. https://doi.org/10.1007/978-1-60327-009-0_14
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DOI: https://doi.org/10.1007/978-1-60327-009-0_14
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