Conséquences d’une restriction de croissance intra-utérine et du sexe biologique sur le métabolisme des acides gras dans les cardiomyocytes de rats foetaux
It is widely accepted that an adverse fetal environment predisposes to chronic diseases that occur in adulthood. In our laboratory, it has been shown that a decrease in placental perfusion induced blood flow redistribution to the heart in fetus as well as an intrauterine growth restriction. Furthermore, remodeling and decreased contractility of cardiomyocytes were observed in adult offspring females. In perinatal period, the use of fatty acids as an energy substrate becomes more important than glucose in cardiomyocytes. Whereas a mechanism is in place in utero, we proposed the hypothesis that the transfer from the use of glucose as fuel towards fatty acids occurs earlier in intrauterine growth restriction fetuses. The objective of this study is to measure, in fetal hearts, the components of fatty acid metabolism, the main carrier of fatty acids, carnitine palmitoyltransférase‒1α, and its associated proteins namely acyl‒coenzymeA synthase‒1 and voltage‒dependant anion channel 1. We will measure the cytochrome c oxidase activity and the number of mitochondria. Influence of sex and fetal condition (intrauterine growth restriction vs control) will be compared. We observed that protein expression of carnitine palmitoyltranferase-1α and acyl-coenzyme A synthetase long-chain 1 is significantly increased, but not that of the voltage-dependant anion channel 1, in hearts of female fetus IUGR. The number and the activity of mitochondria are similar in all the groups. These results suggest that fetal condition and sex alter the quantity of the acid transporter carnitine palmitoyltranferase-1α has at the translation level without affecting the activity of the cytochrome c oxidase and the number of mitochondria.
Low-sodium diet Pregnancy Mitochondria Carnitine palmitoyltransferase-1-alpha