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Experimental study reveals enhanced glycolytic capacity and hypoxia resistance in fetal compared to newborn rat hearts, indicating developmental maturation of cardiac energy metabolism.
Glycolysis was assessed in the rat heart during the perinatal period: in the fetus of 16.5 days postcoitum (dpc) and 21.5 dpc (term = 22 dpc) and in the newborn of 1 day postpartum (dpp) and 7 dpp. Glucose uptake, lactate production and glucose incorporation into glycogen were much higher in the fetal than in the newborn heart. Measurements were made of tissue contents of high energy phosphate compounds, lactate and hexose phosphates. Unchanged contents of glucose-6-phosphate and fructose-6-phosphate during hypoxia in spite of an increased flux through the enzyme phosphofructokinase (PFK) suggest that PFK has a regulatory role in the glycolysis as early as 16.5 dpc. The isolated fetal heart was more resistant to hypoxia than the newborn heart: glucose uptake and lactate production were much higher and high energy phosphate compounds and glycogen were better maintained in the fetal heart.
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Hoerter et al. (2009) studied this question.
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