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Perinatal changes in glycolytic function in response to hypoxia in the incubated or perfused rat heart
Insights
The fetal rat heart exhibits higher glycolytic activity and greater resistance to hypoxia compared to the newborn heart, indicating a crucial regulatory role for phosphofructokinase (PFK) in perinatal cardiac glycolysis.
Area of Science:
- Cardiovascular Physiology
- Perinatal Metabolism
- Biochemistry
Background:
- Cardiac metabolism undergoes significant shifts during the perinatal period, transitioning from fetal to neonatal life.
- Understanding glycolysis regulation is crucial for comprehending cardiac adaptation to oxygen availability.
- The perinatal heart's metabolic flexibility impacts its resilience to hypoxic stress.
Purpose of the Study:
- To investigate the developmental changes in cardiac glycolysis during the perinatal period in rats.
- To assess the role of phosphofructokinase (PFK) in regulating fetal cardiac glycolysis.
- To compare the hypoxic tolerance of fetal and newborn rat hearts.
Main Methods:
- Assessed glycolysis by measuring glucose uptake and lactate production in fetal (16.5 and 21.5 days postcoitum) and newborn (1 and 7 days postpartum) rat hearts.
- Quantified tissue levels of high-energy phosphate compounds, lactate, and hexose phosphates.
- Evaluated the impact of hypoxia on glycolytic flux and enzyme activity, particularly phosphofructokinase (PFK).
Main Results:
- Fetal hearts showed significantly higher glucose uptake, lactate production, and glucose incorporation into glycogen compared to newborn hearts.
- Despite increased flux through phosphofructokinase (PFK) during hypoxia, glucose-6-phosphate and fructose-6-phosphate levels remained stable, suggesting PFK's regulatory role.
- Isolated fetal hearts demonstrated greater resistance to hypoxia, maintaining higher glucose uptake, lactate production, and better preservation of high-energy phosphates and glycogen.
Conclusions:
- Cardiac glycolysis is more active in the fetal period, with phosphofructokinase (PFK) playing a key regulatory role as early as 16.5 days postcoitum.
- The fetal heart possesses a more robust metabolic system, conferring enhanced resistance to hypoxic conditions compared to the neonatal heart.
- These findings highlight critical metabolic adaptations in the perinatal heart that support its function and survival during development and oxygen challenges.
Abstract:
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.