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Figure 1 Changes in energy balance and fatty acid oxidation in the newborn heart. Dominant pathways are indicated by darker typeface, and bold arrows; those indicated in gray are diminished. The inner mitochondrial membrane has been omitted for clarity. ACC = acetyl CoA carboxylase; AMP = adenosine monophosphate; AMPK = 5'-AMP–activated protein kinase; ATP = adenosine triphosphate; CAT = carnitine acyl transferase; CoA = coenzyme A; CoASH = uncombined CoA; CPT 1 = carnitine palmitoyl transferase-1; Pi = inorganic phosphate; TCA = tricarboxylic acid. After birth, a fall in plasma insulin (which is an inhibitor of AMPK expression) levels, together with a decrease in available glucose and lactate substrate lead to a rise in AMPK activity. 5'-Adenosine monophosphate–activated protein kinase phosphorylates and inactivates ACC, resulting in a decrease in malonyl CoA production. Malonyl CoA in turn has a key role in inhibiting the activity of CPT 1, the rate limiting translocating protein which allows acylated long chain fatty acids to enter the mitochondrion. Thus the heart is prepared to utilize fatty acids in the postnatal period, as the level of malonyl CoA, the inhibitor effect of CPT 1, is greatly reduced. With the onset of suckling, a pronounced rise in plasma fatty acid levels, together with these low levels of malonyl CoA, facilitate the influx of fatty acyl CoA into the mitochondrion, and an increase in beta-oxidation occurs. Glycolysis and lactate oxidation, both important pathways in fetal life, decline in their relative contribution as energy sources in the newborn heart.
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