McGarry & Foster5'6 established that octanoate, a medium-chain fatty acid, was oxidized independently of metabolic state, whereas, the oxidation rate of long-chain fatty acids was a function of metabolic status (e.g. fed, fasted, diabetic). Since octanoate bypasses CPT I these authors concluded that this enzyme was a prime candidate for control of oxidative fluxes, including ketogenesis, from long-chain fatty acids. This conclusion was supported by apparent correlations in changes of substrate supply, hormones and in development with parallel changes in ketogenesis and the activity and expression of CPT I.
In the fetus, the rates of hepatic P-oxidation and ketogenesis are low. However, following birth, the capacity of these metabolic pathways increases and results in a significant rise in the concentration of ketone bodies (increasing from 0.2 mM in the rat at birth to 2mM 24h later7). This physiological hyperketonaemia is maintained throughout the suckling period.8 The changes are similar to those in CPT I, where the activity, protein concentration and level of mRNA encoding CPT I are low in the fetus and increase 5fold during the first day of extrauterine life. The enzyme activity and gene expression remain high during the entire suckling period.910 Furthermore, the inhibitory effect of malonyl-CoA (an intermediate compound in the biosynthetic pathway of fatty acids and a potent physiological reversible inhibitor of CPT I11) is decreased in the first 24h following birth. However, these changes are not seen in liver CPT II and the mRNA, immunoreactive protein and activity are not influenced by nutritional and hormonal changes in the postnatal period. CPT II activity is already high in fetal rat liver and does not change after birth. Thumelin et al.9 cite their findings as evidence that CPT I has the potential to control hepatic long-chain fatty acid oxidation.
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