Extra-mitochondrial conversion of Acyl Carnitine to Acyl CoA
The introduction to Ann N Y Acad Sci. (2004) 1033:17–29 lists the various carnitine acyltransferases and mentions CPT-1a, CPT-1b, CPT-1c (tissue specific) but states there is only a single CPT-2 in humans. It does not appear that there is any other variant, so extra-mitochondrial conversion of acyl carnitine to acyl CoA would require a post-translational variant of CPT-2, or CPT-1 working in the reverse direction.
The discussion of carnitine metabolism in Berg et al., Section 22, implies the reaction is near equilibrium. Hence, if the concentrations of substrate and product were appropriate it would be thermodynamically possible for CPT-1 to operate in the reverse direction.
Thermodynamically possible does not necessarily mean enzymically possible. I am not familiar with kinetic studies on CPT-1 and CPT-2, but imagine that CPT-1 has a higher affinity for acyl CoA and carnitine than for the product acyl carnitine, and that the reverse situation holds for CPT-2. I imagine that the ability of CPT-1 (or one particular isoform) to catalyse the reverse reaction in physiological circumstances would depend on its Km for acyl carnitine and the concentration of the latter. It might be worth seeing what kinetic analysis has been done.
The ‘appropriate’ situation for (2) might be if something were preventing utilization of acyl carnitine in the mitochondria of ‘target’ cells.
If you work in this area you will know better than me that there are various clinical conditions and sub-clinical conditions (e.g. obesity) that result in abnormal utilization of acyl carnitine. Could the abnormal instances you observe be for such individuals?