CoA and fatty acyl-CoA derivatives mobilize calcium from a liver reticular pool

The effect of CoA and fatty acyl-CoA esters on Ca²⁺ fluxes has been studied in isolated liver microsomes and in digitonin-permeabilized hepatocytes. When microsomes were loaded with increasing concentrations of Ca²⁺ (6-29 nmol/mg of protein), the extent to which CoA and palmitoyl-CoA released Ca²⁺ increased. At 23 nmol of Ca²⁺/mg of protein, half-maximal [CoA] and [palmitoyl-CoA] were 35 and 50 μM respectively. Under conditions of minimal Ca²⁺ loading, net release of Ca²⁺ was absent, but Ca²⁺ translocation from a CoA-sensitive to a CoA-insensitive pool took place. The effect of CoA required the presence of fatty acids, probably to form fatty acyl esters. In permeabilized hepatocytes, the pool(s) mobilized by CoA (or by palmitoyl-CoA) appeared to be different from that mobilized by Ins(1,4,S)P₃.