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Following the subchronic administration of the non-selective monoamine reuptake inhibitor iprindole (2.5 mg/kg, ip, twice a day for 14 days) we found a pronounced accumulation of acetyl-CoA in the liver of rats. Furthermore, we determined a suppression of the fatty acid utilization rate in the liver resulting in a decrease of plasma triacylglycerol level in iprindole treated animals. Pretreatment with the antidepressant d-penicillamine (20 mg/kg, ip, twice a day for 14 days) did not affect the elevated acetyl-CoA level in the liver of iprindole-pretreated rats. However, d-penicillamine induced a considerable decrease of the fatty acid utilization rate in the liver resulting in a decrease of plasma triacylglycerol level. Similar effects were found after the pretreatment with imipramine (20 mg/kg, ip, twice a day for 14 days) whereas the monoamine synthesis inhibitor clorgyline (10 mg/kg, ip, twice a day for 14 days) was without effect. In contrast, carnitine (200 mg/kg, ip, twice a day for 14 days) which is involved in the control of fatty acid oxidation, induced a considerable increase of the acetyl-CoA level in the liver and a decrease of the fatty acid utilization rate. The carnitine antagonist trimethoxybenzoic acid (10 mg/kg, ip, twice a day for 14 days) partly mimicked the effect of carnitine, whereas the monoamine synthesis inhibitor florinef (10 mg/kg, ip, twice a day for 14 days) suppressed the increase of acetyl-CoA level caused by carnitine. In addition, carnitine partly reversed the effect of d-penicillamine and imipramine on hepatic fatty acid utilization. In
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