Carnitine Stimulated Transport of the Intermediates of Long Chain Fatty Acid β Oxidation in Liver and Heart Mitochondria. ∗

Abstract

Summary

The effects of carnitine and BSA on the oxidation to CO₂ and conversion to acetoacetate of [1-¹⁴C] palmitate, [1-¹⁴C] traws-2-hexadecenoate, [1-¹⁴C] DL-3-hydroxyhexadecanoate and [1-¹⁴C] 3-ketohexadecanoate were examined in liver mitochondria from normal and diabetic rats and in heart muscle mitochondria from normal animals. Carnitine stimulated the oxidation of all substrates except the 3-keto intermediate by normal liver and heart muscle mitochondria; BSA increased basal oxidation and augmented the carnitine effect on the oxidation of these same compounds in both tissues. Carnitine increased the conversion of palmitate and the unsaturated and hydroxy derivatives to acetoacetate in liver mitochondria; BSA greatly increased both basal and carnitine-stimulated acetoacetate production; no acetoacetate accumulated under any conditions in heart mitochondria. Diabetes did not significantly influence the oxidation of, or the accumulation of acetoacetate from, any of the 4 substrates tested in liver mitochondria, nor was the effect of carnitine greater than normal in tissue obtained from diabetic rats.