Rat liver peroxisomes, II. Stimulation of peroxisomal fatty-acid beta-oxidation by thyroid hormones.

From liver homogenates of control and thyroxine-treated rats the light mitochondrial fractions were prepared by differential centrifugation. Mitochondria and peroxisomes of these fractions were further separated by isopycnic sucrose density gradient centrifugation. Analysis of the activities of the peroxisomal marker enzymes catalase and urate oxidase throughout the gradient exhibited completely corresponding distributions with that of peroxisomal palmitoyl-CoA oxidation. Thyroxine treatment did not change the proportion of mitochondria and peroxisomes present in the differential fractions of the homogenate. Consequently, the activities of peroxisomal beta-oxidation in the light mitochondrial fractions of control and thyroxine-treated animals were directly comparable with each other. A 2.5-fold increase in peroxisomal palmitoyl-CoA oxidation raising the activity from 0.089 to 0.220 U/g as estimated in the light mitochondrial fractions was found following treatment of male rats with daily doses of 25 micrograms L-thyroxine (s.c.) over a period of 10 days. Total hepatic peroxisomal fatty-acyl-CoA oxidation was calculated based on estimations in the light mitochondrial fractions. The difficulties encountered herein are discussed. The present result replenishes the broad spectrum of cellular effects exerted by thyroid hormones and indicates that both the mitochondrial and the peroxisomal system contribute to the well known hormone effects such as increase in fatty-acid oxidation, O2 consumption and heat production.