Studies on metabolic abnormalities of the rat liver in fatty liver cirrhosis induced by choline-deficient diet

Part II. Fatty acid oxidation in isolated liver mitochondria

Abstract

The oxidation of long-chain fatty acids is an essential function of the mitochondrion. To examine the metabolic abnormalities of liver mitochondria during development of choline-deficient fatty liver cirrhosis was investigated the oxidation of palmitic and oleic acid in the presence of isolated liver mitochondria during the stages of normal, hypertrophic fatty liver and hypertrophic nodular fatty cirrhosis in rats. The results were as follows:
1. At the stage of hypertrophic fatty liver, β-oxidation in the isolated mitochondria was normal.
2. At the stage of hypertrophic nodular cirrhosis, β-oxidation in the isolated mitochondria was impaired remarkably.
3. It was concluded that the metabolic abnormalities in the hypertrophic fatty liver were not so prominent, but the abnormalities were intense in cirrhotic livers. Long-standing impairment of lecithin synthesis in relation to cholinedeficiency was shown to induce a marked structural change in the mitochondria. Therefore, impairment of the electron transport system of the mitochondria leads to reduced β-oxidation. The overall change in metabolism is thought to be the cause of the transition to cirrhosis.
4. Rats fed a choline-deficient diet, partially supplemented by sucrose with xylitol, remained normal or showed atypical livers. Such rat liver mitochondria showed general restoration of the electron transport function, but β-oxidation was not restored.