Abstract
In order to elucidate the factors which affect oxidation of fatty acid and the mechanism of the regulating system in fatty acid oxidation, we studied oxidation of 14C-palmitate into 14CO2 in isolated rat liver mitochondria under various conditions, especially in connection with the effect of insulin in vitro. Since the report was made on the increase in oxidation of long chain fatty acids by diabetic rats or by liver slices obtained from diabetic rats, insulin appears to have some action on the oxidation of fatty acid besides its effect on the release of fatty acid from adipose tissue.
It is elucidated in this report that insulin stimulated oxidation of palmitate into carbon dioxide 2-fold in intact rat liver mitochondria at the concentration of 10mU/ml which is physiologically observed in pancreatic vein after glucose administration. As the results indicated that insulin enhanced the oxidation of palmitic acid but neither that of acetic acid nor that of pyruvic acid in mitochondria, it is suggested that insulin stimulated the β-oxidation but not citric-acid cycle oxidation.
This stimulative effect of insulin was not observed in sonicated mitochondria. Thus, intactness of mitochondria is assumed to be essential for the effect. As it is shown that insulin binds with mitochondria, the former is assumed to affect the whole structure that favours β-oxidation of palmitate.
It is well known that albumin, too, stimulates not only the oxidation of palmitate, but also that of acetate or pyruvate. However, effective concentration of insulin was found to be different from that of albumin. In the region where albumin effect was the highest, insulin was further stimulative to palmitate oxidation. Also, in case of sonicated mitochondria, palmitate oxidation was lowered by albumin addition, but no effect was observed by insulin addition. So it is highly probable that the mechanism of insulin effect differs from that of albumin.
It was also found that this insulin effect was not substituted by a sulfhydryl reagent such as reduced or oxidized glutathione.
