Abstract
According to Verkade1), the role of ω-oxidation was to make bilateral β-oxidation possible, which was more efficient than unilateral β-oxidation discovered by Knoop. We found that ω-oxidation was enhanced in liver preparations from starved and diabetic rats2). It is known that in starved or diabetic rats, utilization of glucose decreases along with increased utilization of fatty acids and, subsequently, formation of ketone bodies is increased in the liver. On β-oxidation, the last four carbon atoms of fatty acids become acetoacetyl-CoA, while those of dicarboxylic acids become succinyl-CoA. The latter is a member of TCA cycle and can be used for oxidation of acetyl-CoA and for gluconeogenesis in the liver of starved or diabetic rats.
So we examined the effect of dicarboxylic acid administration on ketone body concentration in the blood of these rats. As shown in TABLE I, administration of stearic acid, palmitic acid or capric acid to starved rats did not decrease the concentration of ketone bodies in blood, while administration of 1, 18-octadecadioic acid, 1, 16-hexadecadioic acid or sebacic acid did. In addition, we found that 14C-incorporation from dicarboxylic acid to glucose in blood was much more remarkable than that from monocarboxylic acid to glucose(TABLE II). These results suggest that the physiological significance of ω-oxidation may be to produce succinyl-CoA from fatty acids in mitochondria. From the experimental results shown in TABLE II, it was calculated that about 16 % of palmitic acids injected to starved or diabetic rats were subjected to ω-oxidation and further metabolized by β-oxidation.
