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Metabolism of fatty acids and the levels of ketone bodies in the livers of pyridoxine-deficient rats.

Lipid metabolism was examined in rats fed a high-protein pyridoxine-deficient diet, and their livers were found to contain large amounts of lipids, mainly in the forms of triglycerides and cholesteryl ester. The contents of ketone bodies in the livers of pyridoxine-deficient and the control rats were similar. Their NAD+/NADH ratios, calculated from the amounts of ketone bodies, were also similar in pyridoxine-deficient and control groups when the animals were fed, but the ratio in pyridoxine-deficient rats was lower than that of control rats when the animals were starved. After injection of 14C-linoleic acid, the amounts of expired 14CO2 in pyridoxine-deficient and control rats were similar. The pattern of incorporations of 14C-linoleic acid into various lipid components of the livers were examined; incorporation into the phospho-lipid fraction was similar in control and deficient rats, but the incorporation into the triglyceride fraction was slower, and the incorporation into cholesterol was faster in deficient animals than in controls.

The bands of lipid on the plate were detected with iodine vapor and scrapped off. Free cholesterol, cholesteryl ester and triglyceride were extracted with chloro form-methanol (2:1, by val.), and cholesterol (free and ester) and triglyceride were measured by the method of ZAK (24) and a modification of the method of VAN HANDEL (25), respectively. Phospholipid was either measured directly in the crude lipid fraction as inorganic phosphate by a slightly modification of the method of HOELMAYER-FRIED (26), or it was extracted from the thin-layer chro matogram with chloroform-methanol-acetic acid-water (50:39:1:10, by vol.) (27). The recoveries of cholesterol, cholesteryl ester and triglyceride were over 95 %, and that of phospholipid was about 70%. The cholesteryl ester fraction was hydrolyzed by a modification of the method of FLINT (28); then the hydrolysate was rechromatographed, and the fractions corresponding to cholesterol and cholesteryl ester were eluted and their radioactivities were determined. The radioactivities of the fatty acid and cholesterol moiety were calculated as follows: Where C (e) is the activity of the cholesteryl moiety, F(e) is that of esterified fatty acid, CE is that of cholesteryl ester before hydrolysis, C is that of cholesterol after hydrolysis and F=CE-(C+radioactivity of cholesteryl ester remained after hy drolysis). The rates of hydrolysis were more than 90% under the conditions used.
Determination of expired 14CO2. The expired 14CO2 from a rat injected with 14C-linoleic acid was collected for 1 hour in ethanolamine-ethyleneglycol mono methylether (1:2, by vol.) by application of a negative pressure of 7-8 mmHg (29,30) and the radioactivity was determined.

Contents of liver lipids
As described before (9, 10), the amounts of lipids, and especially triglyceride and cholesteryl ester in the liver were higher in pyridoxine-deficient rats than in the controls ( Table 1)

DISCUSSION
Pyridoxine deficiency is known to disturb lipid metabolism. We previously reported increases in the contents of triglyceride and cholesteryl ester in the liver of rats fed a high-protein pyridoxine-deficient diet (9, 31), and we confirmed these results in the present study (Table 1). Cholesterol and ketone bodies are both synthesized via 3-hydroxy-3-methylglutaryl CoA (32,33). Thus the ac cumulation of cholesteryl ester in the pyridoxine-deficient rats suggested that the syntheses of ketone bodies might be abnormal. But does not seen to be so,   because we could not detect any appreciable difference the levels of ketone bodies in the livers of pyridoxine-deficient and control animals. Recently, CLINKEN BEARD et al. (34) suggested that there might be separate pools of 3-hydroxy-3 methylglutaryl CoA. Fatty liver may also be caused by impaired oxidation of fatty acid: ARTOM (35) reported inhibition of oxidation of stearic acid in animals treated with DL-ethionine and CORREDOR (36) also described impaired oxidation of long chain fatty acid in choline-deficient animals. However, in this work we obtained no evidence for impaired oxidation of fatty acids in pyridoxine-deficient rats from either the mitochondrial NAD+/NADH ratio, calculated from the values for ketone bodies, or results on the oxidation of injected 14C-linoleic acid (Tables 3 and 4). We also observed no difference in the oxidations of acetate in liver slices from pyridoxine-deficient and control rats (31). Studies on the pool sizes of fatty acids in pyridoxine-deficient and control animals are necessary to clarify this problem.
In this work we also examined the incorporation of 14C-linoleic acid into phos pholipids. The radioactivities in phospholipids may be largely due to that in phosphatidic acid, which has a more rapid turnover than other phospholipids (27, 37). The incorporation of 14C-linoleic acid into triglycerides in pyridoxine deficient and control rats were different from 45 minutes after the times of in jection (Fig. 2); the slower removal of radioactivity in deficient rats may be due to impaired oxidation, impaired secretion from the liver or increased influx from extrahepatic tissues. It could also be due to indirect utilization of linoleic acid from fatty ester other than triglyceride (38) or reutilization of acetate produced from linoleic acid. In the latter case the glycerol moiety of triglycerides may also contain radioactivity. Increased cholesterogenesis in the livers of rats fed a pyridoxine-deficient diet has been reported from this laboratory and by others (11-15, 31), and it was confirmed in the present study using 14C-linoleic acid (Fig.  3). As shown in Fig. 4, the rates of esterification of cholesterol in the deficient and control groups were very similar. Thus it seems likely that cholesterol ester accumulates in the liver of pyridoxine-deficient rats because synthesis of the cholesterol moiety increases, rather than because the rate of esterification increases.