1982 Volume 28 Issue 4 Pages 377-390
When weanling rats were given 70% casein diet deficient in pyridoxine, they showed marked accumulation of liver lipid consisting mainly of triglyceride (TG) and cholesterol ester (CE). The serum concentrations of phospholipid (PL) and cholesterol (CH) in pyridoxine-deficient rats were significantly lower than those in pair-fed controls, but their serum levels of TG and free fatty acid (FFA) were not significantly different from those of controls. A significant inverse relation was shown between the concentration of liver TG and PL of pyridoxine-deficient rats. Measurement of incorporation of radioactivity from [1-14C]acetate into lipid in vivo showed that lipogenesis in the liver of pyridoxine-deficient rats was depressed, although the acetate pool was significantly higher than that in pair-fed controls. The incorporations of radioactivity from [1-14C]acetate into liver TG and PL in vivo were also lower in pyridoxine-deficient rats than in the pair-fed controls, but the ratio of the radioactivity in liver TG to that in liver PL was higher in pyridoxine-deficient rats than in pair-fed controls. This higher ratio was not due to increased mobilization of serum FFA from extra-hepatic tissues or decreased hydrolysis of liver TG, because labeling of serum FFA and the activity of liver lipase were not significantly different in deficient and control rats. The ratio of total radioactivity in serum TG to that in liver TG was lower in pyridoxine-deficient rats than in pair-fed controls in the latter period of the experiment. Studies were made on the components of PL contributing to liver TG accumulation in pyridoxine-deficient rats. The concentration of liver phosphatidylcholine (PC) was significantly lower in pyridoxine-deficient rats than in pair-fed controls. In pyridoxine-deficient liver, only PC showed an inverse correlation with the liver lipid concentration. These results suggest that a decreased concentration of liver PC and impaired secretion of TG from the liver into blood may be responsible for the inverse relationship of liver TG and PL concentrations in pyridoxine-deficient rats.
