Studies on the origin of triglyceride in fatty liver caused by pyridoxine-deficiency in rats

Abstract

The effects of pyridoxine-deficiency on the incorporation of oral [1-14C]-linoleate into serum, dextran sulfate and CaCl 2 precipitable lipoprotein (B-lipoprotein) and liver lipid, and on the profiles of serum lipoprotein and apolipoprotein were studied. The incorporation of label into liver lipid in the deficient group was higher than that in the pair-fed controls and tended to be higher than that in the controls fed ad lib. The counts in lipid of B-lipoprotein as a percentage of total liver lipid was significantly lower in pyridoxine-deficient rats than in the two controls. The transport of lipid from the liver to the blood was studied by examining the compositions of lipids and apolipoproteins of various density classes of serum lipoproteins in pyridoxine-deficient, and pair-fed control rats. The concentrations of protein in chylomicrons and very low density lipoproteins (VLDL) were lower than those of pair-fed controls. These findings suggested the possibilities that the secretion of VLDL from liver into blood was impaired or catabolism of VLDL was increased in pyridoxine-deficient rats. The apolipo-protein profiles of VLDL and high density lipoprotein (HDL) as measured by 0.1% SDS, 10% polyacrylamide disc electrophoresis showed that pyridoxine-deficient rats had lower contents of apo-C relative to apo-E in VLDL or to apo-A-I in HDL than those of the pair-fed controls.