Effect of dietary fish oil and corn oil on lipid metabolism and apolipoprotein gene expression by rat liver

Abstract
A 3‐week fish oil diet induced in weanling rats a decrease in plasma lipids and liver triacylglycerol, and an increase in insulinemia, compared to a corn oil diet. At the same time, plasma apolipoprotein (apo) A‐I was slightly lower and plasma heavy apo B/light apo B ratio was higher in fish‐oil‐fed than in corn‐oil‐fed rats. Hepatocytes obtained from fish‐oil‐fed and corn‐oil‐fed rats were used to examine how fish oil affects lipid and apolipoprotein synthesis and secretion. Primary culture of hepatocytes from fish‐oil‐fed rats displayed a lower ability to synthesize and secrete triacylglycerol than hepatocytes from corn‐oil‐fed rats, as measured by mass determination or [U‐14C]glycerol incorporation. Hepatocytes from fish‐oil‐fed rats exhibited a lower synthesis of cholesterol, measured by [14C]acetate incorporation, than hepatocytes from corn‐oil‐fed rats. This impairment was associated with an increase in β‐oxidation, a higher channeling of oleic acid into phospholipids, and a lower triacylglycerol/diacylglycerol ratio in hepatocytes from fish‐oil‐fed rats than in hepatocytes from corn‐oil‐fed rats. Incorporation of [35S]methionine into secreted apoB was reduced in hepatocytes from fish‐oil‐fed rats, but was not paralleled by a decrease in apo B mRNA. The appearance of degradative forms of apo B suggest an increase in apo B degradation in hepatocytes from fish‐oil‐fed rats. Incorporation of [35S]methionine into cellular and secreted apo A‐I was lower in hepatocytes from fish‐oil‐fed rats than in hepatocytes from corn‐oil‐fed rats, and was not paralleled by any difference in the apo A‐I mRNA level. Finally, [35S]methionine incorporation into cellular and secreted forms of apo E and apo A‐I mRNA were reduced in hepatocytes from fish‐oil‐fed rats, compared with hepatocytes from corn‐oil‐fed rats. These combined data show that fish oil diet reduces triacylglycerol synthesis and secretion and affects apo B synthesis at a post‐transcriptional level, and reduces cholesterol synthesis and affects apo E and apo A‐I synthesis at a transcriptional and a post‐transcriptional level.

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