Reduced hepatic triglyceride secretion in rats fed docosahexaenoic acid-rich fish oil suppresses postprandial hypertriglyceridemia.

To evaluate the mechanisms of suppression of postprandial hypertriglyceridemia by fish oil rich in docosahexaenoic acid, the effect on the intestinal absorption of triglyceride, activities of lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) and metabolism of chylomicrons (CM) and CM remnants were compared with that of safflower oil in Sprague-Dawley rats in a series of studies. The feeding of fish oil for 3 wk suppressed postprandial hypertriglyceridemia (study 1). Dietary fish oil did not alter the rate of lymphatic absorption of triglyceride (study 2). The activities of LPL and HTGL were measured at 5 h after the beginning of feeding, when serum triglyceride concentrations were highest in both dietary groups. The activities of LPL in adipose tissue and heart were greater (P < 0.05) and those of HTGL were lower (P < 0.05) in the rats fed fish oil (study 3). In contrast, there were no differences in the activities of LPL and HTGL in postheparin plasma between the fish and safflower oil groups (study 4). The clearance rates of CM and CM remnants were measured by injecting intravenously CM collected from rats fed safflower or fish oils with [14C]triolein and [3H]cholesterol (study 5). Dietary oil did not influence the half-lives of CM or CM remnants. The secretion of triglyceride from the liver of rats injected with Triton WR-1339 was lower (P < 0.05) in the rats fed docosahexaenoic acid, a major component of fish oil, than those fed linoleic acid, a major component of safflower oil (study 6). These observations strongly support the hypothesis that in rats, the principal cause of the suppression of postprandial hypertriglyceridemia by fish oil is the depression of triglyceride secretion from the liver.

Lymphatic absorption of seal and fish oils and their effect on lipid metabolism and eicosanoid production in rats.

Eicosapentaenoic (EPA) and docosahexaenoic acids (DHA) were distributed mainly in the sn-1 and 3 positions of seal oil triglyceride and in the sn-2 position of fish oil triglyceride. In Expt. 1, the structural distribution of EPA and DHA in lymph triglyceride of rats given seal or fish oils was similar to the distribution in the administered oils. In Expt. 2, seal oil-rich or fish oil-rich fats having constant polyunsaturated/monounsaturated/saturated fatty acids and n-6/n-3 polyunsaturated fatty acids ratios were fed to rats for 3 weeks. Seal oil more effectively reduced plasma and liver triglyceride than fish oil. Ratio of the productions of aortic prostacyclin and platelet thromboxane A2 stimulated by thrombin was significantly higher in rats fed seal oil than in those fed fish oil. The results suggested that the different intramolecular distribution of EPA and DHA in dietary fat affected lipid metabolism differently in rats.