I. Hincenbergs

Feeding pure docosahexaenoate or arachidonate decreases plasma triacylglycerol secretion in rats

Essential fatty acid (EFA)-deficient rats were fed highly purified methyl esters of docosahexaenoate (22∶6n−3), arachidonate (20∶4n−6), alpha-linolenate (18∶3n−3) or oleate (18∶1n−9) (100 mg/day, tube fed for 3–10 days), and their plasma triacylglycerol (TG) secretion rates were measured. Secretion rates of TG into plasma were reduced by tube-feeding 22∶6n−3, 20∶4n−6, 18∶3n−3, but not 18∶1n−9, to EFA-deficient rats. A significant reduction occurred after feeding 22∶6n−3 for only three days. Feeding 22∶6n−3 or 18∶3n−3 to EFA-deficient rats for three days also reduced the activities of liver lipogenic enzymes and sharply increased the proportions of 22∶6n−3 and 20∶5n−3 in liver phospholipid fractions. Mechanisms by which these EFA may reduce lipogenesis are discussed.

Increased plasma triglyceride secretion in EFA-deficient rats fed diets with or without saturated fat

Metabolic responses to essential fatty acid-deficiency in rats include an increased rate of triglyceride secretion into the plasma, a large reduction in the HDL1 plasma lipoprotein concentration, and increased concentrations of liver triacylglycerols and cholesteryl esters. Because of differences in the types of EFA-deficient diets used, it is not clear whether these responses were solely due to the absence of EFA from the diet or whether saturated fat, or differences in acyl group chain length in this fat, might be responsible. Therefore, we fed rats diets differing only in amounts and kinds of fat, and measured triacylglycerol secretion rates and liver concentrations of triacylglycerols and cholesteryl esters, for comparison with our earlier measurements of plasma high density lipoprotein subpopulations in rats fed exactly the same diets. The purified diets contained either no fat, 5% by weight hydrogenated coconut oil, 5% hydrogenated cottonseed oil, or each of these three diets supplemented with 1% safflower oil, or 5% corn oil. We also fed some rats a nonpurified stock diet for comparison with literature reports. The present results indicate that the metabolic responses to essential fatty acid deficiency described above are definitely due to essential fatty acid-deficiency and not to the presence or chain length of acyl groups in saturated fat in the diet.

Changes in liver lipid composition with overnight fasting.

Summary Fasting rats overnight from 8 p.m. to 8:30 a.m. produced significant changes in liver weight and liver fatty acid composition in comparison with fed rats killed at 8 p.m. and 8:30 a.m. Feeding and fasting procedures and time of sacrifice of animals should be carefully standardized in studies of liver lipid composition to minimize variations related to the eating patterns of the animals.

Responses of essential fatty acid-deficient rats to fasting-refeeding and partial hepatectomy.

Summary Essential fatty acid-deficient rats were subjected to fasting-refeeding or partial hepatectomy to stimulate liver phos-pholipid and membrane formation under conditions of limited essential fatty acid (EFA) supply. Refeeding after fasting decreased the proportion of arachidonate in liver phospholipid fatty acids only slightly, i.e., from 6.8% in nonfasted rats to 5.3% after 3 or 7 days of refeeding, whereas ei-cosatrienoate decreased from 19.8% in nonfasted rats to 13.0% after 3 days of refeeding, with a return to nonfasted levels after 7 days. Activities of liver glucose-6-phosphate dehydrogenase and fatty acid synthetase in fasted-refed EFA-deficient rats did not differ significantly from values in deficient rats fed ad libitum. Considerable increase in liver weight (ca. 3-8 g or at least 50% of the estimated preoperative weight) occurred after partial hepatectomy of EFA-deficient rats. The proportion of arachidon-ate in phospholipid fatty acids was slightly lower after hepatectomy than before. These results indicate that: (a) little of the arachidonate in EFA-depleted liver is used for lipoprotein formation and transport after fasting-refeeding, whereas eicosatri-enoate is available; (b) fasting-refeeding of EFA-deficient rats does not increase activities of liver glucose-6-phosphate dehydrogenase and fatty acid synthetase above the already elevated levels in EFA-deficient rats fed ad libitum; (c) considerable new liver tissue can be formed after partial hepatectomy even when EFA levels in phospholip-ids are very low. Supported in part by USPHS Grant No. AM 12024.