PubMed Health⌕ Search

Biomedical subjects

I Hincenbergs

Publications and source records attributed to I Hincenbergs.

12 recordsLinked to original sources

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.

Animals↗

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.

ATP Citrate (pro-S)-Lyase↗

Effects of linolenic acid deficiency on the fatty acid patterns in plasma and liver cholesteryl esters, triglycerides and phospholipids in female rats.

These experiments were performed to measure the effects of linolenate deficiency upon neutral lipids of plasma and liver, and to search for a metabolic interaction between dietary choline and linolenic acid. Rats were fed for two generations on a linolenic acid-deficient diet containing methyl linoleate as the only source of lipid. Control rats were supplemented with methyl linolenate. Second-generation linolenate-deficient rats and control rats were fed low-methionine, choline-deficient diets for 2 weeks. Half the animals in each group were given choline-supplemented diets. Plasma and liver total cholesterol, esterified cholesterol, triglyceride and major phospholipid classes, and the fatty acids of these classes were measured. Linolenic acid deficiency reduced the concentrations of plasma triglycerides in both choline-deficient and choline-supplemented rats. Evidence for a metabolic interaction between choline and linolenic acid was not obtained because the rats responded very weakly to the choline deficiency. Linolenate deficiency reduced the proportions of n-3 fatty acids, particularly 22:6n-3, in all the lipids analyzed.

Animals↗

Linolenic acid deficiency.

Linolenic acid deficiency has not been demonstrated clearly in warm blooded animals, yet circumstantial evidence suggests that n-3 fatty acids may have functions in these animals. The fact that several species of fish definitely require dietary n-3 fatty acids indicates that n-3 fatty acids have important and specific functions in these animals and suggests that such functions may also be present in warm blooded animals. It is also true that n-3 fatty acid distribution in tissues of birds and mammals appears to be under strict metabolic control, and that this complex metabolic control mechanism apparently has survived evolutionary pressure for a very long time. So far, attempts to produce linolenic acid deficiency in mammals have not revealed an absolute requirement for n-3 fatty acids. If functions for n-3 fatty acids do exist in warm blooded animals, it seems probable that they may be located in the cerebral cortex or in the retina, because these tissues normally contain high concentrations of n-3 fatty acids.

Animals↗

Linolenic acid deficiency: changes in fatty acid patterns in female and male rats raised on a linolenic acid-deficient diet for two generations.

Rats were fed for two generations a purified, linolenic acid-deficient diet in which the only source of lipid was purified methyl linoleate. This diet contained about 38 mg linolenic acid/kg diet. Control rats were given the same diet supplemented with methyl linolenate (2,500 mg/kg diet). Male and female rats ranged in age from weaning pups to adults. Lipids were extracted from liver, brain, kidney, spleen, heart, muscle, gastrointestinal tract, lung, ovary, testis, adrenal, plasma, erythrocytes, retina, and adipose tissue. Fatty acids of major phospholipid classes (choline phosphoglycerides, ethanolamine phosphoglycerides, and mixed serine phosphoglycerides plus inositol phosphoglycerides) or of total lipid extracts were measured by gas liquid chromatography. Growth rates and organ weights were similar in control and linolenic acid-deficient rats. The major effect of the deficiency was to lower the proportions of n-3 fatty acids, especially 22:6 n-3, in all the organs analyzed. Docosahexaenoic acid (22:6 n-3) was mainly replaced by 22:5 n-6 in deficient rats. The greatest changes in composition were found in brain, heart, muscle, retina, and liver.

Age Factors↗