Classes Of Polyunsaturated Fatty Acids Research Articles

Determination of Total Lipid and Lipid Subclasses in Meat and Meat Products

Current interest in physiological and nutritional activities of the sterol, polyunsaturated fatty acid, and polar lipid fractions of meats and other foods indicates that analytical methods for lipids should be evaluated on their ability to recover and quantitate these classes. Current methods of lipid isolation furnish an extract that is dependent on the solvent(s) used, the type of food material, the temperature of extraction, and the relative proportions of the lipid classes present. Extraction with ethers or other relatively nonpolar solvents removes principally the neutral fats and nonpolar lipids. For an approximation of the crude fat content, such extraction is often sufficient, because the nonpolar fraction generally constitutes over 90% of the total lipids present. The polar lipids include the biochemically important (omega-3) and (omega-6) polyunsaturated fatty acid classes; thus, the method of lipid extraction of food products becomes relevant for a more complete and valuable characterization of their nutritional value. The various methods of lipid determination for meat products are examined for their total recovery of these important lipid groups. A sequential extraction in conjunction with subsequent analytical methods is recommended.

Mitochondrial membrane fatty acid composition in the marmoset monkey following dietary lipid supplementation.

Diets supplemented with high levels of saturated fatty acids derived from sheep kidney (perirenal) fat or unsaturated fatty acids derived from sunflowerseed oil were fed to marmoset monkeys for 22 wk. The effect of such diets on plasma, red blood cell phospholipids, and liver, heart, kidney and brain mitochondrial phospholipid fatty acids was determined. Despite large differences in the level and type of lipid present in the experimental diets, there was little effect on the proportion of saturated to unsaturated fatty acids in the phospholipids of the membranes examined. The diets did, however, alter the proportion of the various classes of polyunsaturated fatty acids in the membrane phospholipids, with the sunflowerseed oil diet elevating and the sheep kidney fat diet reducing the n-6/n-3 unsaturated fatty acid ratio, relative to a low (mixed fat) reference diet. This change occurred in all membranes except brain, in which only a small response to altered dietary lipid intake was observed. Elevation of dietary linoleic acid led to an increase in membrane linoleic acid and a marked decrease in membrane arachidonic acid, such that the membranes from animals fed the sunflowerseed oil diet exhibited the lowest proportion of arachidonic acid. In this latter respect, the response of the marmoset monkey to dietary lipid supplementation differs markedly from the rat. Our inability to alter significantly membrane lipid saturation/unsaturation supports the notion that a homeostatic mechanism is in some way responsible for buffering membranes from the effects of significant changes in the nature of the dietary lipid intake.

Dietary menhaden oil lowers plasma prostaglandins and calcium in mice bearing the prostaglandin-producing HSDM1 fibrosarcoma.

The omega 3 class of polyunsaturated fatty acids, particularly eicosapentaenoic acid (EPA, 20:5), has been shown to alter the patterns of arachidonic acid (20:4) metabolism in both in vitro and in vivo systems. To examine further the role of arachidonic acid conversion to prostaglandins (PG) in hypercalcemic mice bearing the PG-producing HSDM1 fibrosarcoma, we have performed experiments in which control and tumor-bearing animals were fed diets either low (0.1-0.2% of total fatty acid) or high (17%) in EPA. In all five experiments performed, tumor-bearing mice eating control diets had markedly elevated (average sixfold above control) plasma concentrations of 13,14-dihydro-15-keto-PGE2 (PGE2-M), while in mice bearing HSDM1 tumors and eating the EPA-enriched menhaden oil diet, the elevation was reduced to only twice control values. The increase in plasma calcium concentration (approximately 2.5 mg/dl above control) in tumor-bearing animals was also reduced significantly (P less than 0.05) to only 1.3 mg/dl above control in mice eating the diet enriched in EPA. Plasma immunoreactive hydroxy fatty acids (i12-HETE) and sulfidopeptide leukotrienes (iSRS) were not elevated in tumor-bearing mice and were unaffected by diet. The contents of PGE2, PGF2 alpha, and 6-keto-PGF1 alpha were lower in tumor tissue from animals eating the diet high in EPA, whereas the tissue contents of i12-HETE and iSRS were not altered by diet. Fatty acid analysis of liver and tumor tissue revealed marked increases in certain omega 3 fatty acids (20:5, 22:5, and 22:6) from animals eating the enriched diet. Body weights, tumor weights, and tumor histology were not significantly altered by diet. To determine whether dietary calcium played a role in the elevation of plasma calcium in mice bearing the HSDM1 tumor and the reduction of plasma calcium in animals fed EPA, we compared results in mice fed diets containing 0.80% (normal) and 0.015% (deficient) calcium. The increases in plasma calcium and PGE2-M observed in tumor-bearing mice were the same on both normal and very low calcium intakes. We conclude, in mice of the Swiss albino strain bearing the HSDM1 fibrosarcoma, that consumption of a diet enriched in EPA reduces the production of cyclooxygenase products of arachidonic acid metabolism and thereby reduces the elevation of plasma calcium concentration. Dietary enrichment with EPA did not alter the production of serologically determined lipoxygenase products of arachidonic acid.

Choline uptake in cultured human Y79 retinoblastoma cells: effect of polyunsaturated fatty acid compositional modifications.

Choline uptake in Y79 human retinoblastoma cells occurs through two kinetically distinguishable processes. The high-affinity system shows little sodium or energy dependence, and it does not appear to be linked to acetyl CoA; choline O-acetyltransferase. When the cells are grown in a culture medium containing 10% fetal bovine serum, the high-affinity system has a K'm= 2.16 +/- 0.13 microM and V'max = 27.0 +/- 2.9 pmol min-1 mg-1, whereas the low-affinity system has a k'm = 20.4 +/- 1.3 microM and V'max = 402 +/- 49 pmol min-1 mg-1. Under these conditions, the polyunsaturated fatty acid content of the cell membranes is relatively low. When the polyunsaturated fatty acid content of the microsomal membrane fraction was increased by supplementing the culture medium with linolenic or docosahexaenoic acids (n-3 polyunsaturated fatty acids) or arachidonic acid (n-6 polyunsaturated fatty acid), the K'm of the high-affinity choline transport system was reduced by 40--60%. The V'max also was reduced by 20--40%. Supplementation with oleic acid, the most prevalent monounsaturated fatty acid, did not affect either kinetic parameter. The results suggest that one functional effect of the high unsaturated fatty acid content of neural cell membranes is to facilitate the capacity of the high-affinity choline uptake system to transport low concentrations of choline. This effect appears to be specific for polyunsaturated fatty acids but not for a single type, for it is produced by members of both the n-3 and n-6 classes of polyunsaturated fatty acids.

Accumulation of N-3 polyunsaturated fatty acids cultured human Y79 retinoblastoma cells.

The metabolism of the n-3 class of polyunsaturated fatty acids, which occur in relatively high quantities in neural tissues, was studied in human Y79 retinoblastoma cells. These cells contained low levels of n-3 polyunsaturates when grown in culture media supplemented with fetal bovine serum. The cells readily incorporated performed docosahexaenoic acid (22.6 n-3) into phospholipids, but human skin fibroblasts did this to a similar extent. When 10 to 30 mumol/ml linolenic acid (18:3 n-3) was added, the cell also accumulated 22:6 in phospholipids. The capacity to convert appreciable amounts of 18:3 to 22:6 appears to be a unique property of the retinoblastoma cells as compared with other continuously cultured cell lines. More 18:3 than linoleic acid (18:2 n-6) was incorporated into phospholipids by the retinoblastoma cultures, and 18:3 was channeled to a larger extent into the ethanolamine glycerophospholipid fraction. These findings indicate that retinoblastoma cells handle n-3 polyunsaturated fatty acids in a manner very similar to neural tissue in vivo. Based on the results obtained with this model system, it appears that three processes may contribute to the accumulation of 22:6 in retina and neural tissue: increased ability to incorporate 18:3, the capacity to convert 18:3 to 22:6, and channeling of 18:3 and its metabolites into ethanolamine glycerophospholipids.