Studies on liver phosphatidyl cholines: I. Effects of fatty liver induction on phosphatidyl cholines from liver mitochondria and microsomes

Protein, total phospholipid, phosphatidyl cholines and phosphatidyl choline fractions from liver mitochondria and microsomes of female rats were analyzed after treatment with CCl₄ (0.3 ml of CCl₄ suspended in corn oil) or ethionine (50 mg in 0.9% saline) or after feeding a choline deficient, low protein diet for seven days. Phosphatidyl cholines were separated into four fractions differing in the degree of fatty acid unsaturation. Over 50% of total phosphatidyl choline phosphorus was present in fraction 3 of liver mitochondria and microsomes. The major fatty acid in fraction 1 was docosahexaenoic acid. Fraction 4 contains oleic and linoleic acids. Arachidonic acid occurs in fraction 2 and 3. Ethionine decreased the amount of microsomal protein and phosphatidyl choline fraction 1 of mitochondria. Microsomal protein was decreased by CCl₄. The choline deficient, low protein diet caused a decrease in mitochondrial and microsomal phospholipids. The amount of the mitochondrial phosphatidyl choline decreased. Corn oil increased the level of phosphatidyl choline fraction 3. Choline deficiency decreased the amount of phosphatidyl choline fraction 3, increased fraction 4 of mitochondria and microsomes and increased fraction 1 of microsomes.     

Effects of dietary corn oil and salmon oil on lipids and prostaglandin E2 in rat gastric mucosa

Three groups of male rats were fed either a corn oilenriched diet (17%, w/w), a salmon oil-enriched diet (12.5%) supplemented with corn oil (4.5%) or a low-fat diet (4.4%) for eight wk to investigate the possible relationships between dietary fatty acids and lipid composition, and prostaglandin E₂ level and phospholipase A₂ activity in the rat gastric mucosa. High-fat diets induced no important variation in total protein, phospholipid and cholesterol contents of gastric mucosa. Compared with a low-fat diet, corn oil produced a higher n−6/n−3 ratio in mucosal lipids, whereas this ratio was markedly lowered by a fish oil diet. In comparison with the low-fat diet, the production of prostaglandin E₂(PGE₂) in gastric mucosa of rats fed salmon oil was significantly, decreased by a factor of 2.8. In the corn oil group, PGE₂ production tended to decrease, but not significantly. In comparison with the low-fat diet, both specific and total gastric mucosal phospholipase A₂ activities were increased (+18 and 23%, respectively) in the salmon oil group; they were unchanged in the corn oil group. It is suggested that the decrease of gastric PGE₂ in rats fed fish oil is not provoked by a decrease in phospholipase A₂ activity but may be the result of the substitution of arachidonic acid by n−3 PUFA or activation of PGE₂ catabolism.     

The behavior of rat bile phospholipids in the intestine and in incubation media containing pancreatic juice

Samples of radioactive bile were collected from rats after intravenous injection of potassium soaps ([9–10³H₂] or [1¹⁴C] oleate, [1¹⁴C] linoleate or [9–10³H₂] palmitate). These radioactive acids were chosen because it is well established that, in natural phosphatidyl cholines, palmitic acid is located chiefly at the 1 position and linoleic and oleic acids at the 2 position. After incubation of bile with pancreatic juice, the labeling of unchanged biliary phospholipids was higher when native bile was labeled with oleic acid than with palmitic or linoleic acids. These data suggest that monounsaturated molecular species of biliary phospholipids are more resistant than the diunsaturated ones to in vitro hydrolysis by phospholipase A₂. Ninety min after introduction of the radioactive bile into the upper part of the rat duodenum, high labeling of luminal phospholipids was observed regardless of the bile sample used, although labeling of free fatty acids was always low. The passage of intact biliary phospholipids through the intestinal epithelium is discussed.     

Lung surfactant and fatty acid composition of lung tissue and lavage of rats fed diets containing different lipids

Two nutritional models, essential fatty acid (EFA) deficiency and the feeding of saturated vs unsaturated fats, were used to determine the effects of dietary lipids on the fatty acid composition of rat lung and lavage. Semipurified diets containing 7% corn oil, 7% hydrogenated coconut oil (EFA-deficient), 10% butter or 10% safflower oil were fed to dams during lactation and thereafter to their offspring for a total of 24 weeks. Lipids were extracted from the lung lavage and lung tissue and their fatty acid composition was determined. The content of dipalmitoylphosphatidylcholine (DPPC), the main surfactant in the lungs, was also determined. The results show that the levels of DPPC in the lungs of rats fed 10% butter decreased although the decrease in the EFA-deficient rats was greater. Comparing rats fed butter with those fed corn oil, there were also modifications in the fatty acid composition of the total lipids and phospholipids of lung tissue and lavage as well as in phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol +phosphatidylserine fractions isolated from the lung tissue. The changes in fatty acid composition were somewhat fewer in rats fed butter then in those fed an EFA-deficient diet. The results suggest that a marginal EFA deficiency produced in rats by long-term feeding of 10% butter may account for the reduction in DPPC levels and in the changes in fatty acid composition in the lung tissue and lavage.     

Effects of streptozotocin-induced diabetes on phosphoglyceride metabolism of the rat liver

We have studied the effect of streptozotocin (SZ)-induced diabetes on fatty acyltransferase and phospholipase enzyme activities involved in the synthesis and degradation of rat liver phosphoglycerides. Neither mitochondrial nor microsomal acyl-CoA: glycerol 3-phosphate acyltransferase (GPAT) activity was altered, although insulin treatment stimulated mitochondrial GPAT activity. However, microsomal acyl-CoA: 1-acylglycerol 3-phosphate acyltransferase (1-acyl-GPAT) activity increased (24–33 per cent, p<0.01) in the diabetic animals using 3 different acyl-CoA donors: palmitoyl-CoA, oleoyl-CoA and linoleoyl-CoA. SZ-induced diabetes also increased acyl-CoA:1-acylglycerol 3-phosphorylcholine acyltransferase (GPCAT) activity (38–45 per cent, p<0.01) with 3 different acyl-CoA donors: oleoyl-CoA, linoleoyl-CoA and arachidonoyl-CoA. 1-acyl-GPAT and GPCAT activity returned to normal with insulin treatment. In contrast to the increased activity of the microsomal fatty acyltransferases 1-acyl-GPAT and GPCAT, SZ-induced diabetes decreased mitochondrial phospholipase A₂ activity and lysophospholipase activity (49–70 per cent, p<0.01). Insulin treatment of the diabetic rats corrected the decreased lysophospholipase and stimulated phospholipase A₂ activity 35 per cent higher than controls. Since microsomal 1-acyl-GPAT and GPCAT are known to have higher activity toward unsaturated fatty acyl-CoA donors, the increased GPCAT activity coupled with the decreased lysophospholipase activity and the increased 1-acyl-GPAT activity in diabetes would tend to increase the formation of newly synthesized phospholipids containing unsaturated fatty acids. This mechanism plus the decreased fatty acid desaturase (4) may be the factors which alter the fatty acid composition of phosphoglycerides in diabetic rat liver microsomes.     

Influence of medium-chain triglycerides on lipid metabolism in the rat

Lipid metabolism was studied in rats fed diets containing corn oil, coconut oil, or medium-chain triglyceride (MCT), a glyceride mixture containing fatty acids of 8 and 10 carbons in length. The ingestion of MCT-supplemented, cholesterolfree diets depressed plasma and liver total lipids and cholesterol as compared with corn oil-supplemented diets. In rats fed cholesterol-containing diets, plasma cholesterol levels were not influenced by dietary MCT, but liver cholesterol levels were significantly lower than in animals fed corn oil. In vitro cholesterol synthesis from acetate-1-¹⁴C was lower in liver slices of rats that consumed MCT than in similar preparations from corn oil-fed rats. Studies of fatty acid carboxyl labeling from acetate-1-¹⁴C and the conversion of palmitate-1-¹⁴C to C₁₈ acids by liver slices showed that chain-lengthening activity is greater in the liver tissue of rats fed MCT than in the liver of animals fed corn oil. The hepatic fatty acid desaturation mechanisms, evaluated by measuring the conversion of stearate-2-¹⁴C to oleate, was also enhanced by feeding MCT. Adipose tissue of rats fed MCT converts acetate-1-¹⁴C to fatty acids at a much faster rate than does tissue from animals fed corn oil. Evidence is presented to show that the enhanced incorporation of acetate into fatty acids by the adipose tissue of rats fed MCT represents de novo synthesis of fatty acids and not chain-lengthening activity. Data are also presented on the fatty acid composition of plasma, liver, and adipose tissue lipids of rats fed the different fats under study.     

Arachidonic acid,prostaglandin E2 and leukotriene C4 levels in gingiva and submandibular salivary glands of rats fed diets containing n−3 fatty acids

The effect of dietary n−3 fatty acids on prostaglandin E₂ (PGE₂) and leukotriene C₄ (LTC₄) levels in rat salivary glands and gingiva was examined in two separate nutritional studies. In the first set of experiments, two groups of male weanling Sprague-Dawley rats were fed semipurified diets containing 10% corn oil (control group) or 10% menhaden oil (experimental group). Rats were killed after 8 wk on the diets; the fatty acid composition of total phospholipids and the concentrations of PGE₂ and its precursor, arachidonic acid, were measured in gingiva and submandibular salivary glands (SMSG). Dietary n−3 fatty acids were incorporated into the tissue phospholipids. Arachidonic acid levels were reduced by 56% in gingiva and SMSG of rats fed menhaden oil compared with the control rats fed the diet containing corn oil. The concentrations of PGE₂ in SMSG and gingiva of rats fed the diet containing menhaden oil were reduced by 74% and 83%, respectively. In a subsequent nutritional study, we tested whether the diet-induced reduction in tissue arachidonic acid levels would also result in a corresponding decrease in LTC₄ production. Three groups of rats were fed diets containing 5% corn oil (group 1), 4% ethyl ester concentrate of n−3 fatty acids plus 1% corn oil (group 2), or 5% ethyl ester concentrate of n−3 fatty acids (group 3). After 6 wk of feeding, gingiva and SMSG were analyzed for arachidonic acid content andin vitro production of LTC₄. Arachidonic acid content of total phospholipids was about 60% lower in gingiva and 69% lower in SMSG of rats fed the ethyl ester concentrate of n−3 fatty acids (groups 2 and 3) than those of the control group fed the corn oil diet (group 1). Upon incubation with calcium ionophore, gingiva and SMSG from rats fed the n−3 fatty acids rich diet produced significantly less TLC₄ than those from rats of the control group. Because PGE₂ and LTC₄ are believed to be important biochemical mediators of periodontal disease, one may speculate that a diet-induced reduction in their levels may have a beneficial effect upon the course of the disease. The function of salivary glands may also be altered because of the role of these eicosanoids in salivary secretions. Presented in part for the Hatton Award Competition at the American Association for Dental Research Meeting, San Francisco, California, March 15–19, 1989, and at the International Association for Dental Research Meeting, Acapulco, Mexico, April 17–21, 1991.     

Metabolism of epoxidized phosphatidylcholine by phospholipase A2 and epoxide hydrolase

The isolation and measurement of phospholipid epoxides as major peroxidation products in biomembrane preparations prompted an investigation of enzymatic mechanisms which may be responsible for their elimination. Analysis of microsomal epoxide hydrolase and phospholipase A₂ activity against a phospholipid epoxide commonly encountered in tissues indicated it to be a poor substrate for epoxide hydrolase, but rapidly hydrolyzed by phospholipase A₂. Microsomal and purified phospholipase A₂ preparations hydrolyzed the phospholipid epoxide at rates 2-fold greater than were observed with a monoenoic phospholipid from which the epoxide would be derived. The product fatty acid epoxide,cis-9,10-epoxystearic acid, was rapidly hydrated by microsomal and cytosolic epoxide hydrolase. On the basis of earlier reports demonstrating increased phospholipase activity against oxidized phospholipids, and on the results of the present study, a model for the metabolism of oxidized membrane phospholipids is proposed.     

Changes in fatty acid composition of phospholipids from liver microsomes and nuclei in rats fed a choline-free diet

Male F-344 rats were fed a choline-free (CF) diet, and changes in phospholipid content, phospholipid fatty acids and phospholipase A₂ activity in liver nuclei and microsomes were examined during the first 72 hr. Both nuclei and microsomes showed a decrease in phosphatidylcholine (PC) content. Microsomes showed an increase in PC arachidonate while nuclei showed a decrease. Also, microsomes showed increased activity of phospholipase A₂ (PLA₂) while nuclei did not. These observations are consistent with the hypothesis that the absence of diene conjugates in liver microsomes in the rats on the CF diet may reflect the increased rate of removal of peroxidized fatty acids by phospholipase A₂.     

A new criterion in the bioassay of essential fatty acids: the spontaneous swelling of rat liver mitochondria in vitro

The spontaneous swelling in vitro of liver mitochondria from rats deficient in essential fatty acids (EFA) and normal rats is compared using the change in optical density as a criterion. Differences between both groups are observed only if high sucrose concentrations are used for the isolation of the mitochondria. The change in optical density can be described mathematically by the sum of two exponential functions. A correlation is found between the parameters of this function and the dose of sunflower seed oil fed to EFA-deficient rats, which makes the method useful as a criterion in an EFA bioassay. The EFA activities of several synthetic polyunsaturated fatty acids are compared using either growth rate or mitochondrial swelling as a criterion.     

Influence of elaidate and erucate on heart mitochondria

Male, weanling rats were fed, for up to six weeks, corn oil (CO), rapeseed oil (RSO), partially hydrogenated fat (HF), or a mixture of partially hydrogenated fat and corn oil (HF+CO). The respiratory activity of their isolated heart mitochondria, their hormone-sensitive lipase activity, and the fatty acid compositions of the phospholipids of the mitochondria were determined. The results indicated that heart mitochondria isolated from rats which had been fed corn oil (CO) had a higher rate of oxygen uptake, showed higher respiratory control ratios, higher ADP/0 ratios and a higher rate of ATP synthesis than the heart mitochondria isolated from those fed rapeseed oil or hydrogenated fats. The oxygen uptake rates of the rat heart mitochondria isolated from each dietary group of rats was in order: oleyl carnitine ≫ erucyl carnitine > elaidyl carnitine. The decreased capacity to oxidize substrate by heart mitochondria which had been isolated from the hearts of rats fed rapeseed or hydrogenated soybean oil as compared with those fed corn oil as a sole source of dietary fat seemed related to the mitochondria lipid composition. The type of dietary fat fed had a pronounced influence on the mitochondrial fatty acid compositions of phosphatidylcholine, phosphatidylethanolamine, and cardiolipin. The lipase activity of the RSO-fed group did not show any increment with either epinephrine or supplemental ATP treatment. The substrate preference for lipase activity in myocardium was corn oil-triglycerides > trierucin > trielaidin > tripalmitin. However, cardiac lipid accumulation did not seem related to lipase activity in the myocardium. Taken from a thesis submitted by Chi Ming Lee Hsu in partial fulfillment of the Ph.D. degree in Food Science, University of Illinois at Urbana-Champaign.     

Influence of diet on conversion of14C1-linolenic acid to docosahexaenoic acid in the rat

¹⁴C₁-Linolenic acid was incorporated into lipids of hearts, livers, and carcasses of male rats. We studied the influence of diet composition on extent and distribution of radioactivity. A CHOW diet, a purified, essential fatty acid (EFA)-deficient diet, a purified control diet, and EFA-deficient diets with four fatty acid supplements were used. Supplements of 18∶2n−6, 20∶4n−6, 18∶3n−3, and 22∶6n−3 were given as single doses. Radioactivities in liver phosphatidyl ethanolamines (PE), phosphatidyl cholines, and neutral lipids were measured. The distribution of radioactivity among the fatty acids in liver phospholipids was determined. Rats on CHOW diet incorporated far less radioactivity than any other group into lipids of hearts and livers. Most of the activity in livers was recovered as 20∶5n−3 and 22∶6n−3 in all rats. In EFA-deficient rats, the radioactivity in 22∶6n−3 of liver PE was still increasing 36 hr after¹⁴C₁-linolenic acid had been administered. The n−6 supplements (18∶2n−6 and 20∶4n−6) seemed to reduce the conversion of 20∶4n−3 to 20∶5n−3 (desaturation), whereas the n−3 supplements (18∶3n−3 and 22∶6n−3) reduced the conversion of 20∶5n−3 to 22∶5n−3 (elongation). Formation of 22∶6n−3 may be controlled by 22∶6n−3 itself at the elongation of 20∶5n−3 to 22∶5n−3.     

Efficacy of linoleic acid administered rectally as monoglyceride

The potential of the rectal route for administration of essential fatty acids (EFA) as monoglyceride (MG) was investigated. EFA-deficient rats were supplemented with 14 mg linoleic acid/day for 3 days. Supplementation was either by oral administration as corn oil, orally as corn oil-derived MG or rectally as MG. The patterns of polyunsaturated fatty acids (PUFA) in liver and serum lipids, characteristic of EFA deficiency, were altered in the direction of normalcy in similar magnitude by all modes of supplementation, indicating that the rectal route may be useful for administration of EFA. The amounts of phospholipids (PL) and free fatty acids (FFA) in liver changed by all modes of administration. The magnitude of change of total PL and of FFA in liver depended upon the chemical form in which linoleic acid was administered and the route of administration, indicating that these factors affect lipid metabolism.     

Effect of essential fatty acid deficiency on the size and distribution of rat plasma HDL

Rat plasma high density lipoproteins (HDL) are comprised of two major particle size subpopulations, HDL₁ (255 Å?140 Å) and HDL₂ (140 Å?84 Å), in which the proportion of arachidonate in fatty acids of cholesteryl esters is greater than 50%. To determine whether decreased availability of arachidonate for cholesterol esterification would alter the distribution and/or amounts of the HDL subpopulations, we compared HDL subpopulations in EFA-deficient and control rats. To separate the effects of EFA deficiency and fat deficiency and to evaluate effects of different saturated fats, we used EFA-deficient diets that were fat-free or that contained 5% saturated fat. The control diets were the EFA-deficient diets plus 1% safflower oil. The saturated fats were hydrogenated coconut oil, hydrogenated cottonseed oil and saturated medium-chain triglycerides. All EFA-deficient diets decreased the proportion of the HDL₁ subpopulation and the peak diameter of the HDL₂ subpopulation. These changes appeared after quite brief EFA depletion in young rats and may be related to the increased liver cholesteryl ester concentrations typical of EFA-deficient rats.     

Influence of dietary fatty acids on membrane properties and enzyme activities of liver mitochondria of normal and hypophysectomized rats

Studies are reported on the effects of diets containing fatty supplements with (A) a high concentration of arachidonate (46% concentrate of ethyl arachidonate), (B) a high concentration of linoleate (corn oil), and (C) an essential fatty acid deficient, fully saturated fat (hydrogenated coconut oil) upon lipid composition, membrane permeability, and enzyme activities of liver mitochondria of normal and hypophysectomized rats. The fatty supplements produced differences in the fatty acid composition of the liver mitochondria; hypophysectomy, in addition, influenced the neutral and phospholipid composition. Permeability, indicated by swelling properties, correlated generally with the degree of unsaturation and essential fatty acid content of the lipid of the mitochondria of the normal animals. The fatty supplements also influenced the enzyme acitivites of the mitochondria of the normal animals. The mitochondria of the hypophysectomized animals were less responsive to the differences in the dietary fat in both their swelling properties and enzyme activities. Although the relationship was complex, it appeared that the hypophysis was involved in the functions of essential fatty acids in liver mitochondria.     

Study of the two pathways for arachidonate oxygenation in blood platelets

During collagen-induced blood platelet aggregation, arachidonic acid is set free from membrane phospholipids and subsequently converted into 12-hydroxyeicosatetraenoic acid by arachidonate lipoxygenase and into thromboxane A₂, 12-hydroxyheptadecatrienoic acid (HETE) and malondialdehyde by cyclooxygenase and thromboxane synthase. Lipoxygenase and cyclooxygenase have optimal activity at neutral to basic pH, while the thromboxane synthase is pH-independent between 5 and 9. These enzymes are membrane-bound. The cyclooxygenase is rapidly inactivated upon membrane disruption by nonionic detergents or phospholipid degradation with phospholipase A₂. It was found that platelet phospholipase A₂ preferentially splits off fatty acid with four double bonds. Eicosatetraynoic acid was used to investigate the physiological function of the arachidonate lipoxygenase during collagen-induced aggregation of rat blood platelets. This fatty acid is a more efficient inhibitor of lipoxygenase than of cyclooxygenase. At an inhibitor concentration of 0.6 μg/ml, platelet aggreation, 12-hydroxyeicosatetraenoic acid production as well as 15-hydroxytryptamine release are completely inhibited, while there is an apparent stimulation of the cyclooxygenase. These results indicate that arachidonate lipoxygenase is essential for irreversible blood platelet aggregation.     

Analytik plasmalogenhaltiger Phosphatide aus Herzgewebe mittels extracellulärer Phospholipase A2

The Analysis of Phospholipids from Cardiac Membranes by Phospholipase A₂. Phospholipase A₂ from snake venom has been employed to analyse the positional distribution of fatty acids in glycerolipids from guinea pig and pig cardiac membranes. It is known that phospholipase A₂ hydrolyses the fatty acids in sn-2 position of 1,2 diacylglycerophospholipids. In cardiac membranes phosphatidylcholine and phosphatidylethanolamine contain along with diacyl esters the corresponding alkenylether analogues of phospholipids. In the present experiments the alkenylether moieties were slowly hydrolysed by phospholipase A₂ from snake venom. We therefore separated by TLC lysophosphatides from fatty acids and unattacked phospholipids. The latter were the plasmalogens. The separated lipids were characterized by GLC. In some experiments the phospholipids were labelled with ¹⁴C-fatty acids before they were hydrolysed by phospholipase A₂. The alkenyl ether chain of plasmalogens seems to negativly influence the hydrolysis of fatty acids in sn-2 position of those phospholipids.     

Effect of subacute toxic levels of dietary cyclopropenoid fatty acids upon membrane function and fatty acid composition in the rat

The effect of subacute toxicity levels of dietary cyclopropenoid fatty acids upon several physiological parameters was determined in the rat. Diets containing 2% corn oil, 2%Sterculia foetida oil or 2% hydrogenatedSterculia foetida oil were fed.Sterculia foetida oil (50% cyclopropenoid fatty acids) fed rats exhibited retarded growth, elevated organ to body wt ratios, increased saturation of tissue lipid, and abnormal histopathology when compared to corn oil and hydrogenatedSterculia foetida oil fed rats. Growth was retarded 50%, liver/body wt doubled, and the percentage of saturated fatty acids in adipose tissue increased 2.5-fold forSterculia foetida oil vs. corn oil comparisons. Three membrane systems were examined in corn oil andSterculia foetida oil fed rats. Erythrocyte hemolysis rate in 0.3 M glycerol was increased by 30%; induction of mitochondrial swelling by reduced glutathione was inhibited completely and microsomal codeine demethylase activity was depressed nearly 50% inSterculia foetida oil fed rats. The ability of cyclopropenoid fatty acids to inhibit fatty acyl desaturase and influence tissue and membrane lipid composition is discussed. Most of the detrimental effects observed in cyclopropenoid fatty acids fed rats may be associated with alteration of normal lipid metabolism and membrane function.     

Lipid binding in mitochondria from testes of normal and essential fatty acid deficient rats

Essential fatty acid (EFA) deficiency in rat causes severe degeneration of spermatogenic tissue. Previously it was shown that the distribution of lipid classes changes very little during tissue degeneration. However it is well known that the fatty acid spectrum in lipids from testicular tissue is altered drastically during EFA deficiency. The molecular binding of lipids in membrane structures might be altered when a larger amount of ω9-acids is present in the various lipid classes in testes of EFA-deficient rats. In the present studies comparison was made of the binding of lipids in testicular mitochondrial membranes from rats fed a fat-free diet or a diet containing 6% peanut oil for 26 weeks. Isolated mitochondria were coated on glass beads, then dried and packed into a column, whereafter the membrane lipids were eluted with solvents with increasing dielectric constants. The differences between the binding of lipid classes in supplemented and EFA-deficient rats were not pronounced, but a tendency to a weaker binding in the EFA-deficient rats was observed. However for both groups the various extracts showed marked differences in the distribution of lipid classes concurrent with the change of the eluent. This indicates a different kind of binding in the membrane, not only for different lipid classes, but also within a special lipid class. Thus both phosphatidylcholines (PC) and phosphatidylethanolamines (PE) were found in extracts with quite different dielectric constants. The fatty acid composition of PC and PE in the major fractions eluted with chloroform and ethanol, respectively, was essentially the same. This indicates that the successive release of phospholipids (PL) in these two fractions was not based on fatty acid solubility properties but on variable binding in the membrane structure. The introduction of ω9-polyenoic fatty acids instead of ω6-polyenoic fatty acids in the PL of mitochondria membranes from EFA-deficient rats seems to be the only deviation in the lipid pattern of EFA-supplemented and EFA-deficient animals, and might therefore be responsible for the symptons of EFA deficiency. Presented in part at the AOCS-ISF World Congress, Chicago, September, 1970.     

Enzyme‐catalyzed synthesis of structured phospholipids with conjugated linoleic acid

Structured phospholipids were synthesized with the functional lipid conjugated linoleic acid (CLA). The lipase‐ and phospholipase A₂‐catalyzed enzymatic acidolysis reaction between phospholipids (PL) and CLA was used for fatty acid modification. Enzymatic processes were an effective way to produce structured PL. Screening of four lipases and immobilized phospholipase A₂ and a combination of lipase and phospholipase showed that only Lipozyme RM IM and Lipozyme TL IM were effective in incorporation of CLA into PL. The maximum incorporation achieved by the latter enzyme was 16% with soy PL in 72 h.