Rate Of Fatty Acid Incorporation Research Articles

Dietary Content and Type of Lipids and Selenium Supplement on Fatty Acid Profile in Meagre (Argyrosomus regius)

Dietary Content and Type of Lipids and Selenium Supplement on Fatty Acid Profile in Meagre (Argyrosomus regius)

Epicardial fat: properties, function and relationship to obesity

Epicardial fat is a relatively neglected component of the heart. The purpose of this review was to examine the anatomic and biochemical data on epicardial fat; to examine the relationship of epicardial fat to obesity and to explore the potential role of epicardial fat in the relationship of obesity to coronary atherothrombotic disease. Epicardial fat covers 80% of the heart's surface and constitutes 20% of total heart weight. It is present along the distribution of the coronary arteries, over the right ventricle especially along the right border, anterior surface and at the apex. There is three- to fourfold more epicardial fat associated with the right than the left ventricle. Putative physiologic functions of epicardial fat are based on observational data and include: buffering coronary arteries against the torsion induced by the arterial pulse wave and cardiac contraction, facilitating coronary artery remodelling, regulating fatty acid homeostasis in the coronary microcirculation and providing fatty acids to cardiac muscle as a local energy source in times of high demand. A considerable amount of the data on epicardial fat originates from autopsy series that have the inherent problem that conditions leading to death may have altered body composition and adiposity. With this caveat, data indicate that epicardial fat mass increases age until age 20-40 years but thereafter the amount of epicardial fat is not dependent on age. The amount of epicardial fat correlates with heart weight but the presence of myocardial ischemia and hypertrophy does not alter the ratio of epicardial fat to cardiac muscle mass. A number of properties differentiate epicardial fat from other fat depots specifically its smaller adipocytes size; different fatty acid composition, high protein content; high rates of fatty acid incorporation, fatty acid synthesis, insulin-induced lipogenesis or fatty acid breakdown; low rates of glucose utilization, low expression (mRNA) of lipoprotein lipase, stearoyl-CoA desaturase and acetyl-CoA carboxylase-alpha, and slow regression during weight loss. There is a significant direct relationship between the amount of epicardial fat and general body adiposity. Clinical imaging studies have demonstrated a strong direct correlation between epicardial fat and abdominal visceral adiposity. Several lines of evidence support a role for epicardial fat in the pathogenesis of coronary artery disease, namely the close anatomic relationship between epicardial fat and coronary arteries; the positive correlation between the amount of epicardial fat and the presence of coronary atherosclerosis and the ability of adipose tissue to secrete hormones and cytokines that modulate coronary artery atherothrombosis. Thus, epicardial fat maybe an important factor responsible for cardiovascular disease in obesity.

Tissue Specific Interactions of Exercise, Dietary Fatty Acids, and Vitamin E in Lipid Peroxidation

Both physical exercise and ingestion of polyunsaturated fatty acids that play an essential role in free radical-mediated damages cause lipid peroxidation. The intake of specific fatty acids can modulate the membrane susceptibility to lipid peroxidation. Data confirmed that liver, skeletal muscle, and heart have different capabilities to adapt their membrane composition to dietary fatty acids, the heart being the most resistant to changes. Such specificity affects membrane hydroperoxide levels that depend on the type of dietary fats and the rate of fatty acid incorporation into the membrane. Sedentary rats fed a monounsaturated fatty acid-rich diet (virgin olive oil) showed a higher protection of their mitochondrial membranes against peroxidation than sedentary rats fed a polyunsaturated fatty acid-rich diet (sunflower oil). Rats subjected to training showed higher hydroperoxide contents than sedentary animals, and exhaustive effort enhanced the aforementioned results as well as in vitro peroxidation with a free radical inducer. This study suggests that peroxide levels first depend on tissue, then on diet and lastly on exercise, both in liver and muscle but not in heart. Finally, it appears that α-tocopherol is a less relevant protective agent against lipid peroxidation than monounsaturated fatty acids.

Esterification of fatty acids by bovine intramuscular and subcutaneous adipose tissues.

Exogenous fatty acid esterification in intramuscular and subcutaneous adipose tissues from 72-hr fasted or ad libitum fed Angus cattle was investigated. Intramuscular (interfascicular) and subcutaneous adipose tissue snips were obtained from the longissimus dorsi muscle and were incubated with radioisotopically labeled fatty acids (palmitate, stearate, oleate, linoleate or linolenate) at three different concentrations (0.3 mM, 0.6 mM and 2.0 mM) to assess rates of fatty acid incorporation into glycerolipids. Rates of fatty acid esterification in vitro increased with fatty acid concentration in both intramuscular and subcutaneous adipose tissues. For all of the fatty acids investigated, triglycerides were the predominant products (60-85%). Subcutaneous adipose tissue had larger adipocytes and more actively (P less than 0.05) esterified fatty acids, with the exception of palmitate, than intramuscular adipose tissue. The rate of palmitate esterification was not different between tissues, although intramuscular adipose tissue esterified a greater proportion (P less than 0.10) of palmitate as triglyceride (85%) than did subcutaneous adipose tissue (75%). Relative rates of incorporation of fatty acids into lipids in intramuscular and subcutaneous adipose tissues were: palmitate greater than linolenate greater than linoleate greater than stearate. In general, 72-hr fasting did not significantly reduce the rates of fatty acid incorporation in bovine adipose tissues. Results of this study revealed that:i) rates of exogenous fatty acid incorporation into adipose tissue lipids were dependent on the medium fatty acid concentration and adipose tissue depot; and ii) the relative esterification rates of the various fatty acids in vitro did not necessarily reflect the proportion of these fatty acids in bovine adipose tissues.

The temperature dependence of phospholipid deacylation/reacylation in isolated hepatocytes of thermally acclimated rainbow trout ( Salmo gairdneri)

Rates of glycerol and fatty acid (18:0, 18:1, 18:3 and 20:4) incorporation into phosphatidylcholine (PC), phosphatidylethanolamine (PE) and triacylglycerol were measured in isolated hepatocytes of thermallyacclimated (5° C and 20° C) rainbow trout ( Salmo gairdneri) in order to assess the contribution(s) of the de novo and deacylation/reacylation pathways to the metabolism of membrane lipids. In PC, the effects of acclimation temperature were fatty acid dependent; for 18:0 and 20:4 n − 6 rates of fatty acid incorporation were greater in warm- than cold-acclimated trout, whereas the reverse was true for the incorporation of 18:1. In the case of both PE and triacylglycerol, unsaturated, but not saturated, fatty acids (18:0) were incorporated more rapidly by hepatocytes of cold- than warm-acclimated trout. For PC, ratios of fatty acid / glycerol incorporation were consistently lower than the corresponding ratios for phosphatidic acid regardless of the fatty acid, assay or acclimation temperature. In contrast, fatty acid / glycerol ratios for PE were higher than those for phosphatidic acid in (i) cold- compared to warm-acclimated trout and (ii) in assays conducted at 5°C compared to 20°C for cold-acclimated fish; in addition, ratios generally increased with the degree of unsaturation of the fatty acid in cold-acclimated trout. In the triacylglycerol fraction, fatty acid / glycerol ratios were greater than those for phosphatidic acid in warm-acclimated trout only, and were generally greater in warm- than cold-acclimated fish. These results were interpreted to indicate: (1) an increased contribution of the deacylation/reacylation cycle to the incorporation of unsaturated fatty acids into PE in cold- compared to warm-acclimated fish, and at 5° C compared to 20° C in cold-acclimated trout; and (2) a role for the deacylation/reacylation cycle in excluding the incorporation of unsaturated fatty acids into PC, particularly evident in warm-acclimated trout. The possibility that different metabolic mechanisms are operating to maintain the composition of PE at different temperatures is discussed.

Renomedullary Phospholipases in Salt-Sensitive and Salt-Resistant Dahl Rats

Renomedullary prostaglandin synthesis is lower in salt-sensitive (S) Dahl rats than in age-matched salt-resistant (R) rats on either 0.6% or 8.0% NaCl. The possible role of substrate availability to the cyclooxygenase in determining these differences was examined. S and R rats were started on diets with variable salt content (0.6%, 4.0% or 8.0% NaCl) at five weeks and were sacrified at either 11 or 16 weeks of age for comparisons of renomedullary phospholipase A1 and A2 activities (EC 3.1.1.4. and 3.1.1.32) and arachidonate incorporation into the lipids of renal medulla. Both phospholipase activities were higher in R rats at the two ages examined and for all levels of salt intake. These differences could not be accounted for by variable amounts of endogenous phospholipid substrate. High salt intake did not influence the in vitro A2 deacylating activities per mg protein. Arachidonate incorporation into renomedullary triglycerides remained constant with age in both strains while phospholipid labeling declined with age in S rats only so that, at 16 weeks of age, S rats had significantly lower incorporation into membrane phospholipids. This age-related decline in phospholipid labeling in S rats was prevented by 4.0% NaCl. These results suggest that low renomedullary phospholipase activities in S rats may restrict the release of substrate for prostaglandin synthesis and may also be related to reduced rates of fatty acid incorporation into membrane phospholipids.

Control of fatty acid incorporation in membrane phospholipids. X-ray-induced changes in fatty acid uptake by tumor cells

Lymphosarcoma cells isolated from the spleens of tumor-bearing mice were used to study the effect of a low dose of X-rays (5 Gy) on the incorporation of [ 3H]palmitate and [ 14C]arachidonate into the lipids of the tumor cells. Palmitate and arachidonate were rapidly incorporated especially into the phospholipids of the cells. Between one and three hours after the start of the incubation with radiactive palmitate 80–90% of the label of the total lipids was found in the phospholipid fraction. Already after a few minutes of incubation with radioactive arachidonate, about 95% of the label was incorporated in the phospholipids. Irradiation caused a small but significant increase in the rate of fatty acid incorporation for both fatty acids. Concomitantly, a significantly increased amount of fatty acid was removed from the medium by the cells as a result of the irradiation, and the specific radioactivity of the free fatty acids in the cells was found to be enhanced. The radiation effect on the tumor cells could be mimicked by a hypotonic treatment. The magnitude of the radiation-induced stimulation of the fatty acid incorporation was similar to that of the hypotonically induced effect. Cells which had received a hypotonic treatment before the irradiation, did not show an additional radiation-induced enhancement of fatty acid incorporation into the cellular lipids. When the cells were incubated with serum albumin loaded with a relatively large (non-physiological) amount of complexed fatty acids (fatty acid: albumin molar ratio, ν = 3.7 ), no radiation effect on the fatty acid incorporation could be detected. It is concluded that hypotonic treatment, irradiation, and increased supply of exogenous fatty acids all lead to an enhanced flux of fatty acids into the cells. These results confirm our previous suggestion that the uptake of fatty acids through the plasma membrane is the rate-limiting step in the fatty acid incorporation into the phospholipids and that ionizing radiation is one of the means to enhance fatty acid uptake through the plasma membrane leading to an increased incorporation into the phospholipids.

Phenethyl alcohol inhibition of sn-glycerol 3-phosphate acylation in Escherichia coli.

In vivo and in vitro experiments were performed to determine how phenethyl alcohol (PEA) inhibits phospholipid synthesis in Escherichia coli. This drug drastically reduced the rate of incorporation of sn-glycerol 3-phosphate into the phospholipids of an sn-glycerol 3-phosphate auxotroph. PEA also reduced the rate of fatty acid incorporation into the phospholipids of a fatty acid auxotroph. The kinetics of PEA inhibition of the rate of incorporation of sn-glycerol 3-phosphate were almost identical to those of PEA inhibition of the rate of fatty acid incorporation into phospholipids. The in vivo experiments suggested that the rate-limiting step(s) in phospholipid biosynthesis inhibited by PEA is at the level of the acylation of sn-glycerol 3-phosphate or beyond this step. PEA inhibited the sn-glycerol 3-phosphate acyltransferase with either palmitoyl coenzyme A or palmitoyl-acyl carrier protein as the acyl donor. This drug, however, had no effect on the cytidine 5'-diphosphate-diglyceride:glycerol 3-phosphate phosphatidyl transferase, cytidine 5'-diphosphate-diglyceride:L-serine phosphatidyl transferase, and acyl coenzyme A:lysophatidic acid acyltransferase. The in vitro findings suggested that PEA inhibits phospholipid synthesis primarily at the level of sn-glycerol 3-phosphate acyltransferase.

Differences in free fatty acid and glucose metabolism of human blood neutrophils and lymphocytes

Comparison of isolated human neutrophils and lymphocytes in short-term tissue culture revealed marked differences in their rates of lipid biosynthesis. Ficoll-Hypaque gradients were used to separate lymphocytes and neutrophils from the blood of normal subjects. Neutrophils incorporated more palmitate into cell lipids (151.0 +/- 16.6 nmole/hr/10(8) cells) than lymphocytes (41.6 +/- 4.1). By contrast, the lymphocytes oxidized more palmitate (8.3 +/- 0.5 nmole/hr/10(8) cells) as compared to neutrophils (1.1 +/- 0.1). The greater fatty acid uptake by the neutrophils was due to a sixfold greater rate of incoporation of palmitate into their triglyceride fraction. Triglyceride synthesis by neutrophils increased as the molar ratio of free fatty acid to albumin was raised, whereas incorporation into phospholipids remained relatively constant; there was preferential labeling of neutrophil triglycerides throughout the physiologic range. Studies using linoleate and oleate gave similar results. The distribution of radioactivity into various phospholipids determined by thin-layer chromatography was similar for the two cell types. When labeled glucose was used as a substrate to measure incorporation primarily into the glycerol backbone of the cell lipids, neutrophils incorporated more radioactivity into total lipids and triglycerides than lymphocytes. These results indicate that neutrophils take up much more fatty acid than lymphocytes primarily because they synthesize much larger quantities of triglycerides, a storage form. Since cellular triglycerides may act as a source of fatty acid for lecithin synthesis during phagocytosis, the greater rate of fatty acid incorporation in the neutrophil may reflect a metabolic pattern that permits efficient phagocytosis.

Differences in Free Fatty Acid and Glucose Metabolism of Human Blood Neutrophils and Lymphocytes

Abstract Comparison of isolated human neutrophils and lymphocytes in short-term tissue culture revealed marked differences in their rates of lipid biosynthesis. Ficoll-Hypaque gradients were used to separate lymphocytes and neutrophils from the blood of normal subjects. Neutrophils incorporated more palmitate into cell lipids (151.0 +/- 16.6 nmole/hr/10(8) cells) than lymphocytes (41.6 +/- 4.1). By contrast, the lymphocytes oxidized more palmitate (8.3 +/- 0.5 nmole/hr/10(8) cells) as compared to neutrophils (1.1 +/- 0.1). The greater fatty acid uptake by the neutrophils was due to a sixfold greater rate of incoporation of palmitate into their triglyceride fraction. Triglyceride synthesis by neutrophils increased as the molar ratio of free fatty acid to albumin was raised, whereas incorporation into phospholipids remained relatively constant; there was preferential labeling of neutrophil triglycerides throughout the physiologic range. Studies using linoleate and oleate gave similar results. The distribution of radioactivity into various phospholipids determined by thin-layer chromatography was similar for the two cell types. When labeled glucose was used as a substrate to measure incorporation primarily into the glycerol backbone of the cell lipids, neutrophils incorporated more radioactivity into total lipids and triglycerides than lymphocytes. These results indicate that neutrophils take up much more fatty acid than lymphocytes primarily because they synthesize much larger quantities of triglycerides, a storage form. Since cellular triglycerides may act as a source of fatty acid for lecithin synthesis during phagocytosis, the greater rate of fatty acid incorporation in the neutrophil may reflect a metabolic pattern that permits efficient phagocytosis.

Fatty acids incorporation into human adipose tissue in hypertriglyceridaemia.

The fatty acid and glucose incorporation into glycerides and glycerol release from adipose tissue were determined in a middle-aged population of 109 men and 41 women. 43 men and 19 women were normolipidaemic. The same analysis was also carried out in 13 male and 9 female normolipidaemic students. Needle biopsy specimens of adipose tissue were incubated in vitro in an albumin medium containing 3H-fatty acids and 14C-glucose. After two hours of incubation values for fatty acid and glucose incorporation were calculated from the incorporation of 3H-activity into the fatty acids and 14C-activity into the glycerol moiety of extracted glycerides. The mean values for fatty acid incorporation were lower in all types of hypertriglyceridaemic subjects (II B, III, IV and V) than in the normolipidaemic control subjects. In the male hypertriglyceridaemic population 36% had values for fatty acid incorporation below the 5th percentile of the normolipidaemic group and 14% had values below the lowest normal value. The rate of fatty acid incorporation was negatively correlated with the serum triglyceride concentration. This correlation remained unchanged when partial correlation was performed when the influence of body weight was eliminated. Fatty acid and glucose incorporation correlated positively. Incorporation of glucose behaved in the same way as described above for incorporation of fatty acids. Glycerol and fatty acid release was the same in the normo- and hypertriglyceridaemic groups. It is likely that the removal of plasma triglycerides from blood requires hydrolysis of triglycerides to fatty acids and the subsequent removal of the fatty acids. The hypothesis has been formulated that when the former process is normal, a defect of fatty acid removal (a low rate of fatty acid incorporation into glycerides) may be responsible for an impaired removal of plasma triglyceride-fatty acids. A low rate of fatty acid incorporation may contribute to the development of hypertriglyceridaemia, according to this hypothesis.

HEMATOLOGY: Irreversible oxidant injury in the erythrocytes of the newborn infant

It is generally recognized that the red cells of the newborn are more susceptible to injury, i.e. the appearance of Heinz bodies and glutathione instability, upon exposure to oxidant compounds. A more complete examination of the extent and nature of this injury was made. RBC's were incubated for 2 hours with and without glucose in the presence of acetylphenhydrazine (APH) or menadione (K3) and then reincubated in glucose media. Red cell hexokinase, phosphofructokinase, and glyceraldehyde-3-phosphate dehydrogenase activity, all SH containing enzymes, were irreversibly lost in the cells of the newborn when incubated in APH or K3 with no glucose in the medium. The cell's ability to consume glucose was reduced from 50 to 95%. The red cells of adults showed som fall in enzyme activity during drug exposure but full acitivity was restored and red cell glycolysis was unimpaired when reincubated in glucose. Incubation of the cells of the newborn in a carbon monoxide atmosphere during drug exposure prevented their adverse effects. In addition, in the presence of glucose, K3 increased the rate of fatty acid incorporation into adult cells and depressed the rate in newborn cells. Oxidant drugs apparently through alterations in the cells of the newborn and their use in the neonatal period appears contraindicated.

The existence of a long-chain acyl-CoA synthetase in homogenates of human blood platelets.

The presence of a long-chain acyl-CoA synthetase in human platelets is demonstrated. The activity was reproducibly assayed in small samples by the formation of acyl-carnitine from fatty acids, CoA, ATP, and carnitine in the presence of carnitine palmityltransferase. The activity increased with increasing carbon number from C10 to C16, suggesting only one long-chain acyl-CoA synthetase in human platelets. The enzyme is probably localized within the cell membrane as the enzyme was latent in intact platelets. The activity in 22 fasting, healthy individuals was 8 to 23 nmol/min/109 platelets, or about 0.5 to 1.5 U/ml packed cells. The activity is compatible with the activity found in several organs from the rat, and with reported rates of fatty acid incorporation into platelet lipids.

Lysophosphatidylcholine concentrations and metabolism in aortic intima plus inner media: effect of nutritionally induced atherosclerosis

The concentration of lysophosphatidylcholine (monoacyl sn-glycerol 3-phosphorylcholine) in intima plus inner media of atherosclerotic aorta from squirrel monkeys was nearly eight times that in comparable control tissue. Plasma levels of the same compound were somewhat elevated in the atherosclerotic group. The metabolism of fatty acyl CoA's and lysophosphatides was studied in cell-free preparations of intima plus inner media from squirrel monkey aorta. Linoleic acid was incorporated predominantly into phosphatidylcholine (as opposed to other phospholipids) when linoleoyl-1-(14)C CoA was the substrate. The extent of this reaction was dependent on the concentration of lysophosphatidylcholine. Lysophosphatidylethanolamine (monoacyl sn-glycerol 3-phosphorylethanolamine) stimulated the incorporation of linoleate into phosphatidylethanolamine. 1-Palmitoyl-1'-(14)C sn-glycerol 3-phosphorylcholine ((14)C-lysophosphatidylcholine) was incorporated into phosphatidylcholine only in the presence of acyl CoA's or ATP plus CoA. Incorporation of (14)C with (14)C-lysophosphatidylcholine plus linoleoyl CoA equaled that with linoleoyl-1-(14)C CoA and lysophosphatidylcholine. Various other lines of evidence are presented to support the importance of the fatty acyl CoA:lysophosphatide fatty acyl transferase mechanism in aortic phospholipid metabolism. Cell-free preparations of aortic intima plus inner media from squirrel monkeys with early, nutritionally-induced atherosclerosis utilized linoleoyl-1-(14)C CoA more than preparations from control monkeys when incubations were carried out without added lysophosphatidylcholine and for long periods (30 min). With optimum levels of labeled linoleoyl CoA and unlabeled lysophosphatidylcholine, or unlabeled linoleoyl CoA and labeled lysophosphatidylcholine, there were no differences in substrate utilization between control and atherosclerotic tissues. We conclude that the concentrations of lysophosphatidylcholine, which are higher in atherosclerotic than in control aortic tissues, could be a factor controlling rates of fatty acid incorporation into phosphatidylcholine.

Incorporation of fatty acids into phospholipids by cell-free and subcellular fractions of squirrel monkey and rat aorta: Importance of endogenous lysophosphatidylcholine

Summary Mechanisms involved in the incorporation of fatty acids into the phospholipids by cell-free preparations of the intima plus inner media of aorta were studied in the rat and squirrel monkey. Stein et al.8 first demonstrated this activity in cell-free preparations of aorta. The cell-free system used in the present study had an absolute requirement for ATP and CoA and was markedly stimulated (in the incorporation of [1-14C]linoleic acid into phosphatidylcholine) by lysophosphatidylcholine but not by glycerol-3-phosphate. Apparent Michaelis constants for linoleic acid and for lysophosphatidylcholine were determined. The incorporation of fatty acids into different phospholipids and different positions was studied. Linoleic acid was shown to be more efficiently incorporated into phosphatidylcholine than oleic or palmitic acids. There appeared to be competition of the different fatty acids for some common aspect of the enzyme system. The greatest fatty acid-incorporating activity was in the microsomes. Phospholipid, RNA, and protein concentrations of the aortic and liver microsome fractions were compared. Aortic cell-free preparations from squirrel monkeys (Sqimiri sciureus) with atherosclerosis had greater [l-14C]linoleic acid incorporation into aortic phosphatidylcholine than controls when lysophosphatidylcholine was not added. With levels of added lysophosphatidylcholine which resulted in maximum rates of fatty acid incorporation there was no difference in activity between diet groups.

Metabolism of fatty acids in the isolated perfused rat heart

1. 1. Rat hearts were perfused with a medium containing two different radioactive fatty acids, labeled with 14C and 3H, respectively. 2. 2. No preference was found for the extraction from the medium of the following acids tested: palmitic, stearic, oleic and linoleic acid. However, the distribution of these acids in the heart lipids differed. 3. 3. In the neutral lipids of the heart, over 96% of the fatty acids incorporated were found in the triglyceride fraction. In this fraction the incorporation of palmitic acid exceeded that of its competitors: stearic, oleic and linoleic acids. 4. 4. In the phospholipids of the heart, the lecithin fraction contained over 70% of the fatty acids incorporated. Here, stearic and linoleic acid incorporation exceeded that of palmitic acid, while oleic acid was incorporated to a similar extent. 5. 5. In the lecithin molecule labeled linoleic acid was confined practically to the β-position, while labeled palmitic acid was distributed evenly between the α- and β-positions. 6. 6. A faster turnover of linoleic acid than of palmitic acid in the lecithin molecule was suggested by results obtained from perfusing the prelabeled heart without radioactive substrates. The presence of enzyme systems in the myocardium which remove fatty acids from the β-position of lecithin ( i.e., primarily linoleic acid) was demonstrated. 7. 7. The rate of fatty acid incorporation into lipids was independent of the heart beat. 8. 8. Lowering of the surrounding temperature decreased the esterification of palmitic acid into neutral glycerides to a greater extent than into phospholipids.

Metabolism of fatty acids in the isolated perfused rat heart

1. 1. Rat hearts were perfused with a medium containing two different radioactive fatty acids, labeled with 14C and 3H, respectively. 2. 2. No preference was found for the extraction from the medium of the following acids tested: palmitic, stearic, oleic and linoleic acid. However, the distribution of these acids in the heart lipids differed. 3. 3. In the neutral lipids of the heart, over 96% of the fatty acids incorporated were found in the triglyceride fraction. In this fraction the incorporation of palmitic acid exceeded that of its competitors: stearic, oleic and linoleic acids. 4. 4. In the phospholipids of the heart, the lecithin fraction contained over 70% of the fatty acids incorporated. Here, stearic and linoleic acid incorporation exceeded that of palmitic acid, while oleic acid was incorporated to a similar extent. 5. 5. In the lecithin molecule labeled linoleic acid was confined practically to the β-position, while labeled palmitic acid was distributed evenly between the α- and β-positions. 6. 6. A faster turnover of linoleic acid than of palmitic acid in the lecithin molecule was suggested by results obtained from perfusing the prelabeled heart without radioactive substrates. The presence of enzyme systems in the myocardium which remove fatty acids from the β-position of lecithin ( i.e., primarily linoleic acid) was demonstrated. 7. 7. The rate of fatty acid incorporation into lipids was independent of the heart beat. 8. 8. Lowering of the surrounding temperature decreased the esterification of palmitic acid into neutral glycerides to a greater extent than into phospholipids.