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PubMed1967

Utilization of endogenous lipid by the isolated perfused rat heart.

1. The lipids of the rat heart have been studied with regard to amount, classes present and fatty acid composition of free fatty acids, triglycerides and phospholipids. Myocardial lipid contained 300mumoles of total fatty acid/g. dry wt. of which only 2-4mumoles were free; the remainder was esterified, chiefly as phospholipid. Neutral esters, of which triglyceride was the principal form, made up 15% of the total fatty acids. 2. When normal hearts were perfused with a nutrient-free medium until exhaustion, the triglyceride concentration declined from 43 to 13mumoles/g. dry wt. The content of phospholipids, partial glycerides and cholesteryl esters did not change. When the lipids of the rat heart were labelled with [1-(14)C]palmitate before perfusion with non-nutrient medium, radioactivity disappeared from the triglyceride, diglyceride and free fatty acid fractions, but not from the phospholipid or other ester classes. 3. These experiments support the view that only a small fraction of the total cardiac lipid, principally triglycerides and to a smaller extent diglycerides, is available as a source of fuel in the absence of exogenous substrate.

Animals↗
PubMed1970

The sensitivity of acetyl-coenzyme A carboxylase to citrate stimulation in a homogenate of rat liver containing subcellular particles.

1. Although citrate is known to activate purified preparations of acetyl-CoA carboxylase, it had no stimulatory effect on the incorporation of [(14)C]acetate into long-chain fatty acids in a whole homogenate of rat liver (S(0.7)) under conditions in which the activity of acetyl-CoA carboxylase was rate-limiting for fatty acid synthesis. 2. The rate of incorporation of acetyl carbon into fatty acids was estimated in S(0.7) preparations incubated with [(14)C]acetate, by measuring the specific radioactivity of the acetyl carbon of acetyl-CoA and the incorporation of (14)C into fatty acids. These estimates were compared with estimates of acetyl-CoA carboxylase activity in the S(0.7) preparation obtained by direct assay in conditions in which the enzyme was in the fully activated state. 3. In the absence of citrate, incorporation of acetyl carbon into fatty acids was about 75% of the value expected if the acetyl-CoA carboxylase in the S(0.7) preparation were in the fully activated state. 4. Incorporation of acetyl carbon into fatty acids in the S(0.7) preparation was stimulated by citrate, but the effect was many times less than the stimulation of [(14)C]acetate incorporation by citrate in particle-free preparations. 5. When the mitochondria and microsomes were removed from the S(0.7) preparation, [(14)C]acetate incorporation into fatty acids fell to a negligible value and the preparation became highly sensitive to stimulation by citrate. 6. It is suggested that in the presence of mitochondria and microsomes, and in the intact liver cell, the degree of activation of acetyl-CoA carboxylase is such that citrate activation may not be of physiological significance.

Acetates↗
PubMed1986

Fluxes through the prokaryotic and eukaryotic pathways of lipid synthesis in the '16:3' plant Arabidopsis thaliana.

The kinetics of [1-14C]acetate incorporation in Arabidopsis thaliana L. (Heyn) showed almost equal labelling of phosphatidylcholine (PC) and diacylgalactosylglycerol (DGG) at early times and the transfer of radioactivity from PC to DGG and diacyldigalactosylglycerol (DDG) at longer times. These kinetics demonstrated the parallel operation of the prokaryotic and eukaryotic pathways of lipid synthesis [Roughan & Slack (1982) Annu. Rev. Plant Physiol. 33, 97-132] in this tissue. At 2 h after the application of [1-14C]acetate, more than 85% of the radioactivity at the sn-2 position of each chloroplast lipid was in 16-carbon fatty acids. However, after 60 h, molecular species containing labelled C18 fatty acids at position sn-2 and presumably derived from microsomal PC made a large contribution (20-70%) to each chloroplast lipid except phosphatidylglycerol. These findings are consistent with the contention that the chain length of the fatty acid at the sn-2 position of glycerol is an accurate predictor of whether a particular lipid molecule has been synthesized by the prokaryotic or eukaryotic pathway. At 30 min after the start of [1-14C]acetate labelling, only 12.3% of the radioactivity in PC was in saturated fatty acids, but the proportion increased steadily to 24.3% after 142 h. It is suggested that steps involved in the conversion of PC to chloroplast lipids on the eukaryotic pathway discriminate against palmitate-containing species. The step involved does not appear to be transfer of PC to the chloroplast because extrachloroplastic and chloroplast membranes purified from Arabidopsis mesophyll protoplasts each contained PC with a fatty acid composition similar to that of the same lipid from leaves. Positional analysis of unlabelled lipids, together with the information summarized above, is used to construct a quantitative scheme of the fluxes through the prokaryotic and eukaryotic pathways during lipid synthesis in Arabidopsis. This scheme shows that 38% of the fatty acids synthesized de novo in the chloroplast enter the prokaryotic pathway in the chloroplast envelope. Of the 62% which are exported as acyl-CoA species to enter the eukaryotic pathway, 56% (34% of the total) are returned to complete synthesis of the chloroplast's complement of glycerolipids.

Acetates↗
PubMed1978

Studies in Tetrahymena membranes substrates for desaturation of fatty acyl chains in Tetrahymena pyriformis microsomes.

[1-14-C]Palmitoyl-Co A was incubated with Tetrahymena microsomes containing the complete enzyme system for desaturation during various time periods. The level of [1-14C]palmitoleoyl-CoA increased to a maximum during the 1--3 min incubation time, while [1-14C]palmitoleic acid in the phospholipid reached a maximum level during 6--7 min incubation time. The radioactivity of [1-14C]palmitoleic acid in free fatty acid and the triglyceride fraction was not significantly observed upon 3 min incubation. Incubation of [1-14C]palmitoyl-CoA with microsomes in the absence of NADH produced [1-14C]palmitoyl lipid without desaturation. Radioactive palmitic acids in the microsomal lipids were not converted to palmitoleic acids after addition of NADH by the complete enzyme system. When microsomes prepared from cells labeled with [1-14C]palmitic acid or [1-14C]stearic acid were incubated alone in the presence of O2 and NADH, no significant increase in [1-14C]palmitoleic acid in the phospholipid was observed, wherease an increase in [1-14C]linoleic acid and gamma-[1-14C]linolenic acid did occur at the expense of [1-14C]oleic acid in the phospholipid. From these results it can be concluded that the enzyme involving desaturation of palmitic acid to palmitoleic acid requires palmitoyl-CoA as the substrate. However, the possibility of oleoyl and linoleoyl phospholipids being substrates in the desaturation of Tetrahymena microsomes was suggested.

Acyl Coenzyme A↗
PubMed1981

Fatty acid metabolism in phorbol ester-differentiating human leukemia cells.

Human promyelocytic leukemia cells (HL-60) undergo differentiation when treated with the tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA). As the primary target for TPA action is membranes, studies were undertaken to determine whether phorbol ester exposure would influence fatty acid metabolism in these cells. In cells incubated with labeled fatty acids for 1 hr, the percentage of distribution of lipid radioactivity is highest in the phospholipid fraction of control cultures, whereas in TPA-supplemented cells, substantially more label is associated with triacylglycerols. The specific activity of phospholipids and triacylglycerols was lower in treated than in control cells; however, the amount of cellular triacylglycerols increased 3.2-fold (lipid per mg protein). The increase in the amount of cellular phospholipids in TPA-treated cells is not as pronounced (approximately 50% above control), and this only occurs at higher concentrations of TPA. At early times after TPA exposure, there is no stimulation of the cellular uptake of labeled fatty acids; however, differentiating cells (24 to 48 hr of TPA), when incubated with label, contained more radioactivity than did control cultures. Cells treated with TPA for 48 hr show a marked decrease in the conversion of [1-14C]stearic acid to monoenoic product (22% of control); this decrease is dose dependent and occurs within 24 to 48 hr of treatment. Although the phospholipid fatty acid composition of differentiating cells was similar to control cells, acyl groups of triacylglycerols isolated from treated cells showed a marked decrease in the percentage of unsaturates. These data provide evidence which demonstrates that TPA treatment of HL-60 cells has a profound effect on fatty acid metabolism. The lack of an effect of TPA on fatty acid metabolism after short-term exposure to the promoter suggests that the modifications observed may be the result of cellular differentiation rather than a direct effect exerted by the presence of TPA in the culture media.

Carcinogens↗
PubMed1985

Enhanced utilization of 14-methylhexadecanoic acid for the synthesis of lipids during the growth of Walker 256 carcinoma in rats.

Labeled 14-methylhexadecanoic acid was administered to normal rats, animals bearing the Walker 256 tumor at various stages of its growth and to tumor-resistant rats and its distribution in lipids (free fatty acids, triglycerides, phospholipids and cholesteryl esters) was studied during 15 min to 3 hours following its injection in the liver, blood and tumor tissue. The period of the most active tumor growth was associated with a significantly better utilization of this fatty acid for the synthesis of lipids. The quantities of radioactive triglycerides, phospholipids and cholesteryl ester in the liver were highly increased during this time. In tumor-resistant animals the levels of radioactive lipids were similar to those in control normal animals but the turn-over of 14-methylhexadecanoic acid was considerably slower than in controls. The turn-over of the cholesteryl 14-methylhexadecanoate in the liver was significantly changed at the late stages of the tumor growth. The level of this cholesteryl ester in the blood decreased progressively during the tumor growth whereas that of triglycerides increased. No significant changes were associated with the free fatty acid and phospholipids in the blood. The total radioactivity present in the tumor increased from 0.05% up to nearly 1% of the administered 14-methylhexadecanoic acid during the growth of the Walker 256 tumor. The level of radioactive cholesteryl 14-methylhexadecanoate in the tumor tissue increased progressively during 3 hours following the injection of 14-methylhexadecanoic acid. Thus the tumor growth is apparently accompanied by significant changes in the metabolism of 14-methylhexadecanoic acid and results in an enhanced synthesis of lipids in the liver tissue. The newly synthesized lipids, in particular cholesteryl 14-methylhexadecanoate, are transported in the blood stream into the tumor where they accumulate.

Animals↗
PubMed1969

Phospholipid metabolism during bacterial growth.

Haemophilus parainfluenzae incorporates glycerol and phosphate into the membrane phospholipids without lag during logarithmic growth. In phosphatidyl glycerol (PG), the phosphate and unacylated glycerol moieties turn over and incorporate radioactivity much more rapidly than does the diacylated glycerol. At least half the radioactivity is lost from the phosphate and unacylated glycerol in about 1 doubling. The total fatty acids turn over slightly faster than the diacyl glycerol. In phosphatidyl ethanolamine (PE), which is the major lipid of the bacterium, ethanolamine and phosphate turn over and incorporate radioactivity at least half as fast as the phosphate in PG. The glycerol of PE did not turn over in 4 bacterial doublings. In phosphatidic acid the glycerol turns over at one-third the rate of phosphate turnover. By means of a modified method for the quantitative recovery of 1,3-glycerol diphosphate from cardiolipin, the phosphates and middle glycerol of cardiolipin were shown to turn over more rapidly than the acylated glycerols during bacterial growth. There is no randomization of the radioactivity in the 1- and 3-positions of the glycerol in the course of 1 doubling. The fatty acids of PG turn over faster than those in PE. In both lipids the 2-fatty acids turn over much faster than the 1-fatty acids. At both positions the individual fatty acids have their own rates of turnover. The distribution of fatty acids between the 1- and 2-positions is the same as in other organisms, with more monoenoic and long-chain fatty acids at the 2-position. The different rates of turnover and incorporation of radioactivity into different parts of the lipids suggest that exchange reactions may be important to phospholipid metabolism.

Amino Alcohols↗
PubMed1982

Isolation and characterization of an acyl carrier protein from pigeon liver fatty acid synthetase by controlled proteolysis with elastase.

Controlled proteolytic cleavage of 4'-phospho[14C]pantetheine-labeled pigeon liver fatty acid synthetase generates two 4'-phospho[14C]pantetheine-labeled peptides, Ec1 and Ec2. These are separated from each other and the core enzyme by gel permeation chromatography on a Sephadex G-75 column. The two radioactively labeled peptides constitute 50% of the radioactivity initially present in the 4'-phospho[14C]pantetheine-labeled fatty acid synthetase. The remaining label in the core enzyme is released quantitatively by proteolytic cleavage with trypsin. The molecular weights of Ec1 and Ec2 peptides, as determined by size exclusion chromatography and SDS-polyacrylamide gel electrophoresis, are 12000 and 6000, respectively. Both the higher and lower molecular weight peptides are homogeneous with respect to size and charge, as shown by polyacrylamide gel electrophoresis in the presence and absence of SDS. The higher molecular weight peptide, Ec1, is characterized as an acyl carrier protein by the transacylation reaction between the unlabeled Ec1 peptide and radioactively labeled acetyl- and malonyl-CoA. Since Ec2 peptide also contains the prosthetic group present in the Ec1 peptide, the Ec2 peptide appears to result from the proteolytic cleavage of the higher molecular weight peptide, Ec1. Amino acid composition of the acyl carrier protein shows the presence of 1 mol of 4'-phosphopantetheine per mol of protein. 2 mol of acyl carrier protein are present per mol of the fatty acid synthetase. The amino acid analysis is in good agreement with the molecular weight of the Ec1 peptide, as determined by gel filtration and SDS-polyacrylamide gel electrophoresis. N-Terminal amino acid analysis of this peptide shows the presence of an arginine residue.

Acyl Carrier Protein↗
PubMed1982

The modulating influence of vitamin E in biological membrane unsaturated phospholipid metabolism.

A tissue culture system in which the composition of the medium, with respect to vitamin E, linoleic acid, and cholesterol, can be manipulated at will, was used to study the effect of vitamin E on the fatty acid profiles of fibroblast membrane phospholipids. The effect was studied of alpha-tocopherol, and of butylated hydroxytoluene, on the uptake of isotopically labeled linoleic acid and cholesterol, and of the effect of these antioxidants on the metabolic interconversion of linoleic acid with other unsaturated fatty acids. Butylated hydroxytoluene was without effect on any of the parameters measured, alpha-tocopherol caused a large enhancement in the content and radioactivity of the arachidonyl residues of phosphatidyl choline, phosphatidyl serine, and phosphatidyl ethanolamine, generally at the expense of linoleic acid in the same phospholipids. There was no effect of alpha-tocopherol on the unsaturated fatty acids of the neutral lipids, suggesting that there was no general effect on the chain elongation and desaturation of linoleic acid. The results are thought to demonstrate a specific effect of alpha-tocopherol upon the architecture of membrane phospholipids by controlling the profiles of their unsaturated fatty acid components. The uptake of radioactive cholesterol, and the content of cholesterol and cholesterylesters in cultured cells was also significantly increased by the presence of alpha-tocopherol in the medium.

Animals↗
PubMed1990

In vivo utilization of D(-)-3-hydroxybutyrate by chick brain and spinal cord.

The in vivo utilization of D-3-hydroxy[3-14C]butyrate for oxidation in the whole animal and for lipid and amino acid synthesis in brain and spinal cord of overnight-fasted 15-day-old chicks has been measured. Appreciable amounts of injected 3-hydroxy[3-14C]butyrate were expired as 14CO2 one hour after injection, the total amount of which increased with increasing dosages. Lipid synthesis was high in both brain and spinal cord. Free cholesterol and phospholipids were the main lipids labeled in both tissues, increasing with time after injection up to 120 min. The incorporation of radioactivity into triglycerides, esterified cholesterol and free fatty acids was not time-dependent. Increased concentrations of 3-hydroxybutyrate gave rise to higher synthetic rates both in brain and spinal cord. The rate of amino acid synthesis was slightly higher in brain than in spinal cord. Glutamate was always the major amino acid formed.

3-Hydroxybutyric Acid↗
PubMed1975

Electron microscope autoradiographic study of intestinal absorption of decanoic and octanoic acids in the rat.

Intestinal absorption of [3H]octanoic acid and [3H]decanoic acid was investigated in the rat by electron microscope autoradiography. The common duct (bile and pancreatic common duct) of the rats was diverted and a loop of the duodenum was cannulated 24 h later. The lipid mixture to be investigated was introduced into each experimental loop, and after 15 min or less the loop was removed. One part of each loop was used to determine the distribution of radioactivity in different lipid fractions, and an autoradiographic study was performed on the other part of the loop. Radioactivity distribution studies confirmed that medium chain fatty acids are absorbed in their nonesterified form and established that these fatty acids are absorbed much more rapidly than oleic acid. Autoradiographic studies indicated that the medium chain fatty acids are taken up in a molecular or aggregate molecular form, leave the epithelial cells by way of the lateral plasma membrane, and are next found in the blood capillaries. Our results suggest that the Golgi complex does not play an important role in the absorption of unesterified fatty acids.

Animals↗
PubMed1993

Medium-chain fatty acid oxidation in colostrum-deprived newborn piglets: stimulative effect of L-carnitine supplementation.

To investigate the role of L-carnitine in medium-chain fatty acid (MCFA, fatty acids with 6-12 carbons) metabolism, 16 newborn pigs were fitted with umbilical arterial catheters. Pigs were placed in respiration chambers, and [1-14C]MCFA were infused for 9-12 h providing energy equivalent to 50-175% of the animals' metabolic rate. After 5-7 h (carnitine-free infusion period) of MCFA infusion, a primed (12.5, 25 or 50 mumol) co-infusion of L-carnitine [5, 10 or 20 mumol/(h.kg0.75), respectively] was started and maintained for 4-5 h (carnitine infusion period). The fatty acid oxidation rate (MCFA-derived CO2/total CO2 x 100) was calculated based on the specific radioactivity of expired CO2 (measured per 20-min interval) and the specific radioactivity of the MCFA infused. A single-pool exponential curve was fitted to the fatty acid oxidation rate of the carnitine-free infusion period and was extrapolated to the carnitine infusion period. For each piglet, the average difference between fatty acid oxidation rate during the carnitine infusion period and the extrapolated curve was calculated and tested for significance using a t test. Under steady state conditions, MCFA oxidation accounted for 40% of MCFA infused. Carnitine, independent of the level, increased the fatty acid oxidation rate by as much as 20% if the energy provided as MCFA exceeded 50% of the metabolic needs of the pig (P < 0.01), and the response above 50% was proportional to the relative rate of fatty acid infusion (increase in fatty acid oxidation rate = -3.9 + 0.07 x infusion rate, r0.76).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Serum phospholipases A2 in inflammatory diseases.

Phospholipase A2 (EC 3.1.1.4; PLA2) is detected in serum by determination of either the catalytic activity of the enzyme or the concentration of the enzyme protein by immunoassays. The most sensitive methods for determining PLA2 catalytic activity are radiometric assays, with a substrate of synthetic phospholipid (e.g., phosphatidylcholine or phosphatidylethanolamine) containing a 14C- or 3H-labeled fatty acid at the sn-2-position. Membranes of autoclaved Escherichia coli grown in the presence of radioactive oleic acid may also be used as a substrate. The released fatty acids are separated from the unreacted substrate and quantified by liquid scintillation counting. PLA2 catalytic activities are increased in serum in sepsis, acute pancreatitis, peritonitis, multiple injuries, rheumatoid arthritis, and other arthropathies. Immunoassays--radioimmunoassay, enzyme-linked immunosorbent assay, or time-resolved fluoroimmunoassay--are based on the use of either polyclonal or monoclonal antibodies to purified PLA2s. Specific assays have been developed for both pancreatic group I PLA2 (PLA2-I) and nonpancreatic group II PLA2 (PLA2-II). The cellular source of PLA2-I in serum is the pancreatic acinar cell. Increased serum PLA2-I values have been reported in acute pancreatitis, pancreatic cancer, and abdominal trauma. Increased PLA2-II values are found in conditions involving inflammation, e.g., sepsis, infections, acute pancreatitis, various forms of arthritis, cancer, complications of pregnancy, and postoperative states. Good correlations have been found in serum samples between the catalytic activity of PLA2 and the concentration of PLA2-II but not PLA2-I. PLA2-II may represent an acute-phase protein. The cellular source of the PLA2-II in serum is unknown; it is present in large amounts in cartilage and Paneth cells, prostatic gland cells, seminal fluid, lacrimal gland cells, and tears, but cannot be demonstrated by immunohistochemical or immunochemical methods in inflammatory cells.

Humans↗
PubMed1984

Gastric handling of medium-chain triglycerides and subsequent metabolism in the suckling rat.

We have previously shown that preduodenal lipases account for 50% of the lipolytic capacity of 14-day-old rats. The present investigation was designed to study the kinetics of and optimal conditions for absorption of fat in the stomach of suckling rats and its subsequent distribution in the body. After the simultaneous instillation of medium-chain triglycerides (MCT) containing 1.25 microCi 2,3-[3H]trioctanoate and of long-chain triglycerides containing 1.25 microCi 1-[14C]glycerol trioleate into the stomach ligated at the pylorus, we were able to show that gastric absorption of fat is limited to MCT. Two and a half minutes after injection, 88.6% of the radioactivity in the wall of the stomach was associated with free fatty acids, proving that lipolysis had preceded the absorption of the majority of the MCT. The remainder of the radioactivity was found in mono-, di-, and triglycerides as well as with cholesterol ester and phospholipids. In the plasma, peak radioactivity was attained within 2.5 min and a steady state ensued which lasted at least 30 min. Over this time period, specific radioactivity continued to rise in the liver, suggesting that hepatic uptake proceeded at the same rate as gastric absorption. Uptake could also be demonstrated in the three other organs tested, the lungs, the heart, and the kidneys. Absorption of MCT at pH 3 was only 20% of absorption at pH 6, which is the physiological pH in the suckling rat stomach within the first 10 min after a feed. Both at pH 3 and at pH 6, the addition of sodium taurocholate increased absorption of MCT over threefold. It is likely that the absorption of MCT by the stomach is a physiological event in the suckling rat.

Absorption↗
PubMed1978

The role of holotrichs in the metabolism of dietary linoleic acid in the rumen.

The uptake and metabolism of linoleic acid by rumen holotrichs (mainly Isotricha prostoma and I. intestinalis) has been examined in in vitro infusion experiments. Maximum absorption and metabolism of [1-14C]linoleate by 2 . 10(6) Isotricha suspended in 100 ml buffer was obtained using an infusion rate of 1.6 mg linoleate/h. After 90 min, 84% of the added substrate was recovered within the cells, mainly as free fatty acid or phospholipid. There was a rapid incorporation of radioactivity into phospholipid, mainly phosphatidylcholine, at the commencement of linoleate infusion but no further incorporation after about 40 min. The presence of bacteria during incubations, in approximately the same Isotricha/bacteria ratio as found in the rumen, reduced the uptake of linoleate and the accumulation of free fatty acid by holotrichs but the incorporation into phospholipid remained similar to that obtained in the absence of bacteria. Very little biohydrogenation of linoleic acid occurred in incubations with holotrichs alone. Bacterial suspensions converted linoleic acid to mainly trans monoene and a small amount of stearic acid, but in incubations containing both bacteria and holotrichs, both stearic acid and trans monoene were major products. Using the latter mixed culture, about 20% of the added [1-14C]linoleic acid was present in holotrich phospholipid of which 62% remained as octadecadienoic acid. The Isotricha population was 3 . 10(3)--2 . 10(4)/ml rumen fluid and it contributed about 23% of the linoleic acid in the rumen of a cow on a hay diet.

Animals↗
PubMed2000

Extracellular release of free fatty acids by rat T lymphocytes is stimulus-dependent and is affected by dietary lipid manipulation.

[(3)H]-Arachidonic acid-labelled rat T lymphocytes released radioactivity extracellularly when stimulated by the calcium ionophore A23187 or by monoclonal antibodies to some cell surface structures (CD2, CD5, CD11a, CD18, CD54, T-cell receptor) but not to others (CD49d, CD62L); release was greater with the calcium ionophore. Almost all of the radioactivity released from anti-CD2-stimulated lymphocytes was recovered in the free fatty acid fraction, whereas only about 50 per cent of that released after A23187 stimulation was recovered in this fraction. A23187 stimulation resulted in release of arachidonic acid from a variety of phospholipids (phosphatidylinositol, phosphatidylcholine and perhaps phosphatidylethanolamine), while the monoclonal antibody stimulation released arachidonic acid from phosphatidylinositol and perhaps phosphatidylcholine. Unstimulated lymphocytes released a range of fatty acids extracellularly, with palmitic acid accounting for 35-40 per cent and arachidonic acid for 5 per cent of released fatty acid. Stimulation of lymphocytes with either anti-CD2 or A23187 increased total fatty acid release 1.5- to 1.8-fold. In both cases palmitic acid remained the most predominant fatty acid released but the contribution of arachidonic acid increased. The type of lipid fed to the rats significantly influenced the amount and type of fatty acid released. Fish oil feeding significantly reduced extracellular fatty acid release by stimulated lymphocytes.

Animals↗
PubMed1973

Fat absorption in essential fatty acid deficiency: a model experimental approach to studies of the mechanism of fat malabsorption of unknown etiology.

Male rats were made deficient in essential fatty acids by feeding them a fat-free diet supplemented with 4% tripalmitin for 8-12 wk from the time of weaning. After feeding 0.5 ml of [(14)C]triolein or [(3)H]oleic acid, 72-hr stool recoveries of radioactivity were significantly greater in deficient rats than in chow-fed controls. Essential fatty acid deficiency did not reduce the absorptive capacities for triolein or for a medium-chain fat, trioctanoin, measured after 3 and 2 hr of maximal-rate duodenal infusion. In everted jejunal slices from essential fatty acid-deficient rats, uptake of micellar [(14)C]oleic acid at 0-1 degrees C was similar to that of controls, but the rate of incorporation of fatty acid into triglyceride after rewarming to 37 degrees C was significantly reduced. The specific activities of the microsomal esterifying enzymes, acyl CoA:monoglyceride acyltransferase and fatty acid CoA ligase in jejunal mucosa were 30% lower in essential fatty acid-deficient rats. However, the total microsomal enzyme activity adjusted to constant weight did not differ significantly in deficient rats compared with controls. After intraduodenal perfusion of triolein, accumulation of lipid in the intestinal wall was increased in the deficient rats. Because over 90% of the absorbed mucosal lipid was present as triglyceride, essential fatty acid deficiency appears to affect the synthesis or release of chylomicron lipid from the intestine. Analysis of regions of intestine showed that this delay in transport was most marked in the midportion of the small intestine.

Acyltransferases↗