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PubMed2001

Docosahexaenoic acid induces apoptosis in Jurkat cells by a protein phosphatase-mediated process.

Docosahexaenoic acid (DHA) is an omega-3 fatty acid under intense investigation for its ability to modulate cancer cell growth and survival. This research was performed to study the cellular and molecular effects of DHA. Our experiments indicated that the treatment of Jurkat cells with DHA inhibited their survival, whereas similar concentrations (60 and 90 microM) of arachidonic acid and oleic acid had little effect. To explore the mechanism of inhibition, we used several measures of apoptosis to determine whether this process was involved in DHA-induced cell death in Jurkat cells. Caspase-3, an important cytosolic downstream regulator of apoptosis, is activated by death signals through proteolytic cleavage. Incubation of Jurkat cells with 60 and 90 microM DHA caused proteolysis of caspase-3 within 48 and 24 h, respectively. DHA treatment also caused the degradation of poly-ADP-ribose polymerase and DNA fragmentation as assayed by flow cytometric TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) assay. These results indicate that DHA induces apoptosis in Jurkat leukemic cells. DHA-induced apoptosis was effectively inhibited by tautomycin and cypermethrin at concentrations that affect protein phosphatase 1 (PP1) and protein phosphatase 2B (PP2B) activities, respectively, implying a role for these phosphatases in the apoptotic pathway. Okadaic acid, an inhibitor of protein phosphatase 2A, had no effect on DHA-induced apoptosis. These results suggest that one mechanism through which DHA may control cancer cell growth is through apoptosis involving PP1/PP2B protein phosphatase activities.

Apoptosis↗
PubMed1977

Inactivation and inhibition of replication of the enveloped bacteriophage phi6 by fatty acids.

The enveloped bacteriophage phi6 has been shown to be an interesting model system for the study of chemical agents that might have specific antiviral effects against lipid-containing mammalian viruses. In this report, we describe two types of antiviral activity exhibited by several fatty acids against bacteriophage phi6. Oleic acid (18:1) and palmitoleic acid (16:1) were potent inactivators of the virus. Treatment with either fatty acid at 50 mug/ml at 25 or 0 degrees C for 30 min reduced the virus titer to about 0.1% of the initial titer. Oleic acid at a concentration as low as 3 mug/ml ( approximately 10(-2) mM) reduced the virus titer to <1% of the initial titer within 30 min. Ultracentrifugation analyses of (14)C-amino acid- and (32)P-labeled virus treated with oleic acid indicated that the virion is largely disassembled by the treatment. Myristic acid (14:0) and palmitic acid (16:0) did not inactivate phi6 at 50 mug/ml, but nevertheless did prevent phi6 plaque production. Single-step virus growth experiments in which fatty acid was added at various times before or after infection indicated that it was an early stage of the phi6 replication cycle that was inhibited by the presence of myristic acid and that the inhibition occurred only if the myristic acid concentration in the extracellular growth medium was greater, similar10 mug/ml. phi6 could attach to its host cell in the presence of myristic acid at 50 mug/ml. We conclude that the fatty acids that prevent phi6 replication probably do so by interfering with the entry of the viral genome into the host cell.

Coliphages↗
PubMed1995

Giant peroxisomes in oleic acid-induced Saccharomyces cerevisiae lacking the peroxisomal membrane protein Pmp27p.

We have purified peroxisomal membranes from Saccharomyces cerevisiae after induction of peroxisomes in oleic acid-containing media. About 30 distinct proteins could be discerned among the HPLC- and SDS-PAGE-separated proteins of the high salt-extracted peroxisomal membranes. The most abundant of these, Pmp27p, was purified and the corresponding gene PMP27 was cloned and sequenced. Its primary structure is 32% identical to PMP31 and PMP32 of the yeast Candida biodinii (Moreno, M., R. Lark, K. L. Campbell, and M. J. Goodman. 1994. Yeast. 10:1447-1457). Immunoelectron microscopic localization of Pmp27p showed labeling of the peroxisomal membrane, but also of matrix-less and matrix containing tubular membranes nearby. Electronmicroscopical data suggest that some of these tubular extensions might interconnect peroxisomes to form a peroxisomal reticulum. Cells with a disrupted PMP27 gene (delta pmp27) still grew well on glucose or ethanol, but they failed to grow on oleate although peroxisomes were still induced by transfer to oleate-containing media. The induced peroxisomes of delta pmp27 cells were fewer but considerably larger than those of wild-type cells, suggesting that Pmp27p may be involved in parceling of peroxisomes into regular quanta. delta pmp27 cells cultured in oleate-containing media form multiple buds, of which virtually all are peroxisome deficient. The growth defect of delta pmp27 cells on oleic acid appears to result from the inability to segregate the giant peroxisomes to daughter cells.

ATP-Binding Cassette Transporters↗
PubMed1990

Effect of eicosapentaenoic acid on triacylglycerol transport in CaCo-2 cells.

The human intestinal cell line, CaCo-2, was used to study the effect of the n-3 fatty acid, eicosapentaenoic acid, on triacylglycerol secretion. In cells incubated with 250 microM eicosapentaenoic acid, the incorporation of [3H]glycerol into triacylglycerols secreted into the medium was decreased by 58% compared to cells incubated with 250 microM oleic acid. The incorporation of [3H]glycerol into cellular triacylglycerols was decreased 32% in cells incubated with eicosapentaenoic acid. In cells preincubated with [3H]glycerol to label existing triacylglycerols, the rates of secretion of preformed triacylglycerols were similar in response to the addition of either fatty acid. Initial uptake rates of the n-3 fatty acid were higher than for oleic acid. Both eicosapentaenoic acid and oleic acid were minimally oxidized to CO2. Oleic acid was predominantly incorporated into cellular triacylglycerols (62% vs. 47%), whereas more eicosapentaenoic acid was incorporated into cellular phospholipids (46% vs. 30%). Phospholipids of microsomes prepared from cells incubated with eicosapentaenoic acid were enriched in this fatty acid. The rate of synthesis of triacylglycerol and diacylglycerol acyltransferase activities were significantly less in microsomes prepared from cells incubated with eicosapentaenoic acid. Triacylglycerol mass secreted by CaCo-2 cells incubated with either fatty acid was similar. In CaCo-2 cells, eicosapentaenoic acid decreases the synthesis and secretion of newly synthesized triacylglycerol without decreasing the secretion of triacylglycerol mass. Modification of microsomal membrane phospholipid fatty acid composition is associated with a decrease in microsomal triacylglycerol synthesis and diacylglycerol acyltransferase activities.

Biological Transport↗
PubMed1979

Reversible effects of fatty acids on respiration, oxidative phosphorylation, and heat production of rat liver mitochondria.

1. Oleic acid at low concentrations (0--70 nmol/mg protein) stimulated mitochondrial state 4 respiration 4-fold, increased the apparent enthalpy change of the respiration per gram atom of oxygen consumed from -112 to -208 kJ/O and completely inhibited ATP synthesis without significant effect on the Mg-ATPase activity of mitochondria. 2. Similar effects on mitochondrial respiratory activities were observed with other fatty acids. 3. Bovine serum albumin (BSA) protected mitochondria from the effects of oleic acid irrespective of the order of addition of oleic acid and BSA to mitochondria. The capacity of BSA to bind oleic acid was calculated to be 3.6--7.1 (mean, 4.9) mol of oleic acid/mol of BSA. 4. The response time of mitochondrial respiration to added oleic acid or BSA was 20--25 s.

Adenosine Triphosphatases↗
PubMed2026

Epithelial-Mesenchymal Transition Shapes the Lipotoxic Response of Colon Cancer Cells to Palmitic Acid.

Saturated fatty acids such as palmitic acid (PA) can induce lipotoxic stress, whereas monounsaturated fatty acids like oleic acid (OA) often promote adaptive responses through lipid droplets (LDs) formation. Here, we reveal that epithelial-mesenchymal transition (EMT) profoundly influences the lipotoxic response of colorectal cancer cells. Using the epithelial-like HCT15 and mesenchymal-like HCT116 cell lines, we combined proteomic, metabolic, and imaging analyses to elucidate how EMT status determines lipid storage capacity and resistance to PA-induced toxicity. A basal proteomic profiling highlighted a striking divergence in metabolic changes: HCT15 cells displayed enhanced glycolysis and reduced expression of LDs biogenesis proteins, while HCT116 cells exhibited oxidative metabolism and a "lipid-rich" proteomic signature enriched in PLIN2, GPAT3, and DGAT1. Functionally, PA triggered massive cytotoxicity and failed to induce LDs in HCT15 cells, correlating with DGAT1/2 downregulation and suppressed triacylglycerol synthesis. In contrast, HCT116 cells showed modest LDs accumulation, preserved mitochondrial function, and strong resistance to lipotoxic stress. OA treatment restored LDs formation and cell viability in both models, underscoring the protective role of unsaturated fatty acids. Notably, forced EMT induction in HCT15 cells by PMA markedly enhanced LDs accumulation and reduced PA-induced death, confirming that EMT confers metabolic plasticity and lipid-buffering capacity. These findings demonstrate that EMT status modulates differential lipid handling and stress adaptation in colon cancer cells, linking mesenchymal transition to enhanced LDs biogenesis and survival under lipotoxic conditions. Data are available via ProteomeXchange with identifier PXD071641.

Humans↗
PubMed2001

Pluronic F-127 gels incorporating highly purified unsaturated fatty acids for buccal delivery of insulin.

The present study investigated the release profiles of insulin from Pluronic F-127 (PF-127) gel containing unsaturated fatty acids such as oleic acid (18:1), eicosapentaenoic acid (20:5) or docosahexaenoic acid (22:6) and the hypoglycemic effect of insulin following the buccal administration of the gel formulations in normal rats. Insulin release from the gels decreased in the presence of unsaturated fatty acids. Remarkable and continuous hypoglycemia was induced by all PF-127 gels (insulin dose, 25 IU/kg) containing unsaturated fatty acids. PF-127 gels containing oleic acid showed the highest pharmacological availability (15.9+/-7.9%). Our finding demonstrate that 20% PF-127 gels containing unsaturated fatty acids are potential formulations for the buccal delivery of insulin.

Animals↗
PubMed1992

Inhibition of steroid 5 alpha-reductase by specific aliphatic unsaturated fatty acids.

Human or rat microsomal 5 alpha-reductase activity, as measured by enzymic conversion of testosterone into 5 alpha-dihydrotestosterone or by binding of a competitive inhibitor, [3H]17 beta-NN-diethulcarbamoyl-4-methyl-4-aza-5 alpha-androstan-3-one ([3H]4-MA) to the reductase, is inhibited by low concentrations (less than 10 microM) of certain polyunsaturated fatty acids. The relative inhibitory potencies of unsaturated fatty acids are, in decreasing order: gamma-linolenic acid greater than cis-4,7,10,13,16,19-docosahexaenoic acid = cis-6,9,12,15-octatetraenoic acid = arachidonic acid = alpha-linolenic acid greater than linoleic acid greater than palmitoleic acid greater than oleic acid greater than myristoleic acid. Other unsaturated fatty acids such as undecylenic acid, erucic acid and nervonic acid, are inactive. The methyl esters and alcohol analogues of these compounds, glycerols, phospholipids, saturated fatty acids, retinoids and carotenes were inactive even at 0.2 mM. The results of the binding assay and the enzymic assay correlated well except for elaidic acid and linolelaidic acid, the trans isomers of oleic acid and linoleic acid respectively, which were much less active than their cis isomers in the binding assay but were as potent in the enzymic assay. gamma-Linolenic acid had no effect on the activities of two other rat liver microsomal enzymes: NADH:menadione reductase and glucuronosyl transferase. gamma-Linolenic acid, the most potent inhibitor tested, decreased the Vmax. and increased Km values of substrates, NADPH and testosterone, and promoted dissociation of [3H]4-MA from the microsomal reductase. gamma-Linolenic acid, but not the corresponding saturated fatty acid (stearic acid), inhibited the 5 alpha-reductase activity, but not the 17 beta-dehydrogenase activity, of human prostate cancer cells in culture. These results suggest that unsaturated fatty acids may play an important role in regulating androgen action in target cells.

5-alpha Reductase Inhibitors↗
PubMed1988

Dietary fat in relation to fatty acid composition of red cells and adipose tissue in colorectal cancer.

Fatty acids were determined in erthrocytes in 49 patients with colorectal cancer and compared with age and sex-matched controls. Marginally increased levels of stearic acid (P = 0.057) and oleic acid (P = 0.064) and decreased arachidonic acid (P = 0.043) occurred in cancer patients. There was no difference in the stearic to oleic acid ratio between the two groups. Dietary intake, assessed by dietary recall and adipose tissue analysis was also not different. In control subjects the polyunsaturated:saturated (P:S) fatty acid ratio correlated between diet and adipose tissue (P less than 0.01, at least). In contrast cancer patients showed different correlations; in particular dietary and erythrocyte P:S fatty acid ratios correlated (P less than 0.01). These findings may indicate disturbed fat metabolism in cancer patients. The erythrocyte stearic to oleic acid ratio is of no diagnostic value.

Adenocarcinoma↗
PubMed1987

Metabolism in humans of cis-12,trans-15-octadecadienoic acid relative to palmitic, stearic, oleic and linoleic acids.

Mixtures of triglycerides containing deuterium-labeled hexadecanoic acid (16:0), octadecanoic acid (18:0), cis-9-octadecenoic acid (9c-18:1), cis-9,cis-12-octadecadienoic acid (9c, 12c-18:2) and cis-12,trans-15-octadecadienoic acid (12c,15t-18:2) were fed to two young-adult males. Plasma lipid classes were isolated from samples collected periodically over 48 hr. Incorporation and turnover of the deuterium-labeled fats in plasma lipids were followed by gas chromatography-mass spectrometry (GC-MS) analysis of the methyl ester derivatives. Absorption of the deuterated fats was followed by GC-MS analysis of chylomicron triglycerides isolated by ultracentrifugation. Results were the following: (i) endogenous fat contributed about 40% of the total fat incorporated into chylomicron triglycerides; (ii) elongation, desaturation and chain-shortened products from the deuterated fats were not detected; (iii) the polyunsaturated isomer 12c,15t-18:2 was metabolically more similar to saturated and 9c-18:1 fatty acids than to 9c,12c-18:2; (iv) relative incorporation of 9c,12c-18:2 into phospholipids did not increase proportionally with an increase of 9c,12c-18:2 in the mixture of deuterated fats fed; (v) absorption of 16:0, 18:0, 9c-18:1, 9c,12c-18:2 and 12c,15t-18:2 were similar; and (vi) data for the 1- and 2-acyl positions of phosphatidylcholine and for cholesteryl ester fractions reflected the known high specificity of phosphatidylcholine acyltransferase and lecithin:cholesteryl acyltransferase for 9c,12c-18:2. These results illustrate that incorporation of dietary fatty acids into human plasma lipid classes is selectively controlled and that incorporation of dietary 9c,12c-18:2 is limited. These results suggest that nutritional benefits of diets high in 9c,12c-18:2 may be of little value to normal subjects and that the 12c,15t-18:2 isomer in hydrogenated fat is not a nutritional liability at the present dietary level.

Adult↗
PubMed1987

Effects of breathing 80% oxygen on water and albumin accumulation in oleic acid-injured rabbit lungs.

This study was done to determine whether breathing 80% oxygen would enhance edema formation in oleic acid (OA) lung injury. Rabbits breathed air (n = 51) or 80% oxygen (n = 51) for 1 to 7 days after OA lung injury (0.09 ml/kg iv). Control groups breathed 80% oxygen (n = 37) or room air (n = 8) without OA injury. Pulmonary vascular permeability was assessed by measuring 131I-albumin (RISA) concentration in extravascular, extracellular lung water (EVECW) relative to plasma (RISAL/RISAPL). EVECW (ml/g dry lung) was measured by 24Na, and total lung water (TLW) by wet/dry weight (g/g dry lung). Air-breathing control values were 4.53 +/- 0.25 (SD) for TLW and 0.40 +/- 0.09 for RISAL/RISAPL. In the air-breathing OA group, TLW and RISAL/RISAPL increased to 8.32 +/- 0.85 and 0.93 +/- 0.16, respectively, 2 h after OA (p less than .001) but by 24 h, were equal to air-breathing controls. TLW and RISAL/RISAPL in the oxygen treated OA group did not differ from the air breathing OA group on days 2 through 7 inclusive, suggesting that 80% oxygen had no effect on edema formation in the OA-injured lung. Breathing 80% oxygen alone, without OA injury, significantly (p less than .005) increased TLW and RISAL/RISAPL on days 5 and 6. Thus, preexisting lung injury had a protective effect against edema formation from a high fraction of inspired oxygen.

Albumins↗
PubMed1983

Influence of dietary lipids on intestinal bile acid absorption.

The enterohepatic circulation and the inability of upper small intestine to actively absorb bile acid are physiological adaptations for maintaining adequate bile acid concentrations in the intestinal lumen for use in lipid digestion and absorption. Certain lipids inhibit bile acid absorption suggesting a possible role of lipids in this scheme. Using isolated intestinal villi preparations of hamster ileum, experiments were conducted to assess the degree of inhibition of bile acid absorption by lipids of various classes and to determine the possible mechanism of inhibition. At an initial bile acid concentration of 10.0 mM, triolein significantly reduced villus uptake of taurocholic acid by 50% and cholic acid by 38%. This inhibition was similar to the degree of inhibition produced by oleic acid (58 and 48%, respectively). Likewise, representative medium-chain and short-chain triglycerides inhibited taurocholic acid uptake by 35 and 39%, respectively. Results show that triglycerides as well as oleic acid inhibit ileal bile acid uptake. Neither oleic acid nor triolein altered bile acid uptake when micelles were absent from incubation solutions. Furthermore, lipids did not alter absorption of a nonmicelle-forming bile acid, taurodehydrocholic acid. These data imply that dietary lipids in general may inhibit intestinal bile acid absorption. Oleic acid significantly reduced the intermicellar bile acid concentration from 8.9 +/- 0.2 mM to 3.9 +/- 0.2 mM while tributyrin, tricaprylin, and triolein had no effect. Results from these studies suggest that the mechanism of inhibition appears to be an enhancement of micelle formation. We speculate that this mechanism may be an additional mechanism for maintaining adequate luminal bile acid concentrations and may be the pathophysiologic mechanism contributing to bile acid malabsorption in cystic fibrosis.

Animals↗
PubMed2001

Pulmonary administration of prostacyclin (PGI2) during partial liquid ventilation in an oleic acid-induced lung injury: inhalation of aerosol or intratracheal instillation?

OBJECTIVE: The purpose of this study was to investigate the effects of aerosolized prostacyclin (A-PGI2) and intratracheally instilled prostacyclin (I-PGI2) during partial liquid ventilation (PLV) on gas exchange and pulmonary circulation in rabbits with acute respiratory distress. DESIGN: Prospective control study. SETTING: A research laboratory at a university medical centre. SUBJECTS: Sixty-nine Japanese white rabbits. INTERVENTION: Lung injury was induced by oleic acid and the animals were divided into five groups of ten each: a mechanical gas ventilation (GV) group, an A-PGI2 group, a PLV group, an A-PGI2+PLV group and an I-PGI2+PLV group. PLV, A-PGI2+PLV and I-PGI2+PLV groups received 15 ml/ kg perflubron intratracheally while receiving mechanical GV. A-PGI2 and A-PGI2+PLV groups received aerosolized PGI2 (50 ng/kg/min) in combination with GV or PLV, respectively. The I-PGI2+PLV group was instilled 50 ng/kg/min PGI2 intratracheally in combination with PLV. RESULT: After lung injury, all animals developed hypoxia, hypercarbia and pulmonary hypertension. The improvement of partial pressure of arterial oxygen (PaO2) in the A-PGI2 and PLV groups was transient, whereas the A-PGI2+PLV and I-PGI2+PLV groups showed consistent improvement throughout the experiment. The PaO2 values of the I-PGI2+PLV group were significantly higher than those of the other groups 120 min after treatment. The mean pulmonary artery pressure (PAP) significantly decreased after treatment in the A-PGI2, APGI2+PLV and I-PGI2+PLV groups. CONCLUSIONS: The results suggest that both aerosolized and intratracheally instilled PGI2 improve oxygenation and reduce PAP during PLV in oleic acid lung injury.

Administration, Inhalation↗
PubMed1982

Fatty acid requirement of Treponema denticola and Treponema vincentii.

Treponema denticola and Treponema vincentii were cultured in a medium supplemented with either 0.2 or 0.4% (w/v) alpha globulin in place of serum. The active factor(s) in alpha globulin was stable at pH 7.0 to autoclaving and was nondialyzable. Extraction of lipids from alpha globulin showed that both protein and lipid, supplied by the alpha globulin, were required for maximal growth of these two oral treponemes. The lipid component was investigated by adding sodium salts of long-chain fatty acids to the basal medium supplemented with 0.4% delipified alpha globulin. The lipid component of alpha globulin was replaced by either oleic acid (cis-18:1(9)) or by elaidic acid (trans- 18:1 (9)0. No other saturated or unsaturated fatty acid tested could support good growth. Tween 80 (polysorbitan monooleate) was the only Tween compound able to support maximal growth of T. denticola. The cellular lipids of T. denticola, grown with oleate in broth supplemented with 0.4% delipified alpha globulin, were extracted and analyzed by gas chromatography. The principle fatty acids were myristic, pentadecanoic, and palmitic acids. Lesser amounts of oleic acid, eicosadienoic acid, and an unidentified fatty acid (retention time, 88 min) were also detected. Treponema denticola appears to be capable of limited synthesis of cellular fatty acids such as myristic, pentadecanoic, and palmitic acids from oleic acid.

Alpha-Globulins↗
PubMed1985

Synthesis and biological assessment of long-acting estradiol fatty acid esters in ovariectomized rats.

Diesters of 17 beta-estradiol using palmitic acid (16:0) and oleic acid (18:1, cis-9-Octadecenoic acid) have been synthesized for potential evaluation as long-acting compounds. Female castrated rats were injected 1 mumol of estradiol dipalmitate and estradiol dioleate, using estradiol benzoate and estradiol enanthate as controls. Biological activity was determined by uterine wet weight and uterine diameter as well as on the suppression of serum anterior pituitary gonadotropins. A delayed absorption of estradiol was observed after administration of both diesters which was well correlated with the duration of biological effects. The data demonstrate that esterification with palmitic or oleic acids at 3 and 17 positions provides long-acting properties to 17 beta-estradiol, which could be applied in substitutive therapy and or in hormonal contraception.

Animals↗
PubMed2000

Ligand-dependent interaction of hepatic fatty acid-binding protein with the nucleus.

Our studies were conducted to explore the role of hepatic fatty acid-binding protein (L-FABP) in fatty acid transport to the nucleus. Purified rat L-FABP facilitated the specific interaction of [(3)H]oleic acid with the nuclei. L-FABP complexed with unlabeled oleic acid decreased the nuclear association of [(3)H]oleic acid:L-FABP; however, oleic acid-saturated bovine serum albumin (BSA) or fatty acid-free L-FABP did not. The peroxisome-proliferating agents LY171883, bezafibrate, and WY-14,643 were also effective competitors when complexed to L-FABP. Nuclease treatment did not affect the nuclear association of [(3)H]oleic acid:L-FABP; however, proteinase treatment of the nuclei abolished the binding. Nuclei incubated with fluorescein-conjugated L-FABP in the presence of oleic acid were highly fluorescent whereas no fluorescence was observed in reactions lacking oleic acid, suggesting that L-FABP itself was binding to the nuclei. The nuclear binding of FABP was concentration dependent, saturable, and competitive. LY189585, a ligand for L-FABP, also facilitated the nuclear binding of fluorescein-conjugated L-FABP, although it was less potent than oleic acid. A structural analog that does not bind L-FABP, LY163443, was relatively inactive in stimulating the nuclear binding. Potential interactions between L-FABP and nuclear proteins were analyzed by Far-Western blotting and identified a 33-kDa protein in the 500 mm NaCl extract of rat hepatocyte nuclei that bound strongly to biotinylated L-FABP. Oleic acid enhanced the interaction of L-FABP with the 33-kDa protein as well as other nuclear proteins. We propose that L-FABP is involved in communicating the state of fatty acid metabolism from the cytosol to the nucleus through an interaction with lipid mediators that are involved in nuclear signal transduction.

Acetophenones↗
PubMed1997

Apolipoprotein secretion and lipid synthesis: regulation by fatty acids in newborn swine intestinal epithelial cells.

The IPEC-1 newborn swine intestinal epithelial cell line was used to determine the effects of the uptake of various fatty acids on the secretion of apolipoprotein (apo) B and apo A-I, as well as triglyceride and phospholipid. Long-chain saturated fatty acids were taken up and stimulated triglyceride synthesis, and palmitic (16:0) and stearic (18:0) acids also stimulated phospholipid synthesis. However, these fatty acids did not enhance triglyceride, phospholipid, or apo B or apo A-I secretion. Oleic acid (18:1) was the most effective of all fatty acids tested in stimulating triglyceride synthesis and the secretion of triglyceride, phospholipid, and apo B. Linoleic (18:2) and linolenic (18:3) acids were no more effective than long-chain saturated fatty acids in stimulating these processes. With saturated fatty acids, apo A-I followed the same secretory pattern as apo B. However, among the unsaturated fatty acids, oleic acid was the least effective and linolenic acid was the most effective in stimulating apo A-I secretion. Basolateral secretion of lipid and apolipoproteins by differentiated IPEC-1 cells is differentially regulated by apical exposure to fatty acids.

Animals↗