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Cellular differentiation and I-FABP protein expression modulate fatty acid uptake and diffusion.

The effect of cellular differentiation on fatty acid uptake and intracellular diffusion was examined in transfected pluripotent mouse embryonic stem (ES) cells stably expressing intestinal fatty acid binding protein (I-FABP). Control ES cells, whether differentiated or undifferentiated, did not express I-FABP. The initial rate and maximal uptake of the fluorescent fatty acid, 12-(N-methyl)-N-[(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-octadec anoic acid (NBD-stearic acid), was measured in single cells by kinetic digital fluorescence imaging. I-FABP expression in undifferentiated ES cells increased the initial rate and maximal uptake of NBD-stearic acid 1.7- and 1.6-fold, respectively, as well as increased its effective intracellular diffusion constant (Deff) 1.8-fold as measured by the fluorescence recovery after photobleaching technique. In contrast, ES cell differentiation decreased I-FABP expression up to 3-fold and decreased the NBD-stearic acid initial rate of uptake, maximal uptake, and Deff by 10-, 4.7-, and 2-fold, respectively. There were no significant differences in these parameters between the differentiated control and differentiated I-FABP-expressing ES cell lines. In summary, differentiation and expression of I-FABP oppositely modulated NBD-stearic acid uptake parameters and intracellular diffusion in ES cells.

4-Chloro-7-nitrobenzofurazan↗

Fatty acid composition of goat muscles and fat depots: a review.

In addition to the fat content of muscle and adipose depots, the fatty acid composition of lipids affects meat quality. Furthermore, relevant reports are difficult to use for comparisons, in that samples were collected from muscles and fat depots at various anatomical locations and experiments entailed different objectives, designs, procedures and methodologies. Nonetheless, based on currently available publications, according to a recent classification of meats by concentrations of potentially cholesterol-raising, and neutral, and cholesterol-lowering effects, average values for goat muscles appear better than for beef and lamb. Feeding dry diets seems to increase levels of unsaturated fatty acids and stearic acid in fat depots compared with milk or milk replacer. Increasing concentrate consumption can increase levels of odd-numbered and branched chain fatty acids in subcutaneous fat depots. With increasing age of unweaned kids, the level of stearic acid in fat depots decreases, and with increasing live weight of weaned kids levels of saturated fatty acids increase, and contents of monounsaturated fatty acids decrease in most fat depots. This review of a currently limited database indicates need for further experimentation to characterize interactions among factors such as breed, age and nutritional conditions in the fatty acid composition of carcass lipids of goats so as to gain a fuller understanding of goat meat quality.

Journal Article↗

Absence of unsaturated fatty acid synthesis in murine T lymphocytes.

Stearic acid is toxic for T lymphocytes in vitro but has little effect on B lymphocytes. To investigate the molecular basis for this difference, purified murine T and B lymphocytes were compared for their abilities to incorporate and metabolize stearic acid. Unstimulated T and B cells incorporated identical amounts of stearic acid into six different phospholipids and four neutral lipids. After mitogen stimulation, fatty acid uptake was increased in both lymphocyte types, but cell-specific differences were seen in the distribution of stearic acid among the various cellular lipids. Doses of stearic acid that selectively inhibited T-cell proliferation resulted in a 5-fold greater accumulation of distearoylphosphatidylcholine in T cells than in B cells. Whereas T cells did not desaturate the exogenously derived stearic acid, up to 25% of the saturated fatty acid was converted to oleic acid in B cells. These findings suggested a deficiency of stearoyl-CoA desaturase (acyl-CoA, hydrogen-donor:oxygen oxidoreductase, EC 1.14.99.5) activity in T cells, which was confirmed by subsequent studies. Cell-free extracts from B cells displayed nearly 20-fold more stearoyl-CoA desaturase activity than T-cell extracts, and the level of stearoyl-CoA desaturase mRNA was 30-fold higher in B cells. Collectively, our data indicate that murine T cells are deficient in unsaturated fatty acid synthesis. The deficiency of stearoyl-CoA desaturase in T cells may represent the basis for the differing sensitivities of T and B lymphocytes to inhibition by saturated fatty acids.

Animals↗

Modulation of swarming and virulence by fatty acids through the RsbA protein in Proteus mirabilis.

After sensing external signals, Proteus mirabilis undergoes a multicellular behavior called swarming which is coordinately regulated with the expression of virulence factors. Here we report that exogenously added fatty acids could act as signals to regulate swarming in P. mirabilis. Specifically, while oleic acid enhanced swarming, some saturated fatty acids, such as lauric acid, myristic acid, palmitic acid, and stearic acid, inhibited swarming. We also found that expression of hemolysin, which has been shown to be coordinately regulated with swarming, was also inhibited by the above saturated fatty acids. Previously we identified a gene, rsbA, which may encode a histidine-containing phosphotransmitter of the bacterial two-component signaling system and act as a repressor of swarming and virulence factor expression in P. mirabilis. We found that while myristic acid, lauric acid, and palmitic acid exerted their inhibitory effect on swarming and hemolysin expression through an RsbA-dependent pathway, the inhibition by stearic acid was mediated through an RsbA-independent pathway. Biofilm formation and extracellular polysaccharide (EPS) production play an important role in P. mirabilis infection. We found that RsbA may act as a positive regulator of biofilm formation and EPS production. Myristic acid was found to slightly stimulate biofilm formation and EPS production, and this stimulation was mediated through an RsbA-dependent pathway. Together, these data suggest that fatty acids may act as environmental cues to regulate swarming and virulence in P. mirabilis and that RsbA may play an important role in this process.

Bacterial Proteins↗

Comparative quantitative fatty acid analysis of triacylglycerols using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and gas chromatography.

Quantitative analyses of fatty acids from five triacylglycerol products, coconut oil, palm kernel oil, palm oil, lard and cocoa butter, were carried out using two analytical methods: matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOFMS) and gas chromatography (GC), in an effort to validate the application of MALDI-TOFMS in quantitative fatty acid analysis. For the GC analysis, transmethylated products were used, whereas, for the MALDI-TOF analysis, saponified products were used. Under MALDI-TOF conditions, the acids were detected as sodiated sodium carboxylates [RCOONa + Na](+) consistent with the mode of ionization that was previously reported. Thus, the MALDI-TOF mass spectrum of saponified coconut oil showed the presence of sodiated sodium salts of caprylic acid (7.5 +/- 0.67, m/z 189), capric acid (6.9 +/- 0.83, m/z 217), lauric acid (47.8 +/- 0.67, m/z 245), myristic acid (20.4 +/- 0.51, m/z 273), palmitic acid (9.8 +/- 0.47, m/z 301), linoleic acid (0.9 +/- 0.07, m/z 325), oleic acid (4.8 +/- 0.42, m/z 327) and stearic acid (2.0 +/- 0.13, m/z 329). Saponified palm kernel oil had a fatty acid profile that included caprylic acid (3.5 +/- 0.59), capric acid (4.7 +/- 0.82), lauric acid (58.6 +/- 2.3), myristic acid (20.9 +/- 1.5), palmitic acid (7.2 +/- 1.1), oleic acid (3.8 +/- 0.62) and stearic acid (1.2 +/- 0.15). Saponified palm oil gave myristic acid (0.83 +/- 0.18), palmitic acid (55.8 +/- 1.7), linoleic acid (4.2 +/- 0.51), oleic acid (34.5 +/- 1.5), stearic acid (3.8 +/- 0.26) and arachidic acid (0.80 +/- 0.22). Saponified lard showed the presence of myristic acid (1.5 +/- 0.24), palmitic acid (28.9 +/- 1.3), linoleic acid (13.7 +/- 0.67), oleic acid (38.7 +/- 1.4), stearic acid (12.8 +/- 0.64) and arachidic acid (2.4 +/- 0.35). Finally, for saponified cocoa butter, the fatty acid distribution was: palmitic acid (32.3 +/- 1.0), linoleic acid (2.6 +/- 0.35), oleic acid (34.9 +/- 1.7) and stearic acid (30.3 +/- 1.6). Quantitative gas chromatographic analysis of the corresponding methyl esters from these triacylglycerol products yielded data that were mostly in agreement with the MALDI-TOFMS data. The MALDI-TOF experiment, however, proved to be superior to the GC experiment, particularly with regard to baseline resolution of unsaturated acids. Furthermore, the ability of MALDI-TOFMS to detect low concentrations of fatty acids rendered it more sensitive than the GC methodology.

Animals↗

Effect of acute administration of bile acids on fatty acid composition of biliary phosphatidylcholine in man.

Little is known on variations in fatty acid composition of biliary phosphatidylcholine (PC) during acute administration of particular bile acids (BAs) in man. Bile was collected hourly for 5 h in 6 T-tube patients (prereplacement period). Thereafter particular BAs were infused into the duodenum at a rate of 1 g/h for 5 h and bile collected hourly (replacement period). Each patient received two BAs at an interval of 3 days, following a cross-over design. Three patients received deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) and a second 3 patients cholic acid (CA) and chenodeoxycholic acid (CDCA). Bile acid pool contained mainly the two primary BAs in the prereplacement period and more than 80% administered BAs in the replacement period. Hydrophobic and detergent BAs (DCA and CDCA) increased the secretion rates and the percentage of biliary PC species with arachidonic acid and stearic acid; in contrast less detergent BAs (UDCA and CA) did not significantly alter fatty acid composition of biliary PC. Thus, very hydrophobic and detergent BAs would seem to promote the preferential secretion into the bile of lecithin species present in the liver cell plasma membranes, rich in arachidonic and stearic acid.

Adult↗

Endogenous synthesis cannot compensate for absence of dietary oleic acid in rats.

It is important to know whether an organism is able to synthesize all the oleic acid it needs. To determine this, it is sufficient to feed animals a diet containing essential fatty acids but totally lacking oleic acid, and then determine whether tissue concentrations of fatty acids of the (n-9) series are altered due to insufficient endogenous synthesis of oleic acid from stearic acid. In fact, the effects of a total oleic acid deficiency have not previously been studied because all the vegetable oils used in human and animal nutrition contain this fatty acid in variable amounts. Thus, we fed rats semipurified diets whose lipids (triglycerides) were synthesized chemically. Female rats were fed the diets for 3 wk before mating, and their pups (fed the same diets) were killed when 21 and 60 d old. Generally speaking, oleic acid deficiency resulted in a lower level of this acid in the various organs examined (liver, kidney, testes, heart, muscle and sciatic nerve in 21-d-old rats and liver, kidney, heart, muscle and sciatic nerve in 60-d-old rats). Brain, myelin and nerve endings were not affected at either age. This lower level was accompanied by a higher level of 16:1(n-7) and, to a lesser extent, 18:1(n-7). Dietary supplementation with oleic acid (1666 mg/100 g diet) for up to 21 d resulted in normal levels of this fatty acid in some organs (liver, heart, sciatic nerve) but not in others (kidney, muscle, testes) and a decrease in 16:1(n-7), which returned to about the same levels as in the control group in all organs except liver. Adding small or large amounts of stearic acid to the oleic acid-deficient diet had little or no effect on oleic acid levels in the tissues. We conclude that rats (particularly in liver) do not have sufficient synthesizing potential to guarantee the normal fatty acid composition of certain organs if oleic acid is totally absent in the diet.

Animals↗

Fatty acid composition of cholesteryl esters in serum in boys from 16 developing and developed countries.

The fatty acid composition of the cholesteryl esters in serum was measured in 7- and 8-year-old boys in groups from 16 countries. The ratio of esterified cholesterol: total cholesterol was also measured. All sample collections and analyses were carried out under standardized conditions. The proportion of palmitic acid in the cholesteryl esters was high in the groups from Asia and Africa (0.17-0.26) compared with that in the groups from the U.S.A. and Europe (0.14-0.18). The proportion of linoleic acid in the cholesteryl esters was low in the groups from Asia and Africa (0.39-0.48) and high in the groups from the U.S.A. and Europe (0.45-0.58). The proportion of oleic acid, arachidonic acid, palmitoleic acid and stearic acid showed little variation between the groups. The proportion of linoleic acid in the cholesteryl esters was positively correlated with the concentration of total cholesterol (r = 0.75, n = 26, P < 0.005).

Arachidonic Acids↗

Ruminal fermentation in vivo as influenced by long-chain fatty acids.

Responses of ruminal microbes to long-chain fatty acids in forms of free acids, calcium salts, or triglycerides were measured in trials with rumen cannulated heifers. Addition of fatty acids at 10% to a basal diet of 50% corn silage and 50% grain increased fat content 3 to 10 to 12%. Long-chain fatty acids with a high melting point (stearic acid) and calcium salts of long-chain fatty acids (vegetable fat and tallow) decreased acetate:propionate by about 20%. Long-chain fatty acids with a low melting point (oleic acid) and the triglyceride form of long-chain fatty acid (tallow) decreased acetate to propionate ratio by 50 to 60%. Even though they were not completely inert in the rumen, responses with the hard long-chain fatty acids (stearic acid) and with calcium salts of long-chain fatty acids confirm that these are efficacious for protecting ruminal microbes from adverse effects of fat. With calcium salts of long-chain fatty acids, dietary buffers may be needed to maintain ruminal pH so that dissociation of salts does not occur. Long-chain fatty acid supplementation at 10% of the diet is probably more than the amount needed to optimize productivity and health. With most diets, 6 to 8% supplemental long-chain fatty acid is probably sufficient.

Animals↗

Identification of T-helper cells as the target of stearic acid-inhibition in primary antibody responses in vitro.

We have previously shown that albumin-complexed stearic acid (18:0) inhibited in vitro primary anti-TNP plaque-forming cell (PFC) responses to trinitrophenyl keyhole limpet hemocyanin (TNP-KLH), but did not affect primary PFC responses to trinitrophenyl lipopolysaccharide (TNP-LPS). The present studies were done to identify the cellular target of fatty acid inhibition. The addition of 18:0 at the initiation of antibody cultures exerted a dose-dependent inhibitory effect on subsequent PFC responses to TNP-KLH, and removal of the fatty acid after 20 h did not reverse its inhibitory effect. Preincubation of isolated T-cells with TNP-KLH and 18:0 resulted in a similar inhibition of subsequent PFC responses, but a preincubation of isolated B-cells had no effect. The addition of 18:0 to the culture system in vitro led to a marked reduction in the level of IL-2 detectable in culture supernatants, and PFC responses could be restored by providing exogenous mouse recombinant IL-2. The addition of antigen-primed T-helper cells to antibody cultures partially abrogated the inhibition by 150 microM 18:0, apparently due to their greater production of IL-2. Lastly, following overnight incubation of unfractionated splenic lymphocytes in the presence of TNP-KLH and [1-14C]-18:0, B-cells were shown to contain nearly 5-fold more radiolabeled oleic acid (18:1) than T-cells. Collectively, these findings implicate T-helper cells as the principle target of 18:0-inhibition of primary antibody responses in vitro, possibly as a result of the inability of T-helper cells to avoid an over accumulation of stearic acid in their membrane phospholipids.

Animals↗

Effect of a stearic acid-rich, structured triacylglycerol on plasma lipid concentrations.

BACKGROUND: Structured lipids are being incorporated into foods to reduce their energy value. One such lipid is rich in stearic acid. OBJECTIVE: The objective of this study was to compare the effects on plasma lipids of a stearic acid-rich triacylglycerol and a fat rich in palmitic acid in hypercholesterolemic subjects. DESIGN: Fifteen subjects with an average plasma cholesterol concentration of 6.13 +/- 0.80 mmol/L initially ate a low-fat diet for 2 wk (run-in period), followed in random order and blinded fashion by 2 high-fat diets (for 5 wk each) containing foods derived from margarines rich either in palmitic acid or in the structured, stearic acid-rich triacylglycerol. RESULTS: Plasma cholesterol concentrations with the low-fat, the stearic acid-rich, and the palmitic acid-rich diets were not significantly different (5.35 +/- 0.83, 5.41 +/- 0.78, and 5.52 +/- 0.68 mmol/L, respectively) but were significantly lower (P < 0.001) than those measured during the habitual diet period (ie, 2 wk before the study began). Neither HDL cholesterol nor plasma triacylglycerol differed significantly among the 3 study diets. CONCLUSION: A similar increase in the intake of stearic and palmitic acids (differing by approximately 5% of total energy) to ensure a high fat intake resulted in plasma total and LDL-cholesterol concentrations that did not differ significantly from concentrations measured during a period of low-fat intake.

Cholesterol↗

Lipid protein interactions in mitochondria. VIII. Effect of general anesthetics on the mobility of spin labels in lipid vesicles and mitochondrial membranes.

We have studied the effect of general anesthetics on the mobility of two stearic acid spin labels (5-doxyl stearic acid and 16-doxyl stearic acid) in bovine heart mitochondria and in phospholipid vesicles made from either mitochondrial lipids or commercial soybean phospholipids. The general anesthetics used include nonpolar compounds (alcohols, halothane, pentane, diethyl ether, chloroform) and the amphiphatic compound, ketamine. All anesthetics tested increase the mobility of the spin labels in phospholipid vesicles to a limited extent up to a concentration where the ESR spectra become those of free spin labels. On the other hand, anesthetics have a pronounced effect on mitochondrial membranes at concentrations as low as those known to produce general anesthesia; the effect is lower near the bilayer surface (5-doxyl stearic acid) and very strong in the bilayer core (16-doxyl stearic acid). The effects of anesthetics are mimicked by the detergent, Triton X-100. We suggest that the discrepancy between the action of anesthetics in mobilizing the spin labels in lipid vesicles and in membranes results from labilization of lipid protein interactions.

Anesthetics↗

Substrate control of termination of fatty acid biosynthesis by fatty acid synthetase from Brevibacterium ammoniagenes.

The pattern of fatty acids produced by the fatty acid synthetase complex of Brevibacterium ammoniagenes under several conditions was examined. The fatty acid synthetase obtained from B. ammoniagenes produced oleic acid as well as saturated fatty acids (palmitic and stearic acids). The relative proportions of palmitic to stearic acids varied over a wide range. Such alterations were dependent on the malonyl-CoA concentration and the ratio of acetyl-CoA to malonyl-CoA concentrations. At malonyl-CoA concentrations higher than 100 microM, stearic acid accounted for more than 90% of the saturated fatty acids and the pattern of fatty acid synthesized was independent on the ratio of acetyl-CoA to malonyl-CoA. At malonyl-CoA concentrations lower than 100 microM, raising the acetyl-CoA/malonyl-CoA ratio increased the percentage of palmitic acid. However, the proportion of oleic acid produced remained almost constant under all conditions tested.

Acetyl Coenzyme A↗

Arachidonic acid metabolism in articular chondrocytes.

In this study rabbit articular chondrocytes were cultured and the cells were labeled with 3H-arachidonic acid and 14C-stearic acid. 3H incorporation reached a plateau at four hours and 14C-incorporation reached a plateau at 24 hours. The 3H was associated mainly with phosphatidylcholine (PC), phosphatidylethanolamine (PE), and phosphatidylinositol (PI) at the 2-position while 14C was found at the 1-position. When the double-labeled cells were incubated with bradykinin or ionophore A23187, a significant release of 3H into the medium was observed, while the 14C release was small. Approximately 90% of the 3H released was arachidonic acid. Small amounts of the released 3H were no longer associated with stearic acid; it was converted mainly into prostaglandin E2 (PGE2). When stimulated by either bradykinin or ionophore, a significant 3H loss was observed in cellular PC while there were no significant 3H changes in other phospholipids, triacylglycerols (TGs), or diacylglycerols (DGs). Although 14C of cellular lysophosphatidylcholine (lyso-PC) was not increased significantly, the 3H seemed to be released from the 2-position of PC by the action of phospholipase A2. There was no significant change in the breakdown of PC between palmitoyl-arachidonyl (16:0/20:4) and stearoyl-arachidonyl (18:0/20:4) species. Both A23187 and bradykinin may activate phospholipase A2, releasing arachidonic acid equally from the 2-position of PCs having either palmitic acid or stearic acid at the 1-position. Some of this material is converted to PGE2, but this conversion is low compared to other cell types.

Animals↗

Sterol carrier protein-2 expression modulates protein and lipid composition of lipid droplets.

Despite the critical role lipid droplets play in maintaining energy reserves and lipid stores for the cell, little is known about the regulation of the lipid or protein components within the lipid droplet. Although immunofluorescence of intact cells as well as Western analysis of isolated lipid droplets revealed that sterol carrier protein-2 (SCP-2) was not associated with lipid droplets, SCP-2 expression significantly altered the structure of the lipid droplet. First, the targeting of fatty acid and cholesterol to the lipid droplets was significantly decreased. Second, the content of several proteins important for lipid droplet function was differentially increased (perilipin A), reduced severalfold (adipose differentiation-related protein (ADRP), vimentin), or almost completely eliminated (hormone-sensitive lipase and proteins >93 kDa) in the isolated lipid droplet. Third, the distribution of lipids within the lipid droplets was significantly altered. Double labeling of cells with 12-(N-methyl)-N-[(7-nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-octadecanoic acid (NBD-stearic acid) and antisera to ADRP showed that 70, 24, and 13% of lipid droplets contained ADRP, NBD-stearic acid, or both, respectively. SCP-2 expression decreased the level of ADRP in the lipid droplet but increased the proportion wherein ADRP and NBD-stearic acid colocalized by 3-fold. SCP-2 expression also decreased the lipid droplet fatty acid and cholesterol mass (nmol/mg protein) by 5.2- and 6.6-fold, respectively. Finally, SCP-2 expression selectively altered the pattern of esterified fatty acids in favor of polyunsaturated fatty acids within the lipid droplet. Displacement studies showed differential binding affinity of ADRP for cholesterol and fatty acids. These data suggested that SCP-2 and ADRP play a significant role in regulating fatty acid and cholesterol targeting to lipid droplets as well as in determining their lipid and protein components.

4-Chloro-7-nitrobenzofurazan↗

A comparison of a spin-label and a fluorescent cell membrane probe using pure and mixed monomolecular films.

Monocular films studies of 12-nitroxide stearic acid and 12-(9-anthroyl) stearic acid reveal that deviations from the behavior of the parent molecule (stearic acid) are as much dictated by the polar, or nonpolar, nature of the probe group as by its size. In mixed films under membrane-like conditions, the spin label probe, 12-nitroxide stearic acid, exhibits positive deviations from ideality and should read too high a fluidity. The picture is, however, complicated by a tendency of this probe molecule to adopt a bent conformation, a tendency apparently enhanced by specific interactions with the lecithin zwitterion. 12-(9-anthroyl) stearic acid, in contrast, shows only negative deviations from ideality in mixed dipalmitoyl lecithin films and should read too low a fluidity.

Anthracenes↗

Method development for the analysis of trans-fatty acids in hydrogenated oils by capillary electrophoresis.

A novel capillary electrophoresis methodology using UV indirect detection (224 nm) for the analysis of trans-fatty acids in hydrogenated oils was proposed. The electrolyte consisted of a pH 7 phosphate buffer at 15 mmol x L(-1) concentration containing 4 mmol.L(-1) sodium dodecylbenzenesulfonate, 10 mmol x L(-1) polyoxyethylene 23 lauryl ether (Brij 35), 2% 1-octanol and 45% acetonitrile. Under the optimized conditions, ten fatty acids, C12:0, C13:0 (internal standard), C14:0, C16:0, C18:0, C18:1c, C18:1t, C18:2cc, C18:2tt and C18:3ccc were baseline-separated in less than 12 min. The proposed methodology was applied to monitor the formation of trans-fatty acids during hydrogenation of Brazilnut oil. A crude oil sample (42.1% linoleic acid, 37.3% oleic acid, 13.4% palmitic acid, and 7.0% stearic acid) was mixed with 0.25% of a nickel-based catalyst and submitted to two independent hydrogenation conditions: 175 degrees C, 3 atm, 545 rpm for 60 min (GH(1) sample), and 150 degrees C, 1 atm, 545 rpm for 30 min (GH(2) sample). For the most severe hydrogenation condition (higher temperature and pressure, under longer reactional period), a more complete conversion of linoleic and oleic acids into stearic acid occurred with concomitant formation of the trans-species, elaidic acid (C18:1t). For the milder hydrogenation procedure that generated sample GH(2), larger amounts of linoleic and oleic acids remained, in addition to the transformations already observed in the GH(1) sample.

Electrophoresis, Capillary↗

Increased arachidonic acid levels in phospholipids of human colonic mucosa in inflammatory bowel disease.

1. Colonic mucosa from 19 patients with ulcerative colitis, eight with Crohn's disease and 14 controls were analysed for arachidonic acid (C20:4), linoleic acid (C18:2), oleic acid (C18:1), stearic acid (C18:0) and palmitic acid (C16:0). 2. Gas-liquid chromatography of lipid extracts showed that arachidonic acid was significantly higher in ulcerative colitis (19 +/- 4) and Crohn's disease (20 +/- 3) than in controls (13 +/- 5 micrograms/mg of protein) (means +/- SD). Neither the degree of inflammation nor treatment with sulphasalazine or prednisolone appeared to influence the fatty acid concentrations. 3. Seventy-five to ninety-five per cent of the arachidonic acid was found in the phospholipid fraction after separation by thin-layer chromatography. There were no significant changes in the concentrations of the other fatty acids measured, although oleic acid was lower in inflammatory bowel disease. The ratios of oleic acid to stearic acid and to palmitic acid were lower in inflammatory bowel disease. 4. The alteration in the fatty acid profile may partly explain the increased synthesis of eicosanoids in colonic mucosa in inflammatory bowel disease.

Adolescent↗