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The inhibitory effect of polyunsaturated fatty acids on human CYP enzymes.

The inhibitory effect of saturated fatty acids (SFAs): palmitic acid (PA), stearic acid (SA) and polyunsaturated fatty acids (PUFAs): linoleic acid (LA), linolenic acid (LN), arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on six human drug-metabolizing enzymes (CYP1A2, 2C9, 2C19, 2D6, 2E1 and 3A4) was studied. Supersomes from baculovirus-expressing single isoforms were used as the enzyme source. Phenacetin O-deethylation (CYP1A2), diclofenac 4-hydroxylation (CYP2C9), mephenytoin 4-hydroxylation (CYP2C19), dextromethorphan O-demethylation (CYP2D6), chlorzoxazone 6-hydroxylation (CYP2E1) and midazolam 1-hydroxylation (CYP3A4) were used as the probes. Results show that all the five examined PUFAs competitively inhibited CYP2C9- and CYP2C19-catalyzed metabolic reactions, with Ki values ranging from 1.7 to 4.7 microM and 2.3 to 7.4 microM, respectively. Among these, AA, EPA and DHA tended to have greater inhibitory potencies (lower IC(50) and Ki values) than LA and LN. In addition, these five PUFAs also competitively inhibited the metabolic reactions catalyzed by CYP1A2, 2E1 and 3A4 to a lesser extent (Ki values>10 microM). On the other hand, palmitic and stearic acids, the saturated fatty acids, had no inhibitory effect on the activities of six human CYP isozymes at concentrations up to 200 microM. Incubation of PUFAs with CYP2C9 or CYP2C19 in the presence of NADPH resulted in the decrease of PUFA concentrations in the incubation mixtures. These results indicate that the PUFAs are potent inhibitors as well as the substrates of CYP2C9 and CYP2C19.

Animals↗

Influence of triacylglycerol structure on the postprandial response of factor VII to stearic acid-rich fats.

BACKGROUND: The consumption of a synthetic, randomized, stearic acid-rich triacylglycerol results in decreased postprandial lipemia and activated factor VII (FVII:a) compared with cocoa butter (a nonrandomized, symmetrical, stearic acid-rich triacylglycerol). It was hypothesized that this difference is a consequence of the differences in structure between the 2 triacylglycerols. OBJECTIVE: The objective was to test whether the consumption of randomized cocoa butter decreases postprandial lipemia and FVII:a. DESIGN: A randomized crossover trial with 17 male subjects compared the effects of meals containing 50 g fat provided as a symmetrical (cocoa butter) or an asymmetrical (randomized cocoa butter) triacylglycerol on postprandial changes in lipids, chylomicron composition, and FVII:a. RESULTS: After randomization, the postprandial area under the curve for plasma triacylglycerol decreased by 41% (P < 0.01). At 3 h the plasma concentrations of triacylglycerol, palmitic acid, stearic acid, and oleic acid were 26%, 18%, 34%, and 19% lower, respectively. The proportion of oleic acid in the sn-2 position of the chylomicron triacylglycerol was reduced from 67.4 mol% to 35.9 mol% and resulted in an increase in the proportion of stearic acid in the sn-2 position from 9.2 mol% to 25.4 mol%. FVII:a did not increase 6 h after consumption of the randomized cocoa butter (: 1.2; 95% CI: -2.7, 4.6 U/L) but increased significantly (: 7.7; 95% CI: 2.5,12.9 U/L) 6 h after consumption of the unrandomized cocoa butter. CONCLUSIONS: Symmetrical stearic acid-rich triacylglycerol with oleic acid in the sn-2 position appears to be absorbed more rapidly than is asymmetrical triacylglycerols with long-chain saturated fatty acids in the sn-2 position, which leads to activation of FVII.

Adult↗

Different effects of palmitic and stearic acid-enriched diets on serum lipids and lipoproteins and plasma cholesteryl ester transfer protein activity in healthy young women.

The effects of palmitic and stearic acid-enriched diets on serum lipids, lipoproteins, apolipoproteins (apo) A-I and B, and plasma cholesteryl ester transfer protein (CETP) activity were examined in 12 healthy young women. Subjects followed the two experimental diets for 4 weeks according to a randomized crossover design. Both experimental diet periods were preceded by consumption of a baseline diet for 2 weeks. The diets provided 37% of total energy intake (E%) as fat, and differed only with respect to fatty acid composition. There was a substitution of 5E% of palmitic acid or stearic acid in the experimental diets for 5E% of monounsaturated fatty acids in the baseline diet. After the palmitic acid diet, serum total and high-density lipoprotein (HDL) cholesterol and apo A-I concentrations were higher (8%, P = .015, 9%, P = .040, and 11%,P = .011, respectively) and mean serum low-density lipoprotein (LDL) cholesterol concentration tended to be higher (8%, P = .077) as compared with values after the stearic acid diet. Plasma CETP activity increased in the palmitic acid diet as compared with the stearic acid diet (12%, P = .006). In conclusion, palmitic acid and stearic acid-enriched diets had different effects on serum lipids and lipoproteins and also on plasma CETP activity in young healthy women.

Adult↗

Incorporation of fatty acids into phospholipids in L cells stimulated by antibody.

Binding antibodies to surface membranes stimulated incorporation of fatty acids (FA) into phospholipids of L cells. Antibodies stimulated at least a 3.4-fold greater incorporation of arachidonic acid into phosphatidylinositol than into any other class of phospholipid when compared on a molar basis (p less than 0.003). This enhanced incorporation was selective, depending on the character of the FA, because antibodies stimulated the incorporation of arachidonic acid at least 2.4-fold more than oleic acid, palmitic acid or stearic acid (p less than 0.001). Surprisingly, an antibody-stimulated incorporation of palmitic acid into sphingomyelin (SM) was at least 2.2-fold greater than that into any other class of phospholipid (p less than 0.001) and the antibody-stimulated incorporation of palmitic acid into SM was at least 60-fold greater than that of arachidonic acid, stearic or oleic acid (p less than 0.001). Nontoxic doses of ethylenediamine tetraacetic acid (EDTA), dexamethasone, 4-bromophenacylbromide and indomethacin inhibited the antibody-stimulated incorporation of arachidonic acid into cellular phospholipids, principally phosphatidylinositol (PI), and similarly inhibited the antibody stimulation of DNA synthesis. We conclude that when antibody binds to surface antigens on L cells, a rapid and selective incorporation of fatty acids into certain cellular phospholipids occurs, possibly mediated by calcium-dependent phospholipases. Degradation products of arachidonic acid, i.e., prostaglandins, may be important in these antibody stimulation events, as well. These early changes in phospholipid metabolism may serve as an important signal or mechanism for the subsequent stimulation of DNA synthesis in L cells.

Animals↗

Fatty acid-induced changes in vascular reactivity in healthy adult rats.

Dietary fatty acids (FAs) are known to modulate endothelial dysfunction, which is the first stage of atherosclerosis. However, their exact role in this initial phase is still unclear. The effects of isolated or combined (by 2) purified FAs from the main FA families were studied on the vascular response of isolated thoracic aorta in healthy rats to get a better understanding of the mechanisms of action of dietary FAs in regulating vascular endothelial function. Cumulative contraction curves to phenylephrine and relaxation curves to carbachol and then to sodium nitroprusside were obtained in the absence or presence of the FAs studied allowing endothelium-dependent and endothelium-independent ability of the smooth muscle to relax to be assessed in each experimental group. The endothelium-dependent vasodilator response to carbachol was lowered by eicosapentaenoic acid, whereas it was not altered either by docosahexaenoic acid alone or by combined eicosapentaenoic acid-docosahexaenoic acid, oleic acid, or stearic acid, and it was increased by linoleic acid (LA). A decreased phenylephrine-induced contraction was observed after incubation with arachidonic acid and with stearic acid. On the other hand, the endothelium-dependent relaxation was reduced by the addition of combined LA-arachidonic acid and LA-oleic acid. In conclusion, these data point out the differential effects of different types of FAs and of FAs alone vs combined on vascular reactivity. The complex nature of these effects could be partially linked to metabolic specificities of endothelial cells and to interactions between some FAs.

Animals↗

The hydrogenation of the series of methylene-interrupted cis,cis-octadecadienoic acids by pure cultures of six rumen bacteria.

The hydrogenation of all the methylene-interrupted cis,cis-octadecadienoic acids was examined using pure cultures of six rumen bacteria able to hydrogenate linoleic acid to stearic acid or its immediate precursor, trans-11-octadecenoic acid, after first conjugating the linoleic acid to cis,trans-9,11-octadecadienoic acid. Only the delta 14-cis,17-cis-isomer was not hydrogenated by at least one of the bacteria and no evidence was found that conjugation was necessary before hydrogenation except for the delta 2-cis,5-cis- and delta 9-cis,12-cis-isomers. Several isomers were hydrogenated to an extent close to that achieved with linoleic acid (delta 9-cis,12-cis). Those bacteria only able to hydrogenate linoleic to trans-11-octadecenoic acid gave only octadecenoic acid products and those bacteria able to hydrogenate linoleic acid to stearic gave variable yields of octadecenoic acids and stearic acid except with the isomers delta 12-cis,15-cis and delta 13-cis,16-cis when only octadecenoic acids were detected. At the substrate levels used (20 micrograms/ml), both inhibition and stimulation of growth were found but no common pattern emerged, nor was the growth consistently related to the extent of hydrogenation.

Animals↗

[Sphingolipid changes in rat cerebral cortex during focal ischemia--how does ceramide accumulate in an ischemic condition?].

Levels of ceramide, sphingomyelin, cerebroside and gangliosides were determined in rat cerebral cortex during focal ischemia produced by middle cerebral artery occlusion. Ceramide began to increase at 6 hours of ischemia and increased to 4.5 folds at 96 hours. Amino-linked fatty acids in increased ceramide were composed solely of non-hydroxy fatty acids, and stearic acid was the most prominent. Sphingomyelin, whose amino-linked fatty acids were mostly stearic acid, decreased in a time-dependent manner and became about a half of controls at 96 hours. Hydroxy fatty acid linked cerebroside decreased at and after 6 hours of ischemia, whereas significant decrease of non-hydroxy fatty acid linked cerebroside occurred only at 96 hours of ischemia. There were no measurable changes in the levels of gangliosides. The results suggested that ceramide was produced in the cerebral cortex by the breakdown of sphingomyelin during ischemia.

Animals↗

Palmitic and stearic fatty acids induce Alzheimer-like hyperphosphorylation of tau in primary rat cortical neurons.

Epidemiological studies suggest that high fat diets significantly increase the risk of Alzheimer's disease (AD). In addition, the AD brain is characterized by high fatty acid content compared to that of healthy subjects. Nevertheless, the basic mechanism relating elevated fatty acids and the pathogenesis of AD remains unclear. The present study examines the role of fatty acids in causing hyperphosphorylation of the tau protein, one of the characteristic signatures of AD pathology. Hyperphosphorylation of tau disrupts the cell cytoskeleton and leads to neuronal degeneration. Here, primary rat cortical neurons and astrocytes were treated with saturated free fatty acids (FFAs), palmitic and stearic acids. There was no change in the levels of phosphorylated tau in rat cortical neurons treated directly with these FFAs. The conditioned media from FFA-treated astrocytes, however, caused hyperphosphorylation of tau in the cortical neurons at AD-specific phospho-epitopes. Co-treatment of neurons with N-acetyl cysteine, an antioxidant, reduced FFA-induced hyperphosphorylation of tau. The present results establish a central role of FFAs in causing hyperphosphorylation of tau through astroglia-mediated oxidative stress.

Alzheimer Disease↗

A stearic acid-rich diet improves thrombogenic and atherogenic risk factor profiles in healthy males.

OBJECTIVE: To determine whether healthy males who consumed increased amounts of dietary stearic acid compared with increased dietary palmitic acid exhibited any changes in their platelet aggregability, platelet fatty acid profiles, platelet morphology, or haemostatic factors. DESIGN: A randomized cross-over dietary intervention. SUBJECTS AND INTERVENTIONS: Thirteen free-living healthy males consumed two experimental diets for 4 weeks with a 7 week washout between the two dietary periods. The diets consisted of approximately 30% of energy as fat (66% of which was the treatment fat) providing approximately 6.6% of energy as stearic acid (diet S) or approximately 7.8% of energy as palmitic acid (diet P). On days 0 and 28 of each dietary period, blood samples were collected and anthropometric and physiological measurements were recorded. RESULTS: Stearic acid was increased significantly in platelet phospholipids on diet S (by 22%), while on diet P palmitic acid levels in platelet phospholipids also increased significantly (8%). Mean platelet volume, coagulation factor FVII activity and plasma lipid concentrations were significantly decreased on diet S, while platelet aggregation was significantly increased on diet P. CONCLUSION: Results from this study indicate that stearic acid (19g/day) in the diet has beneficial effects on thrombogenic and atherogenic risk factors in males. The food industry might wish to consider the enrichment of foods with stearic acid in place of palmitic acid and trans fatty acids.

Adult↗

Effects of specific fatty acids on cell transformation induced by an activated c-H-ras oncogene.

An increase in dietary lipid has been associated with an increase in the development of certain forms of cancer, notably breast and colon cancer, both in experimental animal studies and in human epidemiology studies. The underlying mechanisms are not, however, known with certainty. In the present studies we have examined whether certain specific fatty acids (FA) might act by enhancing the role of an activated oncogene in a model cell culture system. We found that when the rat fibroblast cell line Rat 6 was transfected with an activated human c-H-ras oncogene and the cells subsequently grown in medium supplemented with myristic acid, palmitic acid or stearic acid (20-80 microM) there was a marked enhancement of the number of transformed foci obtained. On the other hand arachidonic acid had a marked inhibitory effect in this transformation assay. However, this inhibitory effect can be partially reversed by indomethacin, an inhibitor of cyclo-oxygenase, at dose response manner. Control studies indicated that these results were not simply due to the effects of the FAs on growth of the Rat 6 cells or the process of transfection per se. Lipid analyses of cells grown in the presence of stearic acid indicated that the added FA was extensively incorporated into the major lipid classes of the cell and produced transient changes in lipid composition. This simple cell culture system may be useful for elucidating the mechanisms by which various dietary lipids and nutritional factors influence the carcinogenic process.

Animals↗

Delta 9-fatty acid desaturase from arachidonic acid-producing fungus. Unique gene sequence and its heterologous expression in a fungus, Aspergillus.

Based on the sequence information for delta 9-desaturase genes (from rat, mouse and yeast), which are involved in the desaturation of palmitic acid and stearic acid to palmitoleic acid and oleic acid, respectively, the corresponding cDNA and genomic gene were cloned from the fungal strain, Mortierella alpina 1S-4, which industrially produces arachidonic acid. There was a cytochrome b5-like domain linked to the carboxyl terminus of this Mortierella desaturase, as also seen in the yeast delta 9-desaturase. The Mortierella delta 9-desaturase genomic gene had only one intron, in which a novel phenomenon was observed: there was a GC-end at the 5'-terminus instead of a GT-end that is, in general, found in introns of eukaryotic genes. The full-length cDNA clone was expressed under the control of an amyB promoter in a filamentous fungus, Aspergillus oryzae, resulting in drastic changes in the fatty acid composition in the transformant cells; the contents of palmitoleic acid (16:1) and oleic acid (18:1) increased significantly, with accompanying decreases in palmitic acid (16:0) and stearic acid (18:0). These changes were controlled by the addition of maltose as a carbon source to the medium. Also, the expression of the gene caused a significant change in the lipid composition in the Aspergillus transformant. Genomic Southern blot analysis of the transformant with the Mortierella delta 9-desaturase gene as a probe confirmed the integration of this gene into the genome of A. oryzae.

Amino Acid Sequence↗

Induction of the apolipoprotein AI promoter by Sp1 is repressed by saturated fatty acids.

Insulin induces transcription of the hepatic apolipoprotein AI (apo AI) gene by increasing Sp1 binding to the promoter. To determine the effect of fatty acids on this process, HepG2 cells cotransfected with the plasmid pAI.474.CAT containing the full-length apo AI promoter and the Sp1-expressing plasmid, pCMV-Sp1, were studied. Chloramphenicol acetyl transferase (CAT) activity (% acetylation) increased 1.98-fold in cells receiving the Sp1 expression construct relative to control cells (46.4% +/- 0.6% v 23.4% +/- 1.3%, P < .05). Treatment of cells with 3 saturated fatty acids, stearic, myristic, and palmitic acid, repressed the ability of exogenous Sp1 to induce apo AI reporter gene expression (15.2% +/- 1.7%, 22.5% +/- 0.3%, 22.9% +/- 0.1%, 23.5% +/- 0.8%, respectively, P < .05). Unsaturated fatty acids, oleic, linoleic, or linolenic acid had no effect on Sp1-mediated induction of the apo AI promoter. In the presence of the trans fatty acids, CAT activity in the Sp1-transfected cells was similar to control cells (16.7% +/- 3.3%, 19.3% +/- 0.5%, and 21.0% +/- 2.1% acetylation in cells exposed to elaidic acid, linolelaidic, or linolenelaidic acid, respectively). In cells treated with an equimolar mixture of oleic acid and stearic acid, apo AI promoter activity was suppressed in a manner similar to that observed in stearic acid-treated cells. Insulin (100 microU/mL) induced apo AI promoter activity 2.9-fold (22.4% +/- 1.7% v 7.8% +/- 2.4%, P < .05). However, in the presence of stearic acid, insulin was unable to induce apo AI promoter (6.3% +/- 1.6%). Stearic acid treatment did not alter Sp1-DNA binding as measured by gel shift analysis. Therefore, saturated fatty acids blunt Sp1 induction of apo AI promoter probably at a step beyond DNA binding.

Apolipoprotein A-I↗

Docosahexaenoic acid-induced amelioration on impairment of memory learning in amyloid beta-infused rats relates to the decreases of amyloid beta and cholesterol levels in detergent-insoluble membrane fractions.

We investigated the effects of dietary administration of docosahexaenoic acid (DHA; C22:6n-3) on the levels of amyloid beta (A beta) peptide (1-40) and cholesterol in the nonionic detergent Triton 100 x-insoluble membrane fractions (DIFs) of the cerebral cortex and, also, on learning-related memory in an animal model of Alzheimer's disease (AD) rats infused with A beta peptide (1-40) into the cerebral ventricle. The infusion increased the levels of A beta peptide and cholesterol in the DIFs concurrently with a significant increase in reference memory errors (measured by eight-arm radial-maze tasks) compared with those of vehicle rats. Conversely, the dietary administration of DHA to AD-model rats decreased the levels of A beta peptide and cholesterol in the DIFs, with the decrease being more prominent in the DHA-administered rats. Regression analysis revealed a significant positive correlation between A beta peptide and each of cholesterol, palmitic acid and stearic acid, and between the number of reference memory errors and each of cholesterol, palmitic, stearic and oleic acid; moreover, a significant negative correlation was observed between the number of reference memory errors and the molar ratio of DHA to palmitic plus stearic acid. These results suggest that DHA-induced protection of memory deficits in AD-model rats is related to the interactions of cholesterol, palmitic acid or stearic acid with A beta peptides in DIFs where DHA ameliorates these interactions.

Alzheimer Disease↗

Effect of fatty acid chain length and saturation on the gastrointestinal handling and metabolic disposal of dietary fatty acids in women.

The gastrointestinal handling and metabolic disposal of [1-13C]palmitic acid, [1-13C]stearic acid and [1-13C]oleic acid administered within a lipid-casein-glucose-sucrose emulsion were examined in normal healthy women by determining both the amount and nature of the 13C label in stool and label excreted on breath as 13CO2. The greatest excretion of 13C label in stool was in the stearic acid trial (9.2% of administered dose) whilst comparatively little label was observed in stool in either the palmitic acid (1.2% of administered dose) or oleic acid (1.9% of administered dose) trials. In both the palmitic acid and oleic acid trials, all of the label in stool was identified as being present in the form in which it was administered (i.e. [13C]palmitic acid in the palmitic acid trial and [13C]oleic acid in the oleic acid trial). In contrast, only 87% of the label in the stool in the stearic acid trial was identified as [13C]stearic acid, the remainder was identified as [13C]palmitic acid which may reflect chain shortening of [1-13C]stearic acid within the gastrointestinal tract. Small, but statistically significant, differences were observed in the time course of recovery of 13C label on breath over the initial 9 h of the study period (oleic acid = palmitic acid > stearic acid). However, when calculated over the 24 h study period, the recovery of the label as 13CO2 was similar in all three trials (approximately 25% of absorbed dose). These results support the view that chain length and degree of unsaturation may influence the gastrointestinal handling and immediate metabolic disposal of these fatty acids even when presented within an emulsion.

Adult↗

Influence of liposomes rich in unsaturated or saturated fatty acids on the growth of human xenotransplanted mammary carcinomas and on the levels of heart type fatty acid binding protein.

A panel of 4 human mammary carcinomas passaged in nude mice were subjected to intraperitoneal application of cholesterol-free liposomes enriched with linoleic (unsaturated fatty acid) or stearic acid (saturated fatty acid). The liposomes were examined with regard to their influence on the tumor growth and level of heart type fatty acid binding protein (FABP). Liposomes with different fatty acid composition influenced the growth of mammary carcinomas 3366, BO, 4000 and 4151 in distinct ways. Liposomes with a high content of stearic acid significantly inhibited the growth of mammary carcinomas 3366 and BO, whereas mammary carcinomas 4000 and 4151 were not affected. The growth of mammary carcinoma 3366 was moderately increased after supplementation of liposomes rich in linoleic acid, the tumor BO was significantly inhibited and the growth of MaCa 4000 and 4151 was unchanged. Liposome treatment led to a significant increase in heart type FABP in mammary carcinomas 3366 and BO regardless of whether the animals were treated with liposomes rich in stearic or linoleic acid. Such significant changes of FABP level could not be observed in mammary carcinomas 4000 or 4151. We suggest that the lipid-mediated growth modulation seems to be dependent on an increase of heart type FABPs in these tumor models.

Animals↗

Fatty acids in animals: thrombosis and hemostasis.

Long-chain fatty acids, including stearic acid, can cause thrombosis when they are injected into the systemic circulation of animals. The toxicity is decreased if the fatty acids are bound to albumin. To date, the effect of individual fatty acid feeding is not known. In general, feeding animals diets high in saturated fat followed by the injection of a thrombogenic stimulus is associated with a greater incidence of thrombosis than when a normal diet or a diet high in unsaturated or polyunsaturated fat is fed. A high dietary intake of long-chain polyunsaturated fatty acids of the n-3 family may prevent thrombosis in animals. In assessing the effects of dietary fatty acids, the ability of the organism, be it animal or human, to convert fatty acids to less thrombogenic fatty acids (stearic to oleic) or create an antithrombotic fatty acid (linolenic to eicosapentaenoic) is a major attribute. Further studies should consider the storage of fatty acids in tissues and their release into the blood and the potential impairment of albumin binding and fatty acid transport mechanisms.

Animals↗

Neutral lipids, phospholipids and higher fatty acids in bull's testes.

The lipid fractions were studied in the testicular tissue of mature bulls, of the lowland black-and-white breed. It was found that the main component of neutral lipids was cholesterol (48%) followed by triglycerides (24%), cholesterol esters (16%) and free fatty acids (12%). In cholesterol esters the main component was palmitic acid (41%) followed by oleic acid (22%), stearic acid (14%) and linoleic acid (14%). In phospholipids the main fraction was composed of lecithins (48%) followed by phosphatidylethanolamine (20%) and phosphatidic acids and phosphatidylglycerol (13%). Palmitic acid was found mainly in the fractions of lecithins and sphingomyelins, stearic acid in fractions of phosphatidylethanolamine, phosphatidylserine and phosphatidylinositol. Linoleic acid was found in the fractions of phosphatidylethanolamine, phosphatidylcholine and sphingomyelin. Arachidonic, docosatetraenoic and docosapentaenoic acids in the fractions of phosphatidylethanolamine, phosphatidylserine, phosphatidylinositol and phosphatidylcholine.

Animals↗

Dietary conjugated linoleic acid alters fatty acid composition of pig skeletal muscle and fat.

The dietary dose responsiveness of conjugated linoleic acid (CLA) addition relative to the fatty acid profile of edible lean tissue was examined in grower pigs treated with or without porcine somatotropin (pST). Gilts and barrows were fed CLA at 0, 0.25, 0.5, 1.0, or 2.0% of diet by weight from 20 to 55 kg BW. Additional pigs were administered (pST) at 0 or 100 microg x kg BW x d(-1) and fed either 0.5 or 2.0% CLA. Animals were fed diets containing 18% CP, 1.2% lysine, and 3.5 Mcal of DE/kg at 110% of ad libitum intake. The fatty acid profile in latissimus dorsi and dorsal s.c. adipose tissue samples was determined by gas chromatography. Dietary CLA replacement of corn oil increased the percentage of total fatty acids as stearic acid, whereas the percentages as oleic and linolenic acids were reduced in lattisimus muscle. Treatment with CLA + pST increased the percentages of linoleic and arachidonic acids while reducing the percentages of palmitic and oleic acids in lattisimus muscle. Dietary CLA increased the percentages of palmitic and stearic acids in s.c. adipose tissue while reducing the percentages of oleic, linoleic, linolenic, and arachidonic acids. The percentage of palmitic acid was reduced in s.c. adipose tissue, whereas linoleic acid was increased with CLA + pST. No synergistic effect was detected between CLA and pST for reducing carcass lipid content in grower pigs. However, pST increased the percentage of polyunsaturated fatty acids in lattisimus muscle and s.c. adipose tissue while reducing the percentages of saturated fatty acids in swine fed CLA.

Adipose Tissue↗