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At least 667 records · Page 37Linked to original sources
PubMed2000

Aldosterone alters the phospholipid composition of rat colonocytes.

Previous studies have shown that aldosterone treatment of amphibian epithelial cells results not only in stimulation of Na(+) absorption but also in changes in phospholipid composition which are necessary for the mineralocorticoid action of aldosterone. The present study was designed to investigate the effect of aldosterone on phospholipids of mammalian epithelia. Phospholipid and fatty acid composition was examined in colonic epithelium (mineralocorticoid target tissue) and thymus (non-mineralocorticoid but glucocorticoid target tissue) of rats which had received aldosterone or vehicle by a miniosmotic pump for 7 days. Aldosterone increased the mass of colonic phospholipids relative to cellular proteins with concomitant changes in the percentage distribution of fatty acids, whereas the relative distribution of membrane phospholipds was not changed. Phosphatidylcholine increased the content of polyunsaturated and decreased that of monounsaturated fatty acids, which predominantly reflected the accretion of arachidonic and a decrease in oleic and palmitoleic acids. Within the phosphatidylethanolamine subclass, pretreatment of rats with aldosterone decreased the content of monounsaturated fatty acids (predominantly oleic and palmitoleic acid) and of n-3 fatty acids, and increased the content of saturated fatty acids (palmitic acid). The saturated-to-nonsaturated fatty acid ratio also significantly increased after aldosterone treatment. No changes in thymic phospholipids were seen. The results are consistent with the contention that aldosterone specifically modulates phospholipid concentration and metabolism in mineralocorticoid target tissue. The changes in phospholipid content and its fatty acid composition during the fully developed effect of aldosterone may reflect a physiologically important phenomenon with long-term consequences for membrane structure and function.

Aldosterone↗
PubMed2003

Qualitative investigation on hydrothermal treatment of Hinoki (Chamaecyparis obtusa) bark for production of useful chemicals.

Hydrothermal treatment of an outer layer of a bark of Hinoki (Chamaecyparis obtusa) tree was investigated qualitatively for the possibility of utilizing residual forest biomass to produce valuable chemicals. Experiments were carried out in a semibatch reactor apparatus that allows the study of the effect of reaction temperatures in a single run. Gas chromatography-mass spectrometry analyses show the presence of useful chemicals such as furfural, aromatic compounds (1,3-di-tert-butyl benzene and 2,4-di-tert-butyl phenol), and fatty acids (myristic acid, palmitic acid, and stearic acid) in the products.

Benzene Derivatives↗
PubMed1987

Characterization of cationic albumin in minimal change nephropathy.

The presence of isoalbumins with a less anionic charge than the normal protein (pI = 4.7) is the hallmark of proteinuria in minimal change nephropathy (MCN). Steroid-induced restoration of near normal levels of proteinuria is characterized by the appearance in urines of isoalbumins with a pI still more anionic than the normal. In our search for an explanation for the pI changes, we used preparative isoelectric focusing in granulated gels to split the microheterogeneous bands obtained from nine MCN-affected children into four fractions (A1, A2, A3, A4) with decreasing pI from 5.8 to 4.0 and we have determined their fatty acid content. The least anionic fraction, A1, was the most defatted, followed by A2, A3 and A4 in which fatty acid content progressively increased, A4 being the most fatted fraction. Accordingly, the mean content of fatty acids in urinary albumin in proteinuric children was lower than in both the remission phase and in normal children (2.17 +/- 0.03 vs. 20.91 +/- 0.38 and 20.94 +/- 0.39, respectively) and was lower by a factor of 4 compared to serum albumin in the same phase of the disease (2.17 +/- 0.03 vs. 8.59 +/- 1.64). Among medium and long-chain fatty acids, the ratio between serum and urinary albumin was the highest for linoleic acid (approximately 7), followed by that of oleic acid, palmitic acid and lauric acid. At variance in five other patients affected by non-MCN nephrotic syndrome this ratio was for practically all FAs about 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2002

Stopped-flow kinetic analysis of long-chain fatty acid dissociation from bovine serum albumin.

The kinetics of the interaction of long-chain fatty acids (referred to as fatty acids) with albumin is critical to understanding the role of albumin in fatty acid transport. In this study we have determined the kinetics of fatty acid dissociation from BSA and the BSA-related fatty acid probe BSA-HCA (BSA labelled with 7-hydroxycoumarin-4-acetic acid) by stopped-flow methods. Fatty acid-albumin complexes of a range of natural fatty acid types and albumin molecules (donors) were mixed with three fatty acid-binding acceptor proteins. Dissociation of fatty acids from the donor was monitored by either the time course of donor fluorescence/absorbance or the time course of acceptor fluorescence. The results of these measurements indicate that fatty acid dissociation from BSA as well as BSA-HCA is well described by a single exponential function over the entire range of fatty acid/albumin molar ratios used in these measurements, from 0.5:1 to 6:1. The observed rate constants (k(obs)) for the dissociation of each fatty acid type reveal little or no dependence on the initial fatty acid/albumin ratio. However, dissociation rates were dependent upon the type of fatty acid. In the case of native BSA with an initial fatty acid/BSA molar ratio of 3:1, the order of k(obs) values was stearic acid (1.5 s(-1)) < oleic acid < palmitic acid congruent with linoleic acid<arachidonic acid (8 s(-1)) at 37 degrees C. The corresponding values for BSA-HCA were about half the values for BSA. The results of this study show that the rate of fatty acid dissociation from native BSA is more than 10-fold faster than reported previously and that the off-rate constants for the five primary fatty acid-binding sites differ by less than a factor of 2. We conclude that for reported rates of fatty acid transport across cell membranes, dissociation of fatty acids from the fatty acid-BSA complexes used in the transport studies should not be rate-limiting.

Acetates↗
PubMed1966

The lipids of mammalian pancreas.

1. The total lipids of ox and guinea-pig pancreas were fractionated on silicic acid columns. 2. The high lipid content of both tissues was due to triglyceride. The major fatty acids of this triglyceride were stearic acid, palmitic acid and oleic acid. 3. The pattern of individual phospholipids resembled that of liver, though pancreas contained more plasmalogen.

Animals↗
PubMed1967

The metabolism of n-decane by a Pseudomonas.

The growth of a Pseudomonas on n-decane was found to produce stearic acid, oleic acid, palmitic acid, palmitoleic acid, decanoic acid, octanoic acid, beta-hydroxydecanoic acid, beta-hydroxyoctanoic acid, beta-hydroxyhexanoic acid and beta-hydroxyadipic acid. Small amounts of n-decanamide and n-valeramide were also isolated. The effects of nitrogen and oxygen limitation on the formation of these products in continuous fermentations is reported.

Alkanes↗
PubMed2004

The surprising diversity of Delta6-desaturase substrates.

A single gene encoding a Delta6-desaturase (FADS2) has been isolated and characterized in mammalian species. This Delta6-desaturase plays a major role in the biosynthesis of PUFAs (polyunsaturated fatty acids). It catalyses the rate-limiting desaturation of linoleic acid (C(18:2) n-6) and alpha-linolenic acid (C(18:3) n-3) required for the biosynthesis of long-chain PUFAs. Moreover, recent studies have provided strong evidence that this Delta6-desaturase also acts on 24-carbon PUFAs of both the n-6 and n-3 series. Another substrate of this Delta6-desaturase has been identified through complementary works from different investigators. This Delta6-desaturase acts on a saturated fatty acid, palmitic acid (C(16:0)), leading to the newly characterized biosynthesis of hexadecenoic acid (C(16:1) n-10) or sapienate.

Animals↗
PubMed2004

Binding analyses between Human PPARgamma-LBD and ligands.

The binding characteristics of a series of PPARgamma ligands (GW9662, GI 262570, cis-parinaric acid, 15-deoxy-Delta(12,14)-prostaglandin J(2), LY171883, indomethacin, linoleic acid, palmitic acid and troglitazone) to human PPARgamma ligand binding domain have been investigated for the first time by using surface plasmon resonance biosensor technology, CD spectroscopy and molecular docking simulation. The surface plasmon resonance biosensor determined equilibrium dissociation constants (KD values) are in agreement with the results reported in the literature measured by other methods, indicating that the surface plasmon resonance biosensor can assume a direct assay method in screening new PPARgamma agonists or antagonists. Conformational changes of PPARgamma caused by the ligand binding were detected by CD determination. It is interesting that the thermal stability of the receptor, reflected by the increase of the transition temperature (T(m)), was enhanced by the binding of the ligands. The increment of the transition temperature (DeltaT(m)) of PPARgamma owing to ligand binding correlated well with the binding affinity. This finding implies that CD could possibly be a complementary technology with which to determine the binding affinities of ligands to PPARgamma. Molecular docking simulation provided reasonable and reliable binding models of the ligands to PPARgamma at the atomic level, which gave a good explanation of the structure-binding affinity relationship for the ligands interacting with PPARgamma. Moreover, the predicted binding free energies for the ligands correlated well with the binding constants measured by the surface plasmon resonance biosensor, indicating that the docking paradigm used in this study could possibly be employed in virtual screening to discover new PPARgamma ligands, although the docking program cannot accurately predict the absolute ligand-PPARgamma binding affinity.

Apoproteins↗
PubMed2000

Inhibition by unsaturated fatty acids of type II secretory phospholipase A2 synthesis in guinea-pig alveolar macrophages evidence for the eicosanoid-independent pathway.

The effect of arachidonic acid (C20:4) on the production of secretory type II phospholipase A2 (sPLA2-II) by guinea-pig alveolar macrophages was investigated. We show that incubation of these cells with 1-30 microM of arachidonic acid inhibits the synthesis of sPLA2-II in a concentration-dependent manner with an IC50 of approximately 7.5 microM. The inhibition by low concentrations (5 microM) of arachidonic acid was partially reduced by pretreatment of alveolar macrophages with cyclooxygenase or cytochrome P450 inhibitors (aspirin and 1-aminobenzotriazole, respectively), but not by lipoxygenase inhibitor, BW A4C. However, these inhibitors failed to interfere with the effect of high concentrations (30 microM) of arachidonic acid, suggesting that the latter may act on the expression of sPLA2-II, at least in part, independently of eicosanoid generation. Indeed, a similar inhibitory effect on sPLA2-II activity and mRNA expression was observed with other unsaturated fatty acids such as eicosapentaenoic (C20:5) and oleic (C18:1) acids, but not with the saturated fatty acid, palmitic acid (C16:0). In addition, arachidonic acid partially reduced the secretion of tumor necrosis factor alpha, an important intermediate in the induction of sPLA2-II synthesis by guinea-pig alveolar macrophages. However, addition of recombinant tumor necrosis factor alpha failed to reverse the inhibitory effect of arachidonic acid on sPLA2-II expression, suggesting that this process occurs downstream of tumor necrosis factor alpha secretion. We conclude that the expression of sPLA2-II in alveolar macrophages is down-regulated at the transcriptional level by arachidonic acid either directly or via its cyclooxygenase and cytochrome P450-derived metabolites.

Animals↗
PubMed2003

The influence of dietary fish oil vs. sunflower oil on the fatty acid composition of plasma cholesteryl-esters in healthy, adult cats.

The question addressed was whether the fatty acid composition of plasma cholesteryl esters (CEs) in cats reflects the intake of fatty acids. Diets containing either fish oil or sunflower oil were fed to six healthy, adult cats in a cross-over trial. The dry cat foods contained approximately 18.5% crude fat, of which two-third was in the form of the variable oil. Blood samples were collected at the end of each 4-week feeding period, and the fatty acid composition of plasma CEs and plasma concentrations of lipoproteins were determined. Consumption of the diet with fish oil was associated with significantly greater proportions of eicosapentaenoic acid, arachidonic acid, alpha-linolenic acid, oleic acid, palmitic acid and myristic acid in plasma CEs. The intake of fish oil instead of sunflower oil reduced the percentage of linoleic acid in CEs. The plasma concentrations of total cholesterol, high-density lipoprotein cholesterol, phospholipids and triglycerides were not affected by fish oil vs. sunflower oil feeding.

Animals↗
PubMed1997

Oleic acid inhibits gap junction permeability and increases glucose uptake in cultured rat astrocytes.

The role of oleic acid in the modulation of gap junction permeability was studied in cultured rat astrocytes by the scrape-loading/Lucifer yellow transfer technique. Incubation with oleic acid caused a dose-dependent inhibition of gap junction permeability by 79.5% at 50 microM, and no further inhibition was observed by increasing the oleic acid concentration to 100 microM. The oleic acid-mediated inhibition of gap junction permeability was reversible and was prevented by bovine serum albumin. The potency of oleic acid-related compounds in inhibiting gap junction permeability was arachidonic acid > oleic acid > oleyl alcohol > palmitoleic acid > stearic acid > octanol > caprylic acid > palmitic acid > methyloleyl ester. Oleic acid and arachidonic acid, but not methyloleyl ester, increased glucose uptake by astrocytes. Neither oleic acid nor arachidonic acid increased glucose uptake in the poorly coupled glioma C6 cells. These results support that the inhibition of gap junction permeability is associated with the increase in glucose uptake. We suggest that oleic acid may be a physiological mediator of the transduction pathway leading to the inhibition of intercellular communication.

Animals↗
PubMed1980

Binding of diphtheria toxin to phospholipids in liposomes.

Diphtheria toxin bound to the phosphate portion of some, but not all, phospholipids in liposomes. Liposomes consisting of dimyristoyl phosphatidylcholine and cholesterol did not bind toxin. Addition of 20 mol% (compared to dimyristoyl phosphatidylcholine) of dipalmitoyl phosphatidic acid, dicetyl phosphate, phosphatidylinositol phosphate, cardiolipin, or phosphatidylserine in the liposomes resulted in substantial binding of toxin. Inclusion of phosphatidylinositol in dimyristol phosphatidylcholine/cholesterol liposomes did not result in toxin binding. The calcium salt of dipalmitoyl phosphatidic acid was more effective than the sodium salt, and the highest level of binding occurred with liposomes consisting only of dipalmitoyl phosphatidic acid (calcium salt) and cholesterol. Binding of toxin to liposomes was dependent on pH, and the pattern of pH dependence varied with liposomes having different compositions. Incubation of diphtheria toxin with liposomes containing dicetyl phosphate resulted in maximal binding at pH 3.6, whereas binding to liposomes containing phosphatidylinositol phosphate was maximal above pH 7. Toxin did not bind to liposomes containing 20 mol% of a free fatty acid (palmitic acid) or a sulfated lipid (3-sulfogalactosylceramide). Toxin binding to dicetyl phosphate or phosphatidylinositol phosphate was inhibited by UTP, ATP, phosphocholine, or p-nitrophenyl phosphate, but not by uracil. We conclude that (a) diphtheria toxin binds specifically to the phosphate portion of certain phospholipids, (b) binding to phospholipids in liposomes is dependent on pH, but is not due only to electrostatic interaction, and (c) binding may be strongly influenced by the composition of adjacent phospholipids that do not bind toxin. We propose that a minor membrane phospholipid (such as phosphatidylinositol phosphate or phosphatidic acid), or that some other phosphorylated membrane molecule (such as a phosphoprotein) may be important in the initial binding of diphtheria toxin to cells.

Cardiolipins↗
PubMed1990

Hydrophobic surfactant-associated polypeptides: SP-C is a lipopeptide with two palmitoylated cysteine residues, whereas SP-B lacks covalently linked fatty acyl groups.

Pulmonary surfactant contains two hydrophobic polypeptides, SP-B and SP-C, with known amino acid sequences and with truncated subforms lacking the N-terminal residues. Treatment of SP-C with KOH releases fatty acids (palmitic acid to more than 85%) in molar ratios of 1.8-2.0 relative to the polypeptide. Furthermore, plasma-desorption mass spectrometry shows native SP-C of both the intact and truncated types to be monomers with masses about 500 units higher than those expected for the polypeptide chains. After treatment with KOH, trimethylamine, or dithioerythritol, the polypeptide masses are obtained. These results prove that native SP-C is a lipopeptide with two palmitoyl groups covalently linked to the polypeptide chain. The deacylation conditions, the presence of two cysteine residues in the polypeptide, and the absence of other possible attachment sites establish that the palmitoyl groups are thioester-linked to the two adjacent cysteine residues. In contrast, the major form of porcine SP-B is a dimer without fatty acid components. That SP-C is a true lipopeptide with covalently bound palmitoyl groups suggests possibilities for functional interactions. It gives a direct physical link between SP-C and surfactant phospholipid components. Long-chain acylation may constitute a means for association of proteins with membranes and could conceivably modulate the stability and biological activity of surfactant films.

Amino Acid Sequence↗
PubMed1998

Altered constitutive expression of fatty acid-metabolizing enzymes in mice lacking the peroxisome proliferator-activated receptor alpha (PPARalpha).

Peroxisome proliferator-activated receptor alpha (PPARalpha) is a member of the steroid/nuclear receptor superfamily and mediates the biological and toxicological effects of peroxisome proliferators. To determine the physiological role of PPARalpha in fatty acid metabolism, levels of peroxisomal and mitochondrial fatty acid metabolizing enzymes were determined in the PPARalpha null mouse. Constitutive liver beta-oxidation of the long chain fatty acid, palmitic acid, was lower in the PPARalpha null mice as compared with wild type mice, indicating defective mitochondrial fatty acid catabolism. In contrast, constitutive oxidation of the very long chain fatty acid, lignoceric acid, was not different between wild type and PPARalpha null mice, suggesting that constitutive expression of enzymes involved in peroxisomal beta-oxidation is independent of PPARalpha. Indeed, the PPARalpha null mice had normal levels of the peroxisomal acyl-CoA oxidase, bifunctional protein (hydratase + 3-hydroxyacyl-CoA dehydrogenase), and thiolase but lower constitutive expression of the D-type bifunctional protein (hydratase + 3-hydroxyacyl-CoA dehydrogenase). Several mitochondrial fatty acid metabolizing enzymes including very long chain acyl-CoA dehydrogenase, long chain acyl-CoA dehydrogenase, short chain-specific 3-ketoacyl-CoA thiolase, and long chain acyl-CoA synthetase are also expressed at lower levels in the untreated PPARalpha null mice, whereas other fatty acid metabolizing enzymes were not different between the untreated null mice and wild type mice. A lower constitutive expression of mRNAs encoding these enzymes was also found, suggesting that the effect was due to altered gene expression. In wild type mice, both peroxisomal and mitochondrial enzymes were induced by the peroxisome proliferator Wy-14,643; induction was not observed in the PPARalpha null animals. These data indicate that PPARalpha modulates constitutive expression of genes encoding several mitochondrial fatty acid-catabolizing enzymes in addition to mediating inducible mitochondrial and peroxisomal fatty acid beta-oxidation, thus establishing a role for the receptor in fatty acid homeostasis.

17-Hydroxysteroid Dehydrogenases↗
PubMed1999

Ca(2+)/calmodulin-independent activation of calcineurin from Dictyostelium by unsaturated long chain fatty acids.

This study describes a novel mode of activation for the Ca(2+)/calmodulin-dependent protein phosphatase calcineurin. Using purified calcineurin from Dictyostelium discoideum we found a reversible, Ca(2+)/calmodulin-independent activation by the long chain unsaturated fatty acids arachidonic acid, linoleic acid, and oleic acid, which was of the same magnitude as activation by Ca(2+)/calmodulin. Half-maximal stimulation of calcineurin occurred at fatty acid concentrations of approximately 10 microM with either p-nitrophenyl phosphate or RII phosphopeptide as substrates. The methyl ester of arachidonic acid and the saturated fatty acids palmitic acid and arachidic acid did not activate calcineurin. The activation was shown to be independent of the regulatory subunit, calcineurin B. Activation by Ca(2+)/calmodulin and fatty acids was not additive. In binding assays with immobilized calmodulin, arachidonic acid inhibited binding of calcineurin to calmodulin. Therefore fatty acids appear to mimic Ca(2+)/calmodulin action by binding to the calmodulin-binding site.

Animals↗
PubMed2003

Fusion of lamellar body with plasma membrane is driven by the dual action of annexin II tetramer and arachidonic acid.

Annexin II has been implicated in membrane fusion during the exocytosis of lamellar bodies from alveolar epithelial type II cells. Most previous studies were based on the fusion assays by using model membranes. In the present study, we investigated annexin II-mediated membrane fusion by using isolated lamellar bodies and plasma membrane as determined by the relief of octadecyl rhodamine B (R18) self-quenching. Immunodepletion of annexin II from type II cell cytosol reduced its fusion activity. Purified annexin II tetramer (AIIt) induced the fusion of lamellar bodies with the plasma membrane in a dose-dependent manner. This fusion is Ca2+-dependent and is highly specific to AIIt because other annexins (I and II monomer, III, IV, V, and VI) were unable to induce the fusion. Modification of the different functional residues of AIIt by N-ethylmaleimide, nitric oxide, or peroxynitrite abolished AIIt-mediated fusion. Arachidonic acid enhanced AIIt-mediated fusion and reduced its Ca2+ requirement to an intracellularly achievable level. This effect is due to membrane-bound arachidonic acid, not free arachidonic acid. Other fatty acids including linolenic acid, palmitoleic acid, myristoleic acid, stearic acid, palmitic acid, and myristic acid had little effect. AIIt-mediated fusion was suppressed by the removal of arachidonic acid from lamellar body and plasma membrane using bovine serum albumin. The addition of arachidonic acid back to the arachidonic acid-depleted membranes restored its fusion activity. Our results suggest that the fusion between lamellar bodies with the plasma membrane is driven by the synergistic action of AIIt and arachidonic acid.

Animals↗
PubMed2001

Final report on the safety assessment of Corylus Avellana (Hazel) Seed Oil, Corylus Americana (Hazel) Seed Oil, Corylus Avellana (Hazel) Seed Extract, Corylus Americana (Hazel) Seed Extract, Corylus Avellana (Hazel) Leaf Extract, Corylus Americana (Hazel) Leaf Extract, and Corylus Rostrata (Hazel) Leaf Extract.

These ingredients are all derived from hazelnut trees. The two seed oils are expressed from the nuts of the hazelnut tree of the particular species identified. Most current reported cosmetic uses are of the seed oils. The seed extracts are the extract of the nuts of the identified species tree. There is one current report of use of seed extract in cosmetics. The leaf extracts are the extract from the leaves of the particular species tree. There are no current reports of use of these extracts in cosmetics. Analysis of seed oil from one species identified Oleic Acid, Palmitoleic Acid, Linoleic Acid, Eicosaenoic Acid, Docosenoic Acid, Eicosanoic Acid, Palmitic Acid, Linolenic Acid, Stearic Acid, and Tetraeicosanoic Acid. Little information is available to characterize the extracts, however. The functions of most of these ingredients in cosmetics are not reported. In studies of hazelnuts from Spain and Egypt, aflatoxin was reported as a possible contaminant. Aflatoxins are considered carcinogenic in humans. Virtually no safety test data are available on these ingredients. Negative results in one comedogenicity study using a seed oil are reported. Cross-sensitivity to proteins in peanuts and those in hazelnuts are reported, but the presence or absence of protein in nut extract and plant extract from hazelnut trees is not known. Additional data were provided regarding concentration of use, method of extraction and contaminants, comedogenicity, and ultraviolet (UV) radiation absorption, but these data related to nut oil from only one species, and were not overall sufficient to resolve questions about irritation, sensitization, and photosensitization. Because of the absence of data, it is concluded that the available data are insufficient to support the safety of these ingredients in cosmetic products. Because of the limited information that characterizes any of these oils or extracts, data are needed on each (except that items 1, 2, and 3 below are not needed for Hazel [Corylus Avellana] Nut Oil). The additonal data needs include: (1) current concentration of use; (2) method of extraction/manufacture and quality control (i.e., chemical analyses); (3) contaminants and methods of extraction (especially pesticides and heavy metals); (4) dermal irritation and sensitization; (5) UV absorption; if there is significant absorption, then a photosensitization study will be needed; (6) 28-day dermal toxicity; (7) reproductive and developmental toxicity; and (8) two genotoxicity assays, one in a mammalian system; if positive, then a 2-year dermal carcinogenesis study using National Toxicology Program (NTP) methods may be needed.

Acne Vulgaris↗
PubMed1975

[Qualitative and quantitative studies on the metabolism of fatty acids, in particular on that of linoleic acid in calves].

24 calves of the breed "Deutsche Schwarzbunte Rasse" were used for qualitative and quantitative investigations on the metabolism of fatty acids, particularly that of linoleic acid. The trial comprised 6 calves in 4 groups. The experimental rations consisted of powdered skim milk, oat meal, milk sugar, coco fat and varying proportions of linoleic acid (1.0%, 1.5%, 2.5%). The control group received the basal ration without supplements of linoleic acid. After a short period of adjustment the metabolic trial was started with 9 periods each lasting 7 days. The composition of fatty acids in the faecal lipids was analysed by gas chromatography. The studies led to the conclusion that the fatty acids contained in the faecal fat were not immediately derived from the dietary fat. The results of the trial also showed that the major proportion of all the fatty acids present in the faecal lipids consisted of only 4 fatty acids, viz. oleic acid, palmitic acid, lauric acid and myristic acid. Changes observed for the content of linoleic acid in faecal lipids were negligible so that the assumption may be made that all of the linoleic acid added was completely digested.

Animal Feed↗