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PubMed1981

Propionyl-CoA carboxylase deficiency: case report, effect of low-protein diet and identification of 3-oxo-2-methylvaleric acid 3-hydroxy-2-methylvaleric acid, and maleic acid in urine.

Vomiting, lethargy and metabolic acidosis were the main initial symptoms of metabolic disease in a 1 month old girl. Her older sister had died from a similar disease, considered to be Reye's syndrome, at an age of 15 months. The urine of the present case contained 2-methylcitric acid, 3-hydroxypropionic acid, N-propionylglycine, 2-hydroxy-3-methylbutyric acid, N-tiglylglycine, 3-hydroxyvaleric acid and glutaric acid. These metabolites are all known to be associated with propionyl-CoA accumulation. Free propionic acid was not detected in the urine. In addition, the urine contained 3-oxo-2-methylvaleric acid and 3-hydroxy-2-methylvaleric acid, probably formed by condensation of two molecules of propionyl-CoA. The identity of these metabolites was confirmed by synthesis. An elevated urinary concentration of maleic acid and fumaric acid was another constant abnormality. The activity of propionyl-CoA carboxylase in leucocytes was about 20% of the normal activity. The girl was teated with a low-protein diet since the diagnosis was made at an age of 1 month, and her psychomotor development was satisfactory at an age of 2 1/2 years. She had a few episodes of acidosis during infections.

Amino Acid Metabolism, Inborn Errors↗

PubMed1976

[Effect of ursodeoxycholic acid on bile secretion and bile components. Comparison with chenodeoxycholic acid and dehydrocholic acid].

Effects of some bile acids on the biliary flow, BSP output and composition (phospholipid, cholesterol, bilirubin and bile acids) were studied in dogs. Ursodeoxycholic acid (UD), chenodeoxycholic acid (CD) and dehydrocholic acid (DC) caused a dramatic increase in biliary flow and BSP output. Relative potencies of these effects were DC greater than CD greater than or equal to UD. UD increased the phospholipid, bile acids and cholesterol concentration but had little effect on bilirubin concentration. Furthermore, UD greatly increased the output of four bile components. CD slightly decreased the phospholipid, cholesterol and bilirubin concentration without the bile acids, while CD increased the output of bile components. After UD or CD administration, the bile acid of each appeared markedly in the bile, dose dependently. On the other hand, DC caused a dramatic decrease of phospholipid, cholesterol and bilirubin concentration but had little effect on bile acids concentration. Output of bile components was increased by DC the first 1 hr but decreased at 2 hr. After DC administration, 3alpha, 7alpha-dihydroxy-12keto-5beta-cholanic acid appeared in the bile while DC did not. Therefore, it is concluded that UD and CD are cholanereticas and DC is a hydrocholeretica.

Animals↗

PubMed1990

Dietary linoleic acid and polyunsaturated fatty acids in rat brain and other organs. Minimal requirements of linoleic acid.

Starting three weeks before mating, 12 groups of female rats were fed different amounts of linoleic acid (18:2n-6). Their male pups were killed when 21-days-old. Varying the dietary 18:2n-6 content between 150 and 6200 mg/100 g food intake had the following results. Linoleic acid levels remained very low in brain, myelin, synaptosomes, and retina. In contrast, 18:2n-6 levels increased in sciatic nerve. In heart, linoleic acid levels were high, but were not related to dietary linoleic acid intake. Levels of 18:2n-6 were significantly increased in liver, lung, kidney, and testicle and were even higher in muscle and adipose tissue. On the other hand, in heart a constant amount of 18:2n-6 was found at a low level of dietary 18:2n-6. Constant levels of arachidonic acid (20:4n-6) were reached at 150 mg/100 g diet in all nerve structures, and at 300 mg/100 g diet in testicle and muscle, at 800 mg/100 g diet in kidney, and at 1200 mg/100 g diet in liver, lung, and heart. Constant adrenic acid (22:4n-6) levels were obtained at 150, 900, and 1200 mg/100 g diet in myelin, sciatic nerve, and brain, respectively. Minimal levels were difficult to determine. In all fractions examined accumulation of docosapentaenoic acid (22:5n-6) was the most direct and specific consequence of increasing amounts of dietary 18:2n-6. Tissue eicosapentaenoic acid (20:5n-3) and 22:5n-3 levels were relatively independent of dietary 18:2n-6 intake, except in lung, liver, and kidney. In several organs (muscle, lung, kidney, liver, heart) as well as in myelin, very low levels of dietary linoleic acid led to an increase in 20:5n-3.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

PubMed2005

Stereoblock poly(lactic acid): synthesis via solid-state polycondensation of a stereocomplexed mixture of poly(L-lactic acid) and poly(D-lactic acid).

Stereoblock poly(lactic acid) consisting of D- and L-lactate stereosequences can be successfully synthesized by solid-state polycondensation of a 1:1 mixture of poly(L-lactic acid) and poly(D-lactic acid). In the first step, melt-polycondensation of L- and D-lactic acids is conducted to synthesize poly(L-lactic acid) and poly(D-lactic acid) with a medium-molecular-weight, respectively. In the next step, these poly(L-lactic acid) and poly(D-lactic acid) are melt-blended in 1:1 ratio to allow formation of their stereocomplex. In the last step, this melt-blend is subjected to solid-state polycondensation at temperature where the dehydrative condensation is allowed to promote chain extension in the amorphous phase with the stereocomplex crystals preserved. Finally, stereoblock poly(lactic acid) having high-molecular-weight is obtained. The stereoblock poly(lactic acid) synthesized by this way shows a higher melting temperature in consequence of the controlled block lengths and the resulting higher-molecular-weight. The product characterization as well as the optimization of the polymerization conditions is described. Changes in M(w) of stereoblock poly(lactic acid) (sb-PLA) as a function of the reaction time.

Biocompatible Materials↗

PubMed1999

Renal handling of amino acids in 5/6-nephrectomized rats: stimulation of renal amino acid reabsorption after treatment with triiodothyronine or dexamethasone under amino acid load.

In anaesthetized adult female rats, the renal amino acid handling was measured six days after 5/6 nephrectomy (5/6NX). The distinct rise in blood urea nitrogen as well as the significant reduction in urine flow and GFR indicate an impairment of kidney function. In principle, in 5/6NX rats amino acid plasma concentrations were comparable to those of control animals with two intact kidneys, whereas the fractional excretions (FEAA) of most endogenous amino acids measured were significantly enhanced. After bolus injection of leucine or taurine (each 20 mg/100 g b.wt.) or glutamine (90 mg/ 100 g b.wt.), dissolved in 2 ml normal saline per 100 g b.wt., the FEAA of both the amino acids administered and the endogenous amino acids increased as a sign of overloaded amino acid reabsorption capacity. This effect was more pronounced in 5/6NX rats than in controls. As early as one hour after amino acid load, plasma concentrations and FEAA returned to baseline values of 5/6NX rats. A pretreatment with triiodothyronine (20 micrograms/100 g b.wt.) or dexamethasone (60 micrograms/100 g b.wt.), both given intraperitoneally once daily for 3 days, stimulated the renal amino acid transport capacity in 5/6NX rats: the increase in FEAA after amino acid load was significantly lower compared to non-pretreated animals. This stimulation could be shown for the bolus amino acids and the endogenous amino acids and was more distinct in 5/6NX rats than in controls with two intact kidneys.

Amino Acids↗

PubMed1975

Partial purification and properties of an enzyme from Escherichia coli that catalyzes the conversion of glutamic acid and 10-formyltetrahydropteroylglutamic acid to 10-formyltetrahydropterol-gamma-glutamyglutamic acid.

An enzyme that catalyzes the conversion of L-glutamic acid and 10-formyl-H4folic acid (also known as 10-formyl-H4pteroylglutamic acid) to 10-formyl-H4pteroyl-gamma-glutamylglutamic acid has been purified by 74-fold from extracts of Escherichia coli. ATP, Mg-2+, and a monovalent cation (K+ or NH-4, but not Na+) are required for the enzyme to function. Radioactive and bioautographic analyses revealed the formation of a single product. This product was identified as 10-formyl-H-4pteroyl-gamma-glutamylglutamic acid from its spectral characteristics, its ability to be used effectively as a growth faster for Lactobacillus casei 7469, and from radioactive analysis that indicated the incorporation into the product of 1 mol glutamate/mol of 10-formyl-H-4pteroylglutamic acid utilized. The enzyme functions optimally at pH 9.0-9.8 and at 50 degrees. Its molecular weight is estimated at 42,000-43,000. The Km values are 180 muM for L-glutamic acid and less than 2 muM for (-) 10-formyl-H-4pteroylglutamic acid. The only other naturally occurring folate compounds with significant activity as substrate are H-4pteroylglutamic acid and 5,10-methylene-H-4pteroylglutamic acid; however, these compounds are not used as effectively (K-m values are 10-12 mu-M) as 10-formyl-H-4pteroylglutamic acid.

Adenosine Triphosphate↗

PubMed1984

[Effect of glutamic acid content of the diet on the catabolic rate of isotope-labeled glutamic acid in rats. 2. Time course of 14CO2 excretion following subcutaneous administration of 14C-glutamic acid].

40 rats with a body weight of 100 g received 7 semisynthetic diets with different contents of glutamic acid and one diet contained whole egg. A L-amino acid mixture corresponding to the pattern of egg protein was the protein source of the semisynthetic diets. Glutamic acid was supplemented successively from 0 to 58 mol-% of the total amino acid content. On the 8th day of experimental feeding the animals were labelled by subcutaneous injection of 14C-U-L-glutamic acid. Subsequently the CO2- and the 14CO2-excretion were measured for 24 hours. In this period 64 to 68% of the injected radioactivity were recovered as 14CO2. The curve pattern of 14CO2-excretion indicates two different processes of 14CO2-formation. One characterizing the direct degradation of glutamic acid to CO2 with a high rate constant and a second one with a lower rate constant characterizing the 14CO2-formation via metabolites of glutamic acid. 77% of the total 14CO2-excretion in 24 hours resulted from the direct oxidation of glutamic acid and 23% from the oxidation of intermediates. When 14CO2-formation was measured 10 to 24 hours after injection of 14C-glutamic acid a positive correlation to the content of glutamic acid in the diet was observed. The intestinal tissue contribute considerably to the catabolization of glutamic acid, however, there seems to exist an upper limit for this capacity.

Animal Feed↗

PubMed1981

The antiscorbutic action of L-ascorbic acid and D-isoascorbic acid (erythorbic acid) in the guinea pig.

Female guinea pigs were fed a scorbutigenic diet supplemented with either L-ascorbic acid or D-isoascorbic acid or combinations of these. Their responses were judged by changes in body weight, serum alkaline phosphatase levels, wound healing, and tooth structure. Large additions (100 mg daily) of D-isoascorbic acid to the scorbutigenic diet resulted in normal growth over a 7-wk period and normal serum alkaline phosphatase levels, tooth structure development, and collagen formation after wounding. The addition of 0.5 or 5.0 mg of L-ascorbic acid to this high D-isoascorbic diet improved neither growth rate nor collagen deposition during wound healing. On the basis of changes in tooth structure, D-isoascorbic acid has 1/20 the potency of L-ascorbic acid. Its effect is additive to subminimal maintenance levels of L-ascorbic acid implying that there is no competitive inhibition in the utilization of the two compounds. The relatively weak activity of D-isoascorbic acid is probably due to poor transport to the tissues and ineffective binding to functional sites. This explains why the onset of scurvy is much more rapid after withdrawal of D-isoascorbic acid from the diet when it had been the sole antiscorbutic dietary constituent. It is concluded that D-isoascorbic acid is a "weakly" antiscorbutic agent on the basis that it is both poorly absorbed and retained by the tissue; that in fact it may, to the degree that it is taken up by the tissues and retained, be equal in antiscorbutic potency to L-ascorbic acid.

Alkaline Phosphatase↗

PubMed2004

Analysis of gamma-hydroxybutyric acid, DL-lactic acid, glycolic acid, ethylene glycol and other glycols in body fluids by a direct injection gas chromatography-mass spectrometry assay for wide use.

Analysis of blood of severely intoxicated patients always requires prompt investigation. Diagnosis of intoxication with ethylene glycol, gamma-hydroxybutyric acid or D-lactic acid takes hours, since several different procedures are required. Rapid derivatization of the common hydroxyl function may resolve this analytical problem. Here we describe a fast method for the simultaneous measurement of ethylene glycol, glycolic acid, gamma-hydroxybutyric acid and racemic lactic acid. Only 20 microl of serum, plasma or urine are required for immediate derivatization at 70 degrees C with 750 microl of bis-N,O-trimethylsilyl trifluoroacetamide after adding 20 microl of internal standard solution (1,3-propylene glycol) and 20 microl of the catalyst dimethylformamide. After centrifugation an aliquot is transferred to a gas chromatographic system and analyzed with electron-impact mass spectrometry in selective ion monitoring mode. The derivatized acids and ethylene glycol are well separated and detected with a limit of detection ranging from 0.12 mg/l for ethylene glycol to 0.95 mg/l for gamma-hydroxybutyric acid, while the limit of quantification ranged from 0.4 mg/l for ethylene glycol to 3.15 mg/l for gamma-hydroxybutyric acid. The method is linear from 0.5 to 1800 mg/l blood for ethylene glycol, from 0.7 to 1200 mg/l for lactic acid, from 1.2 to 1800 mg/l for glycolic acid, and from 3.2 to 200 mg/l for gamma-hydroxybutyric acid, with analytical recoveries, accuracy, day-to-day and within-day precision well within the required limits. Total analysis time with one calibrator was 30 min, derivatization time included. This method is very suitable for emergency toxicology, since several toxic substances can be quantified simultaneously in a fast and sensitive manner.

Chromatography↗

PubMed1988

Occurrence of 3 beta-hydroxy-5-cholestenoic acid, 3 beta,7 alpha-dihydroxy-5-cholestenoic acid, and 7 alpha-hydroxy-3-oxo-4-cholestenoic acid as normal constituents in human blood.

Three unconjugated C27 bile acids were found in plasma from healthy humans. They were isolated by liquid-solid extraction and anion-exchange chromatography and were identified by gas-liquid chromatography-mass spectrometry, microchemical reactions, and ultraviolet spectroscopy as 3 beta-hydroxy-5-cholestenoic, 3 beta,7 alpha-dihydroxy-5-cholestenoic, and 7 alpha-hydroxy-3-oxo-4-cholestenoic acids. Their levels often exceeded those of the unconjugated C24 bile acids and the variations between individuals were smaller than for the C24 acids. The concentrations in plasma from 11 healthy subjects were 67.2 +/- 27.9 ng/ml (mean +/- SD) for 3 beta-hydroxy-5-cholestenoic acid, 38.9 +/- 25.6 ng/ml for 3 beta,7 alpha-dihydroxy-5-cholestenoic acid, and 81.7 +/- 27.9 ng/ml for 7 alpha-hydroxy-3-oxo-4-cholestenoic acid. The levels of the individual acids were positively correlated to each other and not to the levels of the C24 acids. The cholestenoic acids were below the detection limit (20-50 ng/ml) in bile and C27 bile acids present in bile were not detected in plasma.

Adult↗

PubMed1985

Docosahexaenoic acid (C22:6 omega 3) and linoleic acid are anti-aggregatory, and alter arachidonic acid metabolism in human platelets.

Effects of various concentrations (12.5-500 uM) of linoleic acid and docosahexaenoic acid (C22:6 omega 3)(sod. salt) were examined on the platelet metabolism of labelled arachidonate (AA) under two different incubation conditions. In the first platelets were pretreated with either fatty acid prior to incubation with labelled AA; and in the second incubation platelets were incubated with a mixture containing a fatty acid (linoleic acid or DHA) and labelled AA. At all concentrations the two fatty acids reduced the formation of TxB2. At lower concentrations (up to 200 uM) the fatty acids inhibited platelet cyclooxygenase as shown by a reduced formation of prostaglandins (PGs) and TxB2. At higher concentrations (400 and 500 uM), however, the fatty acids behaved differently. Although TxB2 formation was reduced, there was observed an increased formation of PGs. In DHA pretreated platelets only PGE2 increased (to double control values). Platelets pretreated with linoleic acid produced increased amounts of all PGs (PGF2 alpha, PGE2, PGD2), and this effect was greatest for PGE2 which increased by 5-6 fold of control values. DHA showed a dose-dependent inhibition of platelet aggregation induced by arachidonate, epinephrine and collagen.

Arachidonic Acid↗

PubMed1991

Lack of dose response by dietary n-3 fatty acids at a constant ratio of n-3 to n-6 fatty acids in suppressing eicosanoid biosynthesis from arachidonic acid.

This study evaluated whether it is the ratio of n-3 to n-6 fatty acids or the absolute amount of n-3 fatty acids in diets that determines the degree of inhibition of eicosanoid biosynthesis from arachidonic acid (AA). Rats were fed diets containing different doses of linolenic acid or menhaden oil for 3 mo. Constant ratios of n-3 to n-6 fatty acids were maintained by concomitant increases in safflower oil as the n-6 fatty acid source. Results showed that AA concentrations in liver, platelet, and lung phospholipids and concentrations of eicosanoids synthesized in tissues were significantly (P less than 0.05) suppressed both by linolenic acid and menhaden oil; however, there was a lack of a dose response within groups fed different amounts of the same dietary fat. These results indicate that the ratio of n-3 to n-6 fatty acids in the diets, rather than the absolute amount of n-3 fatty acids, is the determining factor in inhibiting eicosanoid biosynthesis from AA.

Animals↗

PubMed1992

Effect of simvastatin, ursodeoxycholic acid and simvastatin plus ursodeoxycholic acid on biliary lipid secretion and cholic acid kinetics in nonfamilial hypercholesterolemia.

It has been recently shown that the newest hypocholesterolemic agent, simvastatin, lowers the biliary cholesterol saturation index and that its association with ursodeoxycholic acid renders it more effective. To determine the mechanism by which simvastatin decreases the biliary cholesterol saturation index, we evaluated hepatic secretion rates of cholesterol, bile acids and phospholipids, and cholic acid pool size, turnover and synthesis in eight hyperlipidemic patients (five women and three men, age range = 38 to 65 yr). These assessments were conducted before treatment, after 4 wk of simvastatin (40 mg/day), after 4 wk of ursodeoxycholic acid (600 mg/day) and after a further 4 wk of a combination therapy of simvastatin (40 mg/day) plus ursodeoxycholic acid (600 mg/day). The cholesterol saturation index was significantly reduced with simvastatin (from 1.51 +/- 0.10 to 0.94 +/- 0.05, mean +/- S.E.; p less than 0.02), with ursodeoxycholic acid (from 1.51 +/- 0.10 to 0.86 +/- 0.03, mean +/- S.E.; p less than 0.02) and with the combination of simvastatin plus ursodeoxycholic acid (from 1.51 +/- 0.01 to 0.70 +/- 0.05, p less than 0.02). The cholesterol saturation index during combination therapy was significantly lower (p less than 0.02) than that reached during the use of simvastatin and ursodeoxycholic acid. Both simvastatin and ursodeoxycholic acid significantly reduced the hepatic secretion rate of cholesterol (from 130 +/- 14 mumols/hr to 81 +/- 12 mumols/hr, p less than 0.01, and 70 +/- 9 mumols/hr, p less than 0.01) without affecting bile acid and phospholipid outputs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2006

Effects of milk enriched with omega-3 fatty acid, oleic acid and folic acid in patients with metabolic syndrome.

BACKGROUND & AIMS: Patients with metabolic syndrome (MS) have increased cardiovascular risk factors. Dietary modifications mainly polyunsatturated fatty acids intake, can improve them. The present study was performed to assess the effects of enriched milk with omega-3 and oleic fatty acids, folic acid and vitamin E, in these patients. METHODS: We performed a randomized, placebo-controlled and open clinical trial, among 72 patients with MS for 3 months. Thirty-six of them consumed 500 cm(3) per day of semi-skimmed milk (control group), and the others consumed 500 cm(3) per day of enriched milk (test group). Daily supplements in this group were 5.7 g of oleic acid, 0.2g of omega-3 fatty acid, 150 microg of folic acid and 7.5mg of vitamin E. Serum for total and HDL cholesterol, triglycerol, Apo B, glucose, insulin, hs-CRP, homocysteine and fatty acids contents in serum phospholipids, was obtained at the beginning and at the end of the study. LDL cholesterol was calculated by Friedewald formula. RESULTS: Four patients in the test group, and two in the control group dropped out. In the test group a decrease in serum total cholesterol (-6.2%, P=0.006), LDL cholesterol (-7.5%, P=0.032), triglycerol (-13.3%, P=0.016), Apo B (-5.7%, P=0.036), glucose (-5.3%, P=0.013), and homocysteine (-9.5%, P=0.00) was observed. Any of these parameters changed in the control group. CONCLUSIONS: Dietary supplementation with 500 cm(3) of enriched milk with omega-3 fatty acid, oleic acid and folic acid, reduces serum tryglicerides, total and LDL cholesterol, Apo B, glucose and homocysteine in patients with MS. This milk is well tolerated and accepted by the patients.

Animals↗

PubMed2002

Identification of a novel Na+-independent acidic amino acid transporter with structural similarity to the member of a heterodimeric amino acid transporter family associated with unknown heavy chains.

We identified a novel Na(+)-independent acidic amino acid transporter designated AGT1 (aspartate/glutamate transporter 1). AGT1 exhibits the highest sequence similarity (48% identity) to the Na(+)-independent small neutral amino acid transporter Asc (asc-type amino acid transporter)-2 a member of the heterodimeric amino acid transporter family presumed to be associated with unknown heavy chains (Chairoungdua, A., Kanai, Y., Matsuo, H., Inatomi, J., Kim, D. K., and Endou, H. (2001) J. Biol. Chem. 276, 49390-49399). The cysteine residue responsible for the disulfide bond formation between transporters (light chains) and heavy chain subunits of the heterodimeric amino acid transporter family is conserved for AGT1. Because AGT1 solely expressed or coexpressed with already known heavy chain 4F2hc (4F2 heavy chain) or rBAT (related to b(0,+)-amino acid transporter) did not induce functional activity, we generated fusion proteins in which AGT1 was connected with 4F2hc or rBAT. The fusion proteins were sorted to the plasma membrane and expressed the Na(+)-independent transport activity for acidic amino acids. Distinct from the Na(+)-independent cystine/glutamate transporter xCT structurally related to AGT1, AGT1 did not accept cystine, homocysteate, and l-alpha-aminoadipate and exhibited high affinity to aspartate as well as glutamate, suggesting that the negative charge recognition site in the side chain-binding site of AGT1 would be closer to the alpha-carbon binding site compared with that of xCT. The AGT1 message was predominantly expressed in kidney. In mouse kidney, AGT1 protein was present in the basolateral membrane of the proximal straight tubules and distal convoluted tubules. In the Western blot analysis, AGT1 was detected as a high molecular mass band in the nonreducing condition, whereas the band shifted to a 40-kDa band corresponding to the AGT1 monomer in the reducing condition, suggesting the association of AGT1 with other protein via a disulfide bond. The finding of AGT1 and Asc-2 has established a new subgroup of the heterodimeric amino acid transporter family whose members associate not with 4F2hc or rBAT but with other unknown heavy chains.

Amino Acid Sequence↗

PubMed1998

Membrane fluidity and fatty acid metabolism in kidney cells from rats fed purified eicosapentaenoic acid or purified docosahexaenoic acid.

Rats were given a supplement (1.5 ml/day) of purified eicosapentaenoic acid (EPA, 20:5,n-3), purified docosahexaenoic acid (DHA, 22:6,n-3)), or corn oil for 10 days. Membrane fluidity, measured as the steady-state fluorescence polarization of diphenylhexatriene (DPH), was approximately 20% lower in kidney cells from rats fed purified EPA than in cells from the DHA-fed or corn-oil fed animals. The level of 20:5(n-3) in kidney phospholipids was 18 times higher in rats fed EPA, and four times higher in those fed DHA as compared to the corn-oil group. The level of arachidonic acid (20:4,n-6) was concomitantly decreased, while linoleic acid (18:2,n-6) was increased in kidney-phospholipids in the n-3 fatty acid fed rats. The proportion of 22:6(n-3) in kidney phospholipids was not affected by EPA supplementation, while the DHA diet slightly increased the level of this fatty acid. The distribution of phospholipid subclasses was significantly altered in that phosphatidylcholine was increased and phosphatidylethanolamine was concomitantly decreased. It is suggested that the decrease in 20:4(n-6) is relatively more important in the regulation of fluidity than a concomitant increase in 20:5(n-3). It is also suggested that the compensatory modifications of the phospholipid subclass distribution as a response to decreased 20:4(n-6)/20:5(n-3) ratio was not sufficient to maintain fluidity when the ratio was as low as in the present study. The incorporation of labelled linolenic acid (18:3,n-3) in phospholipids was decreased in cells from the n-3 supplemented rats. Since endogenous 22:5(n-3) in phospholipids was only increased in the EPA group, 22:6(n-3) only in the DHA group, and 20:5(n-3) in both, it is suggested that the decreased incorporation of labelled 18:3(n-3) into phospholipids of the DHA-fed rats in particular is correlated to the increased level of 22:6(n-3) in the membrane phospholipids. The incorporation of fatty acids into phopholipids may thus show substrate specificity, in that 22:6(n-3) is less exchangable with labelled 18:3(n-3) than is 20:5(n-3). These results demonstrate that increasing levels of n-3 fatty acids in membranes affect the uptake and intracellular metabolism of fatty acids as well as membrane fluidity in the kidney.

Animals↗

PubMed1987

Ingestion of fish oil or a derived n-3 fatty acid concentrate containing eicosapentaenoic acid (EPA) affects fatty acid compositions of individual phospholipids of rat brain, sciatic nerve and retina.

The effect of feeding redfish (Sebastes marinus or mantella) oil or a derived n-3 fatty acid concentrate containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on the fatty acid compositions of individual phospholipids in selected neural tissues was studied in growing male rats. Control animals were given sunflower oil in the diet for the 5-wk feeding trial. Lipid analyses revealed that EPA (20:5n-3) became significantly enriched in all phospholipid fractions (phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and phosphatidylinositol) in the tissues studied (brain, retina and sciatic nerve) in the two n-3 fatty acid dietary groups relative to controls. Corresponding changes were also found in the 22:5n-3 contents of these tissues, whereas little or no significant elevation in DHA (22:6n-3) was found. In contrast, the percentages by weight of the n-6 fatty acids including 18:2n-6, 20:4n-6 (arachidonic acid, AA), 22:4n-6 and 22:5n-6 were generally lower in the various phospholipids/tissues of the animals given fish oil or the n-3 fatty acid concentrate; the levels of 22:5n-6 and 22:4n-6 were markedly affected in this regard. These results indicate that dietary n-3 fatty acids (as EPA plus DHA) can greatly affect the fatty acid compositions of the various membrane phospholipids in nervous tissues within a relatively short time. These biochemical alterations may be important for functional changes including altered membrane fluidity, cellular responses, ion transport and the biosyntheses of AA- and EPA-derived prostaglandins and leukotrienes.

Animals↗

PubMed1994

Conjugated linoleic acid (9,11- and 10,12-octadecadienoic acid) is produced in conventional but not germ-free rats fed linoleic acid.

Conjugated linoleic acid (CLA) is an anticarcinogen in several model animal systems. Conjugated linoleic acid occurs naturally in food and is present at higher concentrations in products from ruminant animals. Given that certain rumen microorganisms produce CLA from free linoleic acid, we studied the effect of feeding free or esterified linoleic acid on tissue CLA concentrations using conventional and germ-free rats. Conventional rats were fed a 5% (wt/wt) corn oil control diet alone or supplemented with 5% free linoleic acid or 8.63% corn oil (equivalent to 5% linoleic acid in triglyceride). Germ-free rats were fed autoclavable nonpurified diet alone or supplemented with 5% free linoleic acid. Analyses of CLA concentrations were performed on lipids extracted from liver, lung, kidney, skeletal muscle and abdominal adipose tissue, and on liver phospholipid and neutral lipid fractions. Tissue CLA concentrations were higher in conventional rats fed free linoleic acid (the major isomers were cis-9, trans-11 and trans-9, cis-11) than in control animals. Conjugated linoleic acid concentrations in free linoleic acid-fed rats were maximal at 4 wk, and levels were 5-10 times higher than those of controls. Elevated CLA concentrations were also observed in liver phospholipid and neutral lipid fractions. In contrast, CLA concentrations in the tissues of germ-free rats were not affected by diet. Feeding the corn oil-fortified diet to conventional rats did not increase CLA concentration in the tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗