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Acetyl CoA carboxylase shares control of fatty acid synthesis with fatty acid synthase in bovine mammary homogenate.

The objectives of this research were to determine the flux control coefficients for acetyl CoA carboxylase and fatty acid synthase using an in vitro preparation of bovine mammary homogenate. For an enzyme to be considered rate limiting with the use of metabolic control analysis, its control coefficient would be equal to unity. The hypothesis for this experiment was that the control coefficient for acetyl CoA carboxylase was not equal to unity, and that this enzyme was not, therefore, the rate-limiting step. Mammary tissue was isolated from lactating Holstein cows at slaughter and frozen in liquid nitrogen. Tissue was ground, homogenized, and centrifuged to obtain a postmitochondrial supernatant for use in in vitro incubations containing labeled acetate. Specific inhibitors for acetyl CoA carboxylase and fatty acid synthase were used to fractionally inhibit de novo synthesis for the calculation of flux control coefficients. The composition of fatty acids synthesized in the absence of enzyme inhibitors was similar to the composition of fatty acids in the presence of inhibitors. Calculations following avidin inhibition of acetyl CoA carboxylase determined the flux control coefficient was 0.63 +/- 0.15, which means that 63% of the control of fatty acid synthesis is exerted by acetyl CoA carboxylase. The remaining control (37%) was from fatty acid synthase, which indicates a significant degree of control over the flux of acetate in de novo synthesis resides with this enzyme. The rate-limiting status ascribed to acetyl CoA carboxylase was not supported, because the flux control coefficient was less than unity. Metabolic control analysis, through its use of pathway product measurements, allows for potential interactions in the pathway such as feedback inhibition contribution to the flux control coefficients, which would not otherwise be considered in studies measuring enzyme kinetics with purified enzymes.

Acetates↗

Whole body fatty acid synthesis and fatty acid intake in young rats of the Zucker strain (Fa/- and fa/fa).

The rate of whole body fatty acid synthesis was measured in immature (18- and 25-day-old) lean and obese male Zucker rats. The effect of stress and diurnal variation on the rate of fatty acid synthesis was also determined in 25-day-old animals. In addition, the intake of fatty acid from the diet was also determined. At 16 and 18 days the carcase of the obese rat contained significantly more lipid than its lean counterpart. In neither phenotype was there any significant lipid deposition from 18 to 23 days. Over the period 23 to 27 days the obese rat deposited approximately six times more lipid than its lean counterpart. Consistent with this finding is the observation that at 25 days the obese rat synthesized at least four to five times more fatty acid than its lean littermate. There was no phenotypic difference in the rate of fatty acid synthesis at 18 days. It is suggested that the young obese rat becomes obese before weaning because of a reduced oxidation, and hence increased storage, of dietary fatty acid. After weaning, although this unusual partition persists, hyperlipogenesis is the main cause of the further development of obesity.

Age Factors↗

Complexation of fatty acids and fatty acid-CoAs with synthetic O-methylated polysaccharides.

An experimentally simple, but highly reproducible and reliable method has been developed to follow the complexation event of fatty acid (FA) and FA-CoA with polysaccharides. This method was based on the recent discovery of the unique blue-shifted UV absorption associated with the aggregation of tetraenoic fatty acids (TE-FAs) in aqueous solution. Complexation was monitored by recording the intensity of UV absorption at 250 nm ([free TE-FA]) and 303 nm ([complexed TE-FA]), and the K aggregate of C(20) t,t,t,t-TE-FA exhibited the ideal property for this purpose. Synthetic 3-O-methyl-D-mannose- and 6-O-methyl-D-glucose-containing lipopolysaccharides were found to exhibit a broad range of the binding affinities with C(20) t,t,t,t-TE-FAs as well as saturated FAs/FA-CoAs.

Acyl Coenzyme A↗

Dietary long-chain polyunsaturated fatty acids influence tissue fatty acid composition in rats at weaning.

We studied the fatty acid composition of plasma, plasma phospholipids, erythrocyte membrane lipids, liver microsomal phospholipids and brain lipids in rats fed three different diets varying in their (n-3) and (n-6) long-chain polyunsaturated fatty acid (LCP) concentrations for 0, 2 and 4 wk after weaning. The three diets contained 10% fat; diet HO had a high-oleic acid proportion; diet FO was enriched in n-3 LCP provided by fish oil; and diet FO + BPL contained n-3 and n-6 LCP supplied by fish oil and a brain phospholipid concentrate. At 2 and 4 wk after weaning the proportions of oleic acid in all tissues, except in liver microsomes of the FO + BPL group, were significantly higher than in weanling rats. The absence of (n-3) LCP intake resulted in significantly lower levels of docosapentaenoic [20:5(n-3)] and 22:6(n-3) acids in plasma, plasma phospholipids, erythrocyte membrane lipids and liver microsomal phospholipids but not in brain lipids compared with rats at weaning. Dietary supplementation with (n-3) LCP (FO and FO + BPL groups) for 4 wk led to higher levels of 22:6(n-3) in all tissues compared with rats fed the HO fat. The proportions of 20:4(n-6) and total (n-6) LCP were significantly lower in all tissues from rats fed the FO diet than in rats at weaning and rats fed the HO diet. After 2 and 4 wk, rats fed the FO + BPL diet had significantly higher levels of 20:4(n-6) and total (n-6) LCP in plasma, plasma phospholipids, erythrocyte lipids and liver microsomal phospholipids; the brain also showed a higher content of those fatty acids after 4 wk. Our results suggest that dietary supplementation with 20:4(n-6) and 22:6(n-3) influences the concentration of 20:4-(n-6) and 22:6(n-3) in body tissues of rats after weaning.

Animals↗

Alkylthioacetic acid (3-thia fatty acids)--a new group of non-beta-oxidizable, peroxisome-inducing fatty acid analogues. I. A study on the structural requirements for proliferation of peroxisomes and mitochondria in rat liver.

The induction of peroxisome proliferation was examined in rat liver after administration of equal concentrations (1 mmol/kg body weight) of 1,10-bis(carboxymethylthiodecane) (BCMTD), 1-mono(carboxymethylthiotetradecane) (CMTTD), 1-mono(carboxymethylthiooctane) (CMTO), 1-mono(carboxyethylthiotetradecane) (CETTD), palmitic acid and hexadecanedioic acid (HDDA). BCMTD, a non-beta-oxidizable and non-omega-oxidizable sulphur-substituted fatty acid analogue was considerably more potent than CMTTD (only non-beta-oxidizable) in inducing enlargement of the liver and increasing peroxisomal activities (monitored by peroxisomal beta-oxidation, palmitoyl-CoA hydrolase and catalase activities). Morphometric analysis of randomly selected hepatocytes revealed that BCMTD and CMTTD treatment increased the number and size of peroxisomes and the relative volume fraction of the peroxisomes. All these cellular responses were more marked with BCMTD than compared with CMTTD. CMTO, a non-beta-oxidizable fatty acid analogue containing a lower hydrophobic alkyl-end than CMTTD and CETTD (a beta-oxidizable fatty acid analogue), showed a slight increase (1.4-1.8-fold) of peroxisomal beta-oxidation and caused marginally morphological changes of peroxisomes compared with CMTTD and BCMTD. The most striking effect of the alkylthiopropionic acid (CETTD) was an enhancement of the hepatic triacylglycerol level. Palmitic acid and hexadecanedioic acid only marginally affected the peroxisomal activities, but no morphological changes of peroxisomes and fat droplets were observed. The presented data strongly suggest that a minimal structural requirement for a peroxisome proliferator may be (1) a carboxylic acid group linked to (2) a hydrophobic backbone which (3) cannot be beta-oxidized i.e., the fatty acid analogues have a sulphur atom in the beta-position. It is also conceivable that blockage for omega-oxidation may potentiate the peroxisome-proliferating activities in as much as BCMTD was more potent than CMTTD. Two mitochondrial marker enzymes, carnitine palmitoyltransferase and succinate phenazine methosulphate oxidoreductase were differently affected after administration of the investigated compounds. Furthermore, BCMTD and CMTTD as well as HDDA treatments increased the number of mitochondria, but the mitochondria tended to be smaller. The overall results presented here indicate that the structural requirements for proliferation of mitochondria are not identical to those for proliferation of peroxisomes.

Animals↗

Dietary essential fatty acids change the fatty acid profile of rat neural mitochondria over time.

This experiment examined the time course over which the amount of dietary essential fatty acids (EFA) affects brain mitochondrial fatty acids. Weanling rats were fed 20% (wt/wt) fat diets that contained either 4 or 15% (wt/wt of diet) EFA for 1, 2, 3 or 6 wk or a 10% EFA diet for 3 or 6 wk. The EFA ratio [18:2(n-6)/18:3(n-3)] of all diets was approximately 30. Fatty acid analysis of brain mitochondrial phosphatidylethanolamine, phosphatidylcholine and cardiolipin revealed that the largest dietary effect was on 18:2(n-6), which was 30% higher in rats fed the 15 vs. 4% EFA diets after 1 wk. This difference increased to twofold by 3 wk and was still twofold after 6 wk. These results demonstrate several facts: 1) the response of 18:2(n-6) in cardiolipin to dietary EFA is very fast and large, relative to changes in other quantitatively major fatty acids observed in weanling rats; 2) the 18:2(n-6) level in neural cardiolipin stabilizes after 3 wk of feeding at a level dependent upon the amount of dietary EFA; and 3) at least one neural fatty acid, 18:2(n-6), is very sensitive to amounts of dietary EFA that are well above the animal's EFA requirement.

Animals↗

Lipids of the developing human retina: I. Total fatty acids, plasmalogens, and fatty acid composition of ethanolamine and choline phosphoglycerides.

The total fatty acid composition of the human retina was studied during early normal development and compared to that found in infancy and in adulthood. The retina of an infant undernourished prenatally and of two malnourished postnatally were also studied and compared to the normal values for the age. The fatty acid patterns of ethanolamine phosphoglycerides (EPG) and choline phosphoglycerides (CPG) were also studied. Total and ethanolamine plasmalogens (EP) were estimated by the aldehyde dimethyl acetal (DMA) content of total lipids and of EPG, respectively. After acid methanolysis, analyses of fatty acid methyl esters (FAME) and of DMA were effected by capillary GLC on a single 30 m long, SP-2330, capillary column. The main developmental fatty acid changes were an increase in 22:6 omega 3, 22:5 omega 3 and 20:3 omega 6 and a decrease in 20:4 omega 6. The 22:6 omega 3/20:4 omega 6 ratio increased in a very significant, parabolical way throughout development. In contrast to the brain, the proportion of ethanolamine plasmalogens decreased with maturation, whereas the ratio 18DMA/16DMA increased. The two postnatally malnourished infants had a very significant increase in retinal 22:5 omega 6, but only the child that had been fed on a very unbalanced omega 3/omega 6 diet since 25 weeks of gestation showed an important decrease in retinal 22:6 omega 3.

Aging↗

Peripheral amino acid and fatty acid infusion for the treatment of necrolytic migratory erythema in the glucagonoma syndrome.

Necrolytic migratory erythema (NME), the characteristic rash associated with the glucagonoma syndrome, is a cause of substantial morbidity among patients with this rare malignancy. Treatment options are suboptimal, and often useful for only short or moderate durations. We report the effective, long-term (> 1 year) use of intermittent infusions of amino acids (AA) and fatty acids (FA) administered via peripheral intravenous access for the treatment of NME in the glucagonoma syndrome. Despite resolution of the NME, serum amino acid (initially subnormal) and fatty acid (initially normal) levels remained unchanged. Tumour growth and other symptoms related to the glucagonoma syndrome appear unaffected by such infusions.

Amino Acids↗

Effect of exogenous long-chain fatty acids on individual fatty acid synthesis by dispersed ruminant mammary gland cells.

We investigated the effect of exogenously added fatty acids on de novo synthesis of individual fatty acids and their incorporation into triacylglycerols by dispersed lactating ruminant mammary gland epithelial cells. Palmitate addition strongly stimulated synthesis and incorporation of butyrate and, to a smaller extent, palmitate synthesis and incorporation. Oleic acid strongly inhibited synthesis of all fatty acids except butyrate, whereas the effect of lauric acid was nearly neutral. Free fatty acid depletion of the mammary gland cells potentiated the effect of palmitate and made oleate less inhibitory.

Animals↗

Activation of (Na++K+)-ATPase by long-chain fatty acids and fatty acyl coenzymes A.

Long-chain unsaturated fatty acids and fatty acyl CoA derivatives activated (Na++K+)-ATPase at suboptimal, but not optimal, ATP concentrations. Activation was obtained within a narrow range of fatty acid concentrations; higher acid levels inhibited the enzyme. The various CoA esters, however, activated with K0.5 values in the range of 0.15-10 microM; and with no inhibitory effects at concentrations up to 100 microM. Palmitoyl CoA, binding reversibly to a regulatory site, reduced K0.5 of ATP from 0.37 mM to 0.17 mM; and changed the Hill coefficient of the substrate-velocity curve from 0.86 to 0.63. These compounds may be physiological regulators that desensitize the function of this enzyme to diminishing ATP levels.

Acyl Coenzyme A↗

Sialic acid and fatty acid concentrations in lymphocytes, red blood cells and plasma from patients with multiple sclerosis.

Lipids and constituents of lipids were isolated from peripheral blood lymphocytes (PBL), red blood cells (RBC), plasma and sera from 51 patients with multiple sclerosis (MS) and 51 controls, matched for age, sex and race. The amount of sialic acid released by incubation of intact PBL from MS patients was significantly lower (P less than 0.02) than that of the sialic acid from control lymphocytes. The amounts of sialic acid released by neuraminidase from intact RBC, on the other hand, did not differ significantly between the MS group and the control group. The concentrations of ganglioside sialic acid in PBL from MS and control groups did not vary significantly. Similarly the concentration of ganglioside sialic acid in RBC from MS patients was not significantly different from that in the controls. Analyses of the fatty acids isolated after alkaline methanolysis of the lipids from the PBL of MS patients and controls showed a small but significant decrease (P less than 0.01) in the relative percentage of linoleic acid in patients with MS. Determination of the ester-linked fatty acids in RBC lipids from patients with MS showed a significant decrease (P less than 0.001) in the relative percentage of linoleic acid and an increase (P less than 0.01) in palmitic plus palmitoleic acids compared to control values. The fatty acid composition of the plasma neutral lipids plus free fatty acids showed a very significant decrease (P much less than 0.001) in the relative percentage of linoleic acid, a small decrease (P less than 0.05) in arachidonic acid and significant increases in palmitic (P less than 0.001) and oleic acids (P less than 0.001) in MS, compared to controls. These results are suggestive of possible differences in metabolism of lipids between patients with MS and controls.

Adult↗

Effects of exogenous linoleic acid on fatty acid composition, receptor-mediated cAMP formation, and transport functions in rat astrocytes in primary culture.

We have examined the effects of culturing neonatal rat-brain astrocytes in medium containing delipidated serum, with or without added linoleic acid (LA, 18:2 omega 6), on membrane fatty-acid composition and functions. After 18-21 days in culture, polyunsaturated fatty acids (PUFA) constituted approximately equal to 24 mol% of the total fatty acids in the astrocytes grown in delipidated media ("controls'); these proportions were increased by 35-40% to approximately equal to 33 mol% when the cells were supplemented with 35 microM LA. Notable differences in the PUFA profiles of the cells cultured with or without added LA included: (a) higher proportions of omega 6 PUFA in the LA-supplemented astrocytes (approximately equal to 25%, relative to approximately equal to 10% in controls) that were accompanied by an increase in the ratio of omega 6/omega 3 PUFA (from < 2 in controls to approximately equal to 5), and (b) higher proportions of 20:3 omega 9 and 22:3 omega 9 in the control astrocytes (> 5%) relative to the LA-supplemented cells (approximately equal to 1%). The major metabolites in the omega 6 PUFA-enriched cells were arachidonic (20:4 omega 6), adrenic (22:4 omega 6) and docosapentaenoic (22:5 omega 6) acids (15, 5 & 3 mol%, respectively). Enrichment of the astrocytes in omega 6 PUFA did not alter basal levels of cAMP, nor did it affect the amounts of cAMP formed in response to forskolin, isoproterenol, adenosine or histamine. However, dopamine-dependent increases in cAMP formation in the presence of the phosphodiesterase inhibitor, Ro 20-1724, were reduced by approximately equal to 25% relative to those in controls. LA supplementation modified uptake of [3H]adenosine into the astrocytes; values for Kt for a high affinity transport were increased relative to controls, and maximum capacity of a lower affinity process was reduced. Uptake of [3H]glutamate was not altered in the omega 6 PUFA-enriched astrocytes. This study demonstrated that cultured astrocytes take up exogenous linoleic acid and incorporate its metabolites into phospholipid, and that the resulting changes in membrane PUFA composition modify only specific cell functional properties.

Animals↗

Simultaneous microanalysis of biliary cholesterol, bile acids and fatty acids in lecithin using capillary column gas chromatography: an advantage to assess bile lithogenecity.

Simultaneous determination of biliary lipids was performed by alkaline hydrolysis, the formation of the methyl ester derivatives of fatty acids that are constituents of phospholipids and of the acetylated methyl ester derivatives of bile acids, and subsequent analysis by capillary column gas chromatography. Complete separation and satisfactory recovery of cholesterol, bile acids, and fatty acids were achieved. Also, the accuracy of the calculation of the bile cholesterol saturation index was enhanced by computation. Since the degree of acyl chain unsaturation affects the cholesterol-holding capacity in vesicles, this method provides a unique insight into bile metastability by the quantitative assessment of fatty acids in lecithin.

Bile↗

Polyunsaturated fatty acid inhibition of fatty acid synthase transcription is independent of PPAR activation.

Polyunsaturated fatty acids (PUFA) of the (n-6) and (n-3) families inhibit the rate of gene transcription for a number of hepatic lipogenic and glycolytic genes, e.g., fatty acid synthase (FAS). In contrast, saturated and monounsaturated fatty acids have no inhibitory capability. The suppression of gene transcription resulting from the addition of PUFA to a high carbohydrate diet: occurs quickly (< 3 h) after its addition to a high glucose diet; can be recreated with hepatocytes cultured in a serum-free medium containing insulin and glucocorticoids; can be demonstrated in diabetic rats fed fructose; and is independent of glucagon. While the nature of the intracellular PUFA inhibitor is unclear, it appears that delta-6 desaturation is a required step in the process. Recently, the fatty acid activated nuclear factor, peroxisome-proliferator activated receptor (PPAR) was suggested to be the PUFA-response factor. However, the potent PPAR activators ETYA and Wy-14643 did not suppress hepatic expression of FAS, but did induce the PPAR-responsive gene, acyl-CoA oxidase (AOX). Similarly, treating rat hepatocytes with 20:4 (n-6) suppressed FAS expression but had no effect on AOX. Thus, it appears that the PUFA regulation of gene transcription involves a PUFA-response factor that is independent from PPAR.

5,8,11,14-Eicosatetraynoic Acid↗

Effects of highly purified eicosapentaenoic acid and docosahexaenoic acid on fatty acid absorption, incorporation into serum phospholipids and postprandial triglyceridemia.

Fourteen healthy volunteers were randomly allocated to receive 4 g highly purified ethyl esters of eicosapentaenoic acid (EPA) (95% pure, n = 7) or docosahexaenoic acid (DHA) (90% pure, n = 7) daily for 5 wk in supplement to their ordinary diet. The n-3 fatty acids were given with a standard high-fat meal at the beginning and the end of the supplementation period. EPA and DHA induced a similar incorporation into chylomicrons which peaked 6 h after the meal. The relative uptake of EPA and DHA from the meal was > 90% compared with the uptake of oleic acid. During absorption, there was no significant elongation or retroconversion of EPA or DHA in total chylomicron fatty acids. The concentration of EPA decreased by 13% and DHA by 62% (P < 0.001) between 6 and 8 h after the meal. During the 5-wk supplementation period, EPA showed a more rapid and comprehensive increase in serum phospholipids than did DHA. DHA was retroconverted to EPA, whereas EPA was elongated to docosapentaenoic acid (DPA). The postprandial triglyceridemia was suppressed by 19 and 49% after prolonged intake of EPA and DHA, respectively, indicating that prolonged intake of DHA is equivalent to or even more efficient than that of EPA in lowering postprandial triglyceridemia. This study indicates that there are metabolic differences between EPA and DHA which may have implications for the use of n-3 fatty acids in preventive and clinical medicine.

Adult↗

[Study of the biosynthesis of phleic acids, polyunsaturated fatty acids synthesised by Mycobacterium phlei (author's transl)].

Because of their structures, phleic acids (general formula: CH3-(CH2)m-(CH=CH-CH2-CH2)n-CO2H; main component: m = 14, n = 5) cannot be synthesized by the same kinds of enzymatic systems as other natural polyunsaturated fatty acids. By using specifically labelled 14C compounds, we have tested the ability of different molecules to be incorporated in the phleate skeletons by Mycobacterium phlei. The localisation of radioactive carbon atoms has been studied by chemical degradation of labelled phleates, isolation and purification of the degradation products, and determination of their specific radioactivity. When M. phlei cells are incubated with labelled acetate, the unsaturated and saturated parts of the molecules of phleic acids are unequally labelled. The radioactivity of succinate monoester on the one hand and fatty acids (mixture of myristic and palmitic acids) on the other hand, measured after oxidative degradation of phleate esters, shows a constant ratio under definite conditions. Whether [1-14C]acetate or [2-14C]acetate is used for incubation, the same ratio is observed. Therefore acetate is the precursor of the unsaturated part as well as of the saturated part of the phleate molecules. By using labelled fatty acid esters, it has been found that palmitic acid is the precursor of phleates with m = 14, while myristic acid is the precursor of phleates with m = 12. Stearic and eicosanoic acids are not incorporated without degradation. The hypothesis of a condensation of a saturated fatty acid with a preformed polyunsaturated molecule was examined. Search for such a molecule in the lipids of M. phlei gives negative results. Pentaunsaturated phleate arising from palmitate is more abundant than pentaunsaturated phleate arising from myristate, while the reverse is true for hexaunsaturated phleates. These observations make very unlikely such an hypothesis. An elongation process fits well with the observed facts provided that this process involves elongation by two acetate units simultaneously, making elongation by four carbon atoms at a time. Such a requirement would be easily satisfied if two molecules of acetate are condensed together before their utilization in the elongation process. In such a hypothetical process, crotonate would be the most probable substrate of the elongation reaction.

Acetates↗

Effect of eicosa-5, 8, 11, 14-tetraynoic acid on fatty acid composition of selected organs in the rat.

Eicosa-5, 8, 11, 14-tetraynoic acid or archidonic acid or no supplement (controls) was given orally to rats maintained on a fat free diet and the fatty acid composition of total lipids of several organs determined. No changes were noted in the total fatty acid concentrations of the organs examined in the various groups. A decrease in the amount of arachidonic acid, 22:4omega6 and 22:5omega 6 (as percent of total fatty acids), and an increase in the amount of 20:3omega6 and linoleate were observed in total lipids of several organs. In the group receiving the arachidonate supplement, there was less linoleate and 20:3omega 6 and more archidonate than in the controls. Both eicosa-5, 8, 11, 14-tetraynoic acid and arachidonate supplements resulted in a decrease in 20:3omega9 in most organs studied. Generally, the most marked changes were seen in liver but, of the other organs examined (heart, kidney, testis, brain, and adrenals), only the adrenals failed to show any significant differences between the controls and each of the two supplemented groups. Although the experimental conditions preclude conclusive interpretation of the changes observed, it is suggested that eicosa-5, 8, 11, 14-tetraynoic acid was effective in inhibiting the conversion of linoleate to archidonate and the conversion of arachidonate to 22:4 and 22:5.

5,8,11,14-Eicosatetraynoic Acid↗

De novo fatty acid synthesis and fatty acid elongation catalyzed by subcellular fractions from hog and human aorta.

De novo synthesis and mitochondrial elongation of fatty acids have been demonstrated in subcellular fractions from hog and human aorta. Microsomal fatty acid elongation has been shown in hog aorta. The activity catalyzing the formation of fatty acids from acetyl and malonyl CoA was associated with a high molecular weight complex in the 6 x 10(6) g x min supernatant fraction. The principal product was palmitic acid. Some myristic and stearic acids were also formed. One elongation system was associated with protein which sedimented between 4500 g x min and 150,000 g x min. It used acetyl CoA but not malonyl CoA, and NADH was the preferred reducing agent. Radioactivity from acetyl CoA was incorporated into many fatty acids. In hog aorta a second elongation system was found associated with protein which sedimented at 6 x 10(6) g x min. It used malonyl CoA preferentially as substrate and either NADH or NADPH as reducing agent.

Acetyl Coenzyme A↗