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At least 73 records · Page 4Linked to original sources
PubMed2006

Fatty acid metabolism pathway play an important role in carcinogenesis of human colorectal cancers by Microarray-Bioinformatics analysis.

The present study systematically explored metabolic pathways and altered expressions of genes speculatively participating in colorectal carcinogenesis by using a Microarray-Bioinformatic analysis methods. The results revealed that 157 genes were up-regulated and 281 genes were down-regulated in colorectal cancer (CRC). Gene Ontology (GO) and relevant bioinformatics tools indicated that the functional category to which 438 genes (12%; 438/3800) of the most frequent alteration belonged was metabolism. The analysis of 10 colorectal cancer tissue specimens demonstrated that genes involved in fatty acid metabolic pathways had high rates of overexpression. In addition, we stimulated CRL-1790 cell line with linoleic acid (a polyunsaturated fatty acid) for 12, 24, 48 and 72 h. Cell proliferation was elevated by 5, 25, 28 and 31% (P<0.05), respectively. Further analyses revealed that the genes increasingly expressed in the cell line included enoyl-Coenzyme A, hydratase/3-hydroxyacyl Coenzyme A dehydrogenase (EHHADH), enoyl Coenzyme A hydratase, short chain, 1, mitochondrial (ECHS1); glutaryl-Coenzyme A dehydrogenase (GCDH), acyl-Coenzyme A oxidase 2, branched chain (ACOX2); acyl-Coenzyme A dehydrogenase, C-2 to C-3 short chain precursor (ACADS); carnitine palmitoyltransferase 1B (CPT1B), acyl-CoA synthetase long-chain family member 5 (ACSL5), and cytochrome P450, family 4, subfamily A, and polypeptide 11 (CYP4A11) genes. This indicated that the stimulating effect of linoleic acid on cell proliferation was due to interference with the metabolic pathway of fatty acid metabolism. In conclusion, genes with altered expression levels in CRC were mainly associated with fatty acid metabolic pathways speculated to have an important role linked to carcinogenesis.

Aged↗
PubMed2004

Molecular mechanisms of alcoholic fatty liver: role of peroxisome proliferator-activated receptor alpha.

Normal function of the peroxisome proliferator-activated receptor alpha (PPARalpha) is crucial for the regulation of hepatic fatty acid metabolism. Fatty acids serve as ligands for PPARalpha, and when fatty acid levels increase, activation of PPARalpha induces a battery of fatty acid-metabolizing enzymes to restore fatty acid levels to normal. Hepatic fatty acid levels are increased during ethanol consumption. However, results of in vitro work showed that ethanol metabolism inhibited the ability of PPARalpha to bind DNA and activate reporter genes. This observation has been further studied in mice. Four weeks of ethanol feeding of C57BL/6J mice also impairs fatty acid catabolism in liver by blocking PPARalpha-mediated responses. Ethanol feeding decreased the level of retinoid X receptor alpha (RXRalpha) as well as the ability of PPARalpha/RXR in liver nuclear extracts to bind its consensus sequence, and the levels of mRNAs for several PPARalpha-regulated genes were reduced [long-chain acyl coenzyme A (acyl-CoA) dehydrogenase and medium-chain acyl-CoA dehydrogenase] or failed to be induced (acyl-CoA dehydrogenase, liver carnitine palmitoyl-CoA transferase I, very long-chain acyl-CoA synthetase, very long-chain acyl-CoA dehydrogenase) in livers of the ethanol-fed animals. Consistent with this finding, ethanol feeding did not induce the rate of fatty acid beta-oxidation, as assayed in liver homogenates. Inclusion of WY14,643, a PPARalpha agonist, in the diet restored the DNA-binding activity of PPARalpha/RXR, induced mRNA levels of several PPARalpha target genes, stimulated the rate of fatty acid beta-oxidation in liver homogenates, and prevented fatty liver in ethanol-fed animals. Blockade of PPARalpha function during ethanol consumption contributes to the development of alcoholic fatty liver, which can be overcome by WY14,643.

Animals↗
PubMedDate not supplied

Comparison of lipid and fatty acid metabolism between minimal change nephrotic syndrome and membranous nephropathy.

Polyunsaturated fatty acids have been reported to be associated with atherosclerotic and inflammatory diseases, as they are the major components of cytoplasmic membranes and the precursor fatty acids for prostaglandins and leukotrienes. Nephrotic syndrome is associated with serum lipid disorders, such as hypercholesterolemia due to the increased production of lipoproteins by the liver. However, there are few reports regarding the fatty acid metabolism in patients with nephrotic syndrome. In the present study, serum lipid concentrations and plasma fatty acid composition were measured in patients with minimal change nephritic syndrome (MCNS) and membranous nephropathy (MN). Seven patients with MCNS (MCNS group), 11 patients with MN (MN group) and 8 healthy subjects (control group) were enrolled in the study. All patients were diagnosed by percutaneous renal biopsy. Fasting blood samples were obtained and the serum lipid profile was measured enzymatically. The fatty acid composition of plasma was analyzed by gas-chromatography after transmethylation. There were no significant differences in serum urea nitrogen and creatinine levels among the three groups. Patients with MN were older than those with MCNS. In the serum lipid profile, hypercholesterolemia was observed both in the MCNS and MN groups. Regarding the plasma fatty acid composition, alpha-linolenic acid levels in the MCNS group were significantly higher than those in the control group (1.06 +/- 0.08 wt% vs. 0.77 +/- 0.16 wt%, p = 0.008) and docosahexaenoic acid levels in the MN group were significantly higher than those in the control group (5.51 +/- 1.17 wt% vs. 3.96 +/- 1.07 wt%, p = 0.005). These results suggest that nephrotic syndrome might not only disrupt lipid metabolism but also fatty acid metabolism.

Adult↗
PubMed2006

Loss of the acyl-CoA binding protein (Acbp) results in fatty acid metabolism abnormalities in mouse hair and skin.

Proper fatty acid metabolism is critical for hair and skin development and maintenance. The acyl-CoA binding protein (Acbp) is a widely expressed protein that binds long-chain fatty acyl-CoA esters and plays a role in fatty acyl-CoA transport and pool formation. However, loss of function of Acbp in the whole animal has not been investigated. Here, we show that deletion of Acbp in mouse results in sebocyte hyperplasia and sparse, matted hair with a greasy appearance. Consistent with these gross abnormalities, Acbp is highly expressed in the pilosebaceous units of mouse skin as determined by Northern analysis and in situ hybridization. Loss of Acbp also results in fatty acid metabolism abnormalities, with hair lipid profiles showing altered levels of triacylglycerols and nearly co-migrating lipids. These data suggest that Acbp plays a role in triacylglycerol biosynthesis, and that regulation of this process is important for proper hair and skin development and maintenance in the mouse.

Animals↗
PubMed1997

Thia fatty acids, metabolism and metabolic effects.

(1) The chemical properties of thia fatty acids are similar to normal fatty acids, but their metabolism (see below: points 2-6) and metabolic effects (see below: points 7-15) differ greatly from these and are dependent upon the position of the sulfur atom. (2) Long-chain thia fatty acids and alkylthioacrylic acids are activated to their CoA esters in endoplasmatic reticulum. (3) 3-Thia fatty acids cannot be beta-oxidized. They are metabolized by extramitochondrial omega-oxidation and sulfur oxidation in the endoplasmatic reticulum followed by peroxisomal beta-oxidation to short sulfoxy dicarboxylic acids. (4) 4-Thia fatty acids are beta-oxidized mainly in mitochondria to alkylthioacryloyl-CoA esters which accumulate and are slowly converted to 2-hydroxy-4-thia acyl-CoA which splits spontaneously to an alkylthiol and malonic acid semialdehyde-CoA ester. The latter presumably is hydrolyzed and metabolized to acetyl-CoA and CO2. (5) Both 3- and 4-thiastearic acid are desaturated to the corresponding thia oleic acids. (6) Long-chain 3- and 4-thia fatty acids are incorporated into phospholipids in vivo, particularly in heart, and in hepatocytes and other cells in culture. (7) Long-chain 3-thia fatty acids change the fatty acid composition of the phospholipids: in heart, the content of n-3 fatty acids increases and n-6 fatty acids decreases. (8) 3-Thia fatty acids increase fatty acid oxidation in liver through inhibition of malonyl-CoA synthesis, activation of CPT I, and induction of CPT-II and enzymes of peroxisomal beta-oxidation. Activation of fatty acid oxidation is the key to the hypolipidemic effect of 3-thia fatty acids. Also other lipid metabolizing enzymes are induced. (9) Fatty acid- and cholesterol synthesis is inhibited in hepatocytes. (10) The nuclear receptors PPAR alpha and RXR alpha are induced by 3-thia fatty acids. (11) The induction of enzymes and of PPAR alpha and RXR alpha are increased by dexamethasone and counteracted by insulin. (12) 4-Thia fatty acids inhibit fatty acid oxidation and induce fatty liver in vivo. The inhibition presumably is explained by accumulation of alkylthioacryloyl-CoA in the mitochondria. This metabolite is a strong inhibitor of CPT-II. (13) Alkylthioacrylic acids inhibits both fatty acid oxidation and esterification. Inhibition of esterification presumably follows accumulation of extramitochondrial alkylthioacryloyl-CoA, an inhibitor of microsomal glycerophosphate acyltransferase. (14) 9-Thia stearate is a strong inhibitor of the delta 9-desaturase in liver and 10-thia stearate of dihydrosterculic acid synthesis in trypanosomes. (15) Some attempts to develop thia fatty acids as drugs are also reviewed.

Acyl-CoA Dehydrogenase, Long-Chain↗
PubMed2001

Stable isotope approaches, applications, and issues related to polyunsaturated fatty acid metabolism studies.

The use of stable isotope tracers for investigating fatty acid metabolism in human subjects has increased substantially over the last decade. Advances in analytical instrumentation, commercial availability of labeled substrates, and safety considerations are major reasons for this increased use of stable isotope tracers. Several experimental design options are available for using either deuterium or carbon-13 as tracers for fatty acid and lipid studies. Options include feeding a pulse dose of labeled fat or a mixture containing two or more labeled fats. Multiple doses of the labeled fat can be fed at timed intervals to increase enrichments. Administration by injection or continuous intravenous infusion is an alternative. Another option is to use diets containing foods from plants that have slightly higher natural carbon-13 enrichment. Each basic experimental design has its specific strengths, and the best choice of experimental design depends on the study objectives. Stable isotope studies have been used to address a variety of questions related to unsaturated fatty acid metabolism in humans. Examples are provided that illustrate the use of stable isotopes to investigate oxidation of docosahexaenoic acid, desaturation of linoleic and linolenic acids in infants and adults, incorporation of long-chain n-6 and n-3 fatty acids, bioequivalency of linolenic acid in primates, 13C nuclear magnetic resonance spectra of arachidonic acid in living rat brain, and effect of triacylglycerol structure on absorption. Radioisotope and stable isotope tracer studies in animals and humans are responsible for much of our understanding of fatty acid and lipid metabolism. However, tracer studies have limitations, and there are some unresolved issues associated with isotope studies. Examples of unresolved issues are quantification of isotope data, validity of in vivo fatty acid metabolite results, kinetic modeling, subject variability, and use of blood lipid data as a reflection of tissue lipid metabolism. Resolving these issues, developing novel methodology, and applying stable isotope tracer methods to questions related to PUFA metabolism are broad areas of interesting and challenging research opportunities.

Adult↗
PubMed2000

Effects of intestinal fatty acid-binding protein overexpression on fatty acid metabolism in Caco-2 cells.

Intestinal fatty acid-binding protein (I-FABP) is a cytosolic protein expressed at high levels (up to 2% of cytosolic proteins) in the small intestine epithelium. Despite cell transfection studies, its function is still unclear. Indeed, different effects on fatty acid metabolism depending on the cell type and the amount of I-FABP expressed have been reported. Furthermore, a decrease in fatty acid incorporation has been unexpectedly obtained when I-FABP reached 0. 72% of cytosolic proteins in fibroblasts (Prows et al. 1997. Arch. Biochem. Biophys. 340: 135). In the present study, the effect of a high level of I-FABP similar to amounts present in the small intestine was investigated in the human colon adenocarcinoma cell line, Caco-2. After transfection with human I-FABP cDNA, a clone expressing 1.5% I-FABP and unchanged level of liver FABP was selected. These cells, which had a lower rate of proliferation as compared with mock-transfected cells, developed the typical morphological characteristics of differentiated enterocytes. Incubation of differentiated cells with [(14)C]palmitate showed a 34% reduction (P < 0.01) of fatty acid incorporation, whereas the relative distribution of radiolabel into triglycerides was not affected. A nonsignificant 21% reduction of fatty acid incorporation was observed with another clone expressing 10-fold less I-FABP. In conclusion, a high level of I-FABP expressed in a differentiated enterocyte model inhibited fatty acid incorporation, by a mechanism which remains to be defined.

Caco-2 Cells↗
PubMed2000

Calcium deficiency modifies polyunsaturated fatty acid metabolism in growing rats.

Fatty acid desaturase activities were determined in liver microsomes from calcium-deficient rats and compared to calcium-sufficient ones. The calcium-deprived diet (0.5 g/kg) administered for 60 d caused a 30% inhibition in the delta5 desaturase activity and a 45-55% decrease in delta6 and delta9, respectively, facts that cannot be attributed to a reduction in food intake. In vitro addition of calcium, ethyleneglycol-bis(Beta-aminoethyl ether)N,N-tetraacetic acid, and/or cytosol fractions from control or calcium-deficient rats to microsomes from both groups of animals indicates that the reduced desaturase capacities would be the consequence of an indirect effect of calcium deprivation. The present work shows that the reduced unsaturated fatty acid biosynthesis might be the result of modifications in the physicochemical properties of microsomal membranes. Such changes could also be derived from the inhibition of phospholipase A2 activity induced by calcium deficiency.

Acyl Coenzyme A↗
PubMed2001

Dynamic changes in cardiac fatty acid metabolism in the stunned human myocardium.

BACKGROUND: The chronological changes or mechanisms in cardiac fatty acid metabolism under clinical conditions of hypoxia and ischemia have not been fully elucidated. 123-15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (BMIPP) can be used with single photon emission computed tomography (SPECT) to evaluate myocardial fatty acid metabolism. We investigated chronological changes in energy metabolism in the stunned human myocardium by means of 123I-BMIPP myocardial SPECT. METHODS AND RESULTS: We conducted 123I-BMIPP myocardial SPECT in 10 patients with stunned myocardium during the acute, subacute and chronic phases after onset. The left ventricle was divided into 9 regions on SPECT, and the degree of abnormalities in each region was scored in four grades from normal (0) to defect (4). We also examined wash-out rates on BMIPP images. The scores on early BMIPP images in the acute, subacute and chronic phases were 5.6 +/- 1.8, 13.4 +/- 3.5 and 2.5 +/- 1.1, respectively, and the score was highest in the subacute phase (p < 0.001). Similarly, scores on the late images were 2.3 +/- 1.7, 18.3 +/- 4.5 and 4.7 +/- 2.6, respectively, and highest in the subacute phase (p < 0.001). The wash-out rates (normal: 18.2 +/- 2.1%) in the acute, subacute and chronic phases were 12.1 +/- 4.8%, 44.9 +/- 10.0% and 23.1 +/- 4.6%, respectively, with the value being lowest during the acute phase (p < 0.05), and highest during the subacute phase (p < 0.001). CONCLUSION: These results suggested that fatty acid metabolism in the stunned human myocardium changes dynamically over time.

Aged↗
PubMed1989

Inborn errors of amino acid and fatty acid metabolism with hypoglycemia as a major clinical manifestation.

During the last decade it has become increasingly clear that severe hypoglycemia may be caused by specific enzymatic defects of amino acid and fatty acid metabolism. Several reports have presented hypoglycemic syndromes with reduced fatty acid transport or oxidation, decreased ketogenesis, or abnormalities of the Krebs cycle and electron transport chain. It is of particular interest that several enzymatic defects here discussed may present as Reye's syndrome. An intriguing fact is a highly variable clinical presentation, even in the presence of well-defined enzyme deficiencies. Some patients are desperately ill in the newborn period, whereas in other cases there are symptoms only during catabolic phases later in childhood. The presence of hypoglycemia may be related to low levels of acetyl CoA, with consequently reduced gluconeogenesis; alternatively the glucose-sparing effect of ketones is lost in states of reduced ketone body production. Treatment with pharmacological doses of vitamins may be attempted, depending upon the established or suspected diagnoses. With manifest hypoglycemia i.v. glucose infusion is the treatment of choice. By such means convulsions, and brain damage may be prevented.

Amino Acid Metabolism, Inborn Errors↗
PubMed1982

[Effect of combination therapy of clofibric acid and nicotinic acid derivatives on fatty acid metabolism in hyperlipoproteinemia].

71 patients (42 males and 29 females at the age of 45-76 years) with primary hyperlipoproteinaemia were treated with clofibrin acid and derivatives of nicotinic acid during 3 years. Gas-chromatographic analyses of the composition of fatty acids of their serum cholesterol ester and triglyceride fractions showed an increase of linoleic, linolenic, arachidonic, eicosapentaenic acid as well as a decrease of palmitinic, palmitoleinic, stearic, oleic and eicosatrienic acid under treatment. The changes were more efficient than under monotherapy. Selective competitive inhibition of unesterified fatty acid, blocking of lipolysis, influence on the hepatogenic metabolism of fatty acids and on the LCAT as well as better utilization of the alimentary repeatedly unsaturated fatty acids were discussed as possible mechanism. The increase of the polyunsaturated fatty acids with their interrelations to the prostaglandin metabolism must be seen in the sense of a vasoprotective effect.

Aged↗
PubMedDate not supplied

[Fatty acid metabolism and requirements in childhood].

The metabolism of fatty acids (FA) has a profound impact on the development of the human being. In fact, the lipidic composition of membranes may be modulated by the relative concentrations of available FA. During the last months of the fetal life, an increasing concentration of polyunsaturated very long-chain (VLC) FA is observed from the umbilical cord to the liver and the central nervous system, where they contribute to the qualitative development of the nervous membranes. Therefore, the preterm baby is at particular risk of polyunsaturated VLCFA deficiency. Among polyunsaturated VLCFA, 20:4 n-6 and 22:6 n-3 carry on fundamental roles respectively for cellular growth and visual development. The accretion of VLCFA in the human body is intense also in the term infant during the first months of life. In the period of exclusive milk-feeding fat represents 50% of the daily caloric intake, and the ketonic bodies, resulting from the incremented beta-oxidation of FA, are readily utilized as source of energy by the developing brain. Weaning is now object of study to precise both metabolic needs and dietary intakes of FA families. Recent surveys have revealed that in this period the intakes of linoleic and linolenic acid are at the lower limits of the recommended levels. No upper limit for saturated FA is advisable for the first two years of life.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2001

Characterization of altered myocardial fatty acid metabolism in patients with inherited cardiomyopathy.

Inherited defects in myocardial long-chain fatty acid metabolism are increasingly recognized as a cause of cardiomyopathy and sudden death in children. To evaluate whether the phenotypic expression of these genetic diseases could be delineated using positron emission tomography (PET), 11 patients with inherited defects in fatty acid metabolism were evaluated and results were compared with those of 6 nonaffected siblings. Myocardial perfusion, myocardial oxygen consumption (MVO2), and long-chain fatty acid metabolism were determined noninvasively with PET using quantitative mathematical models. There were no differences in haemodynamics, perfusion, MVO2 or plasma substrate levels between groups. Patients with defects in enzymes of fatty acid beta-oxidation (acyl-CoA dehydrogenase and 3-hydroxyacyl-CoA dehydrogenase deficiencies) (n = 5) had diminished myocardial palmitate oxidation compared with healthy siblings (3.2 +/- 3.0 vs. 13.0 +/- 5.6 nmol/g per min, p < 0.03) and a decrease in the percentage of MVO2 accounted for by palmitate (2% +/- 3% vs. 9% +/- 5%, p < 0.04). In these patients, extracted palmitate was shunted into a slow-turnover compartment (predominantly reflecting esterification to triglycerides) with expansion of palmitate in that pool (185 +/- 246 compared with 27 +/- 67 nmol/g in healthy siblings,p < 0.02). In contrast, myocardium of patients with carnitine deficiency (n = 6) (all on oral carnitine therapy) had normal palmitate extraction but expansion of the interstitial/cytosolic fatty acid pool (617 +/- 399 vs. 261 +/- 73 nmol/g in healthy siblings, p < 0.04), suggesting different mechanisms for handling upstream fatty acyl intermediates. Thus, PET can be used to noninvasively assess abnormal myocardial handling of fatty acids in patients with inherited defects of metabolism. This approach should be useful in the assessment of altered myocardial fatty acid metabolism associated with cardiomyopathy as well as for evaluating the efficacy of therapeutic interventions in affected patients.

Acetates↗
PubMed2004

Fatty acid metabolism assessed by 125I-iodophenyl 9-methylpentadecanoic acid (9MPA) and expression of fatty acid utilization enzymes in volume-overloaded hearts.

BACKGROUND: The peroxisome proliferator-activated receptor (PPAR) alpha is a member of the nuclear receptor superfamily and regulates gene expression of fatty acid utilization enzymes. In cardiac hypertrophy and heart failure by pressure-overload, myocardial energy utilization reverts to the fetal pattern, and metabolic substrate switches from fatty acid to glucose. However, myocardial metabolism in volume-overloaded hearts has not been rigorously studied. The aim of the present study was to examine fatty acid metabolism and protein expressions of PPARalpha and fatty acid oxidation enzymes in volume-overloaded rabbit hearts. METHODS: Volume-overload was induced by carotid-jugular shunt formation. Sham-operated rabbits were used as control. Chronic volume-overload increased left ventricular weight and ventricular cavity size, and relative wall thickness was decreased, indicating eccentric cardiac hypertrophy. (125)I-iodophenyl 9-methylpentadecanoic acid (9MPA) was intravenously administered, and animals were sacrificed at 5 min after injection. The 9MPA was rapidly metabolized to iodophenyl-3-methylnonanoic acid (3MNA) by beta-oxidation. Lipid extraction from the myocardium was performed by the Folch method, and radioactivity distribution of metabolites was assayed by thin-layer chromatography. The protein was extracted from the left ventricular myocardium, and levels of PPARalpha and fatty acid oxidation enzymes were examined by Western blotting. RESULTS: Myocardial distribution of 9MPA tended to be more heterogeneous in shunt than in sham rabbits (P = 0.06). In volume-overloaded hearts by shunt, the conversion from 9MPA to 3MNA by beta-oxidation was faster than the sham-control hearts (P < 0.05). However, protein levels of PPARalpha and fatty acid utilization enzymes were unchanged in shunt rabbits compared with sham rabbits. CONCLUSIONS: These data suggest that myocardial fatty acid metabolism is enhanced in eccentric cardiac hypertrophy by volume-overload without changes in protein expressions of PPARalpha and fatty acid utilization enzymes. Our data may provide a novel insight into the subcellular mechanisms for the pathological process of cardiac remodelling in response to mechanical stimuli.

Animals↗
PubMed1990

Fatty acid metabolism in human lymphocytes. II. Activation of fatty acid desaturase-elongase systems during blastic transformation.

The fatty acid desaturation-elongation ability of human T-lymphocytes during blastic transformation was determined both by gas-liquid chromatography and incubation with radiolabeled precursors. Human peripheral blood mononuclear cells (PBMC) were activated with phytohemagglutinin (PHA) and cultured in media supplemented with different fatty acids (18:0, 18:1(n - 9), 18:2(n - 6), 18:3(n - 3) and 20:4(n - 6)) at a final concentration of 30 microM. All the fatty acids added were elongated by activated PBMC and the maximal activity was observed on 20:4(n - 6) (a 25% of conversion to 22:4(n - 6)). Supplementation with stearic acid increased the proportion of oleic (from 21.4% to 23.7%) and eicosaenoic (from 3.1% to 5.7%) acids in cellular lipids, indicating the existence of a delta 9-desaturase activity. Supplementation with linoleic and linoleic acids increased slightly the cell content in their more unsaturated derivatives. Direct measurement of desaturase activities was performed by incubating quiescent and activated PBMC with [1-14C]stearic, [1-14C]linoleic and [1-14C]linolenic acids. Quiescent cells exhibited a very low delta 9-desaturase and no sign of delta 6-desaturase activity. A moderate and progressive activation of delta 9-, delta 6- and delta 5-desaturases was observed during blastic transformation of human PBMC. Up to 8% of 18:0 was converted to monoenes, 4% and 1.5% of 18:2(n - 6) was converted to trienes and tetraenes, respectively, and 14.5% of 18:3(n - 3) was converted to pentaenes. The maximal relative activities were found after 48 h of PHA-stimulation for delta 9-desaturase (around 90 pmol of 18:0 converted per 10(6) cells in the last 24 h) and at 72 h for delta 6- and delta 5-desaturases (around 75 and 140 pmol of 18:2 and 18:3, respectively, converted per 10(7) cells in the last 24 h). Although these activities are not enough to explain all the changes in fatty acid composition of human PBMC during blastic transformation, they may contribute to a more controlled cell phospholipid composition.

Acetyltransferases↗