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PubMed1992

Essential fatty acid metabolism in cultured human airway epithelial cells.

To characterize essential fatty acid metabolism of human airway epithelium, we examined the capacity of epithelial cells to incorporate and desaturate/elongate 18:2(n - 6) and the turnover of phospholipid fatty acyl chains in these cells. Epithelial cells were cultured for 5-7 days and incubated with [1-14C]18:2(n - 6) (1 microCi, 100 nmol). The essential fatty acid profile of the cells was readily modified by 18:2(n - 6) supplementation to culture medium. After 4 h incubation, 32 +/- 5.6 nmol of [1-14C]18:2(n - 6) was incorporated into phospholipids (65 +/- 9.5%, of which 74% was incorporated into phosphatidylcholine (PC)) and neutral lipid (31 +/- 10%) per mg protein of cultured cells. 30 +/- 8% of [1-14C]18:2(n - 6) incorporated, was converted to homologous trienes, tetraenes and pentaenes, the major products being 20:3(n - 6) and 20:4(n - 6). The conversion of 18:2(n - 6) was time-dependent and donor age-related. A higher proportion of 20:3(n - 6) and 20:4(n - 6) was incorporated into phosphatidylinositol (PI) and phosphatidylethanolamine (PE). About 10-15% of total products formed from 18:2(n - 6) was released from membrane to culture medium. Both 20:4(n - 6) and 20:5(n - 3) inhibited 18:2(n - 6) incorporation and desaturation. Rate of incorporation of 18:2(n - 6) was more than either 18:1(n - 9) or 16:0. With pulse-chase studies, the half-life of 18:2(n - 6) in PC, PI and PE was estimated to be 5.5, 6.0 and 7.3 h, respectively. These data indicate active metabolism of essential fatty acids in human airway epithelial cells. This metabolism may play a key role in the regulation of membrane properties and function in these cells.

Carbon Radioisotopes↗
PubMed1987

l-Carnitine. A preliminary review of its pharmacokinetics, and its therapeutic use in ischaemic cardiac disease and primary and secondary carnitine deficiencies in relationship to its role in fatty acid metabolism.

l-Carnitine occurs naturally as an essential cofactor of fatty acid metabolism which is synthesised endogenously or obtained from dietary sources. In patients with primary carnitine deficiencies, which may be life-threatening, and some secondary deficiencies such as organic acidurias, the exogenously administered compound is clearly beneficial: by abolishing hypotonia, motor skills are improved, as are muscle weakness and wasting. In preliminary clinical trials in patients with ischaemic cardiac disease, therapy with l-carnitine has shown beneficial effects on myocardial function and metabolism and has improved exercise tolerance in patients with angina pectoris-findings which require further substantiation in larger controlled studies. Moreover, while some interesting evidence suggests that l-carnitine may find potential use in such diverse conditions as carnitine deficiencies secondary to prolonged total parenteral nutrition supplementation or chronic haemodialysis, hyperlipidaemias and the prevention of toxicity induced by anthracyclines and valproate, such findings must be regarded as preliminary. Exogenously administered l-carnitine is very well tolerated. Thus, while its role in primary deficiencies is established, with its profile of negligible toxicity l-carnitine is worthy of further investigation to more clearly define its therapeutic applications in a variety of conditions which may be indirectly related to alterations in fatty acid metabolism.

Carnitine↗
PubMed1999

Preliminary characterization of Yor180Cp: identification of a novel peroxisomal protein of saccharomyces cerevisiae involved in fatty acid metabolism.

Here we report the preliminary characterization of Yor180Cp, a novel peroxisomal protein involved in fatty acid metabolism in the yeast Saccharomyces cerevisiae. A computer-based screen identified Yor180Cp as a putative peroxisomal protein, and Yor180Cp targeted GFP to peroxisomes in a PEX8-dependent manner. Yor180Cp was also detected by mass spectrometric analysis of an HPLC-separated extract of yeast peroxisomal matrix proteins. YOR180C is upregulated during growth on oleic acid, and deletion of YOR180C from the yeast genome resulted in a mild but significant growth defect on oleic acid, indicating a role for Yor180Cp in fatty acid metabolism. In addition, we observed that yor180cDelta cells fail to efficiently import the enzyme Delta3,Delta2-enoyl-CoA isomerase (Eci1p) to peroxisomes. This result suggested that Yor180Cp might associate with Eci1p in vivo, and a Yor180Cp-Eci1p interaction was detected using the yeast two-hybrid system. Potential roles for Yor180Cp in peroxisomal fatty acid metabolism are discussed.

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↗
PubMed2001

[Trans isomers of unsaturated fatty acids--metabolic action and clinical effects].

Fatty acids with the trans configuration are formed chiefly during hardening of oils and have been associated with increased risk of ischaemic heart disease. Dietary uptake of such fatty acids increases the level of lipoprotein (a) and LDL cholesterol, at the same time reducing the level of HDL cholesterol in plasma. As the content of saturated fatty acids in margarine is lower than in butter, the former product was for a long time considered as healthier. However, some margarines are rich in trans fatty acids. In other words, the risk of cardiovascular diseases can only be reduced by replacing butter with margarine checked for a low trans fatty acid content. The purpose of this paper was to review the literature dealing with the metabolic actions of trans isomers of unsaturated fatty acids and their clinical effects.

Animals↗
PubMed1980

Effects of exogenous fatty acid concentration on glucagon-induced changes in hepatic fatty acid metabolism.

Studies were conducted to clarify the relationship between the external fatty acid concentration and glucagon in the regulation of hepatic fatty acid metabolism. Hepatocytes from fed rats were incubated with increasing concentrations of oleate (up to 1 mM) in the presence and absence of glucagon and the time sequence of changes in cellular malonyl-CoA levels, fatty acid synthesis, fatty acid oxidation, and ketogenesis were measured. At low concentrations of fatty acid the effect of glucagon was to abolish malonyl-CoA synthesis and lipogenesis and to produce a marked stimulation of fatty acid oxidation and ketogenesis. Similar effects were obtained with high concentrations of fatty acid in the absence of glucagon and, under these conditions, the additional presence of the hormone produced little further response. The results are consistent with the concept that the rate of fatty acid oxidation in liver is dictated largely by the relative concentrations of long-chain acyl-CoA (substrate for carnitine acyltransferase I) and malonyl-CoA (inhibitor of the transferase). They also indicate that the preemptive effect of fatty acids on glucagon-induced changes in fatty acid metabolism stems from their ability to reduce the tissue malonyl-CoA content, probably through long-chain acyl-CoA suppression of acetyl-CoA carboxylase.

Animals↗
PubMed1979

[Fatty acid metabolism in primary hyperlipoproteinemia (HLP) (author's transl)].

The fatty acid spectra of cholesterol ester and triglyceride fractions separated by thin-layer chromatography were analyzed by gas chromatography in the sera of 252 patients with primary HLP (with 53 cases of type IIa, 48 cases of type IIb, and 151 cases of type IV) and 60 healthy persons. Showing significantly increased values in the cholesterol ester fraction for HLP of types IIa and IIb as well as in the triglyceride fraction for HLP of types IIb and IV were palmitic acid, stearic acid, palmitoleic acid, oleic acid, and eicosatrienic acid. Significantly reduced percentages were obtained for linoleic acid, linolenic acid, arachidonic acid, and eicosapentaenic acid in the same fractions for these types. Possible causes include disturbances of the fatty acid metabolism in the liver, increased selective reesterification of fatty acids of the lipolytic process, and partially altered LCAT activity.

Adult↗
PubMed2006

Plasma fatty acid metabolic profiling and biomarkers of type 2 diabetes mellitus based on GC/MS and PLS-LDA.

Metabolic profiling has increasingly been used as a probe in disease diagnosis and pharmacological analysis. Herein, plasma fatty acid metabolic profiling including non-esterified fatty acid (NEFA) and esterified fatty acid (EFA) was investigated using gas chromatography/mass spectrometry (GC/MS) followed by multivariate statistical analysis. Partial least squares-linear discrimination analysis (PLS-LDA) model was established and validated to pattern discrimination between type 2 diabetic mellitus (DM-2) patients and health controls, and to extract novel biomarker information. Furthermore, the PLS-LDA model visually represented the alterations of NEFA metabolic profiles of diabetic patients with abdominal obesity in the treated process with rosiglitazone. The GC/MS-PLS-LDA analysis allowed comprehensive detection of plasma fatty acid, enabling fatty acid metabolic characterization of DM-2 patients, which included biomarkers different from health controls and dynamic change of NEFA profiles of patients after treated with medicine. This method might be a complement or an alternative to pathogenesis and pharmacodynamics research.

Adult↗
PubMed1983

Effect of ischemia on fatty acid metabolism in fetal lung.

The effects of ischemia on in vivo fatty acid metabolism in fetal lung were studied using rabbit fetuses of 25 to 28 gestational age. Ischemia was produced by inflating the aortic balloon thereby reducing the uterine blood flow. Ischemic insult resulted significant increase in lactate/pyruvate and NADH/NAD ratios and decrease in ATP/ADP ratio in fetal lung. Levels of CoA, acetyl CoA, carnitine and acetyl carnitine decreased while those of long chain acyl CoA and long chain acyl carnitine enhanced. Tissue content of these metabolites returned to normal after 2 hr stabilization following 20 min of ischemic insult. Ischemia also caused small increase in lipogenesis and neutral lipid content of fetal lungs. Our results thus suggest that beta-oxidation in fetal lung is inhibited and becomes rate-limiting for fatty acid oxidation during ischemia. Sudden occurrence of hypoxia or ischemia in the fetus is a typical challenge for the obstetricians. The patients occasionally suffer from neurological injury following cerebral hypoxemia. The hypoxic insult may also affect the respiratory activity significantly. For example, acute alveolar hypoxia causes pulmonary vasoconstriction by damaging pulmonary vascular smooth muscle (1) and results in reduction of fatty acid oxidation by limiting the ATP supply required for metabolic processes (2). Hypoxia has also been shown to decrease the rate of palmitate incorporation into phospholipids (3), inhibit rate of fatty acid synthesis (3) and depress rate of incorporation of fatty acid and phosphatidic acid into lipids (4). Despite the fact that fatty acids represent a major substrate for energy metabolism in lung, no work has been done on the fatty acid metabolism in fetal lung. The present study was designed to determine the fate of fatty acid oxidation in fetal lung during ischemic challenge. The levels of acyl CoA and acylcarnitine intermediates were also measured in order to determine the rate-controlling steps of fatty acid metabolism in the fetal lung.

Adenosine Diphosphate↗
PubMed1997

Free fatty acid metabolism during myocardial ischemia and reperfusion.

Long chain free fatty acids (FFA) are the preferred metabolic substrates of myocardium under aerobic conditions. However, under ischemic conditions long chain FFA have been shown to be harmful both clinically and experimentally. Serum levels of free fatty acids frequently are elevated in patients with myocardial ischemia. The proposed mechanisms of the detrimental effects of free fatty acids include: (1) accumulation of toxic intermediates of fatty acid metabolism, such as long chain acyl-CoA thioesters and long chain acylcarnitines, (2) inhibition of glucose utilization, particularly glycolysis, during ischemia and/or reperfusion, and (3) uncoupling of oxidative metabolism from electron transfer. The relative importance of these mechanisms remains controversial. The primary site of FFA-induced injury appears to be the sarcolemmal and intracellular membranes and their associated enzymes. Inhibitors of free fatty acid metabolism have been shown experimentally to decrease the size of myocardial infarction and lessen postischemic cardiac dysfunction in animal models of regional and global ischemia. The mechanism by which FFA inhibitors improve cardiac function in the postischemic heart is controversial. Whether the effects are dependent on decreased levels of long chain intermediates and/or enhancement of glucose utilization is under investigation. Manipulation of myocardial fatty acid metabolism may prove beneficial in the treatment of myocardial ischemia, particularly during situations of controlled ischemia and reperfusion, such as percutaneous transluminal coronary angioplasty and coronary artery bypass grafting.

Animals↗
PubMed2006

Fatty acid metabolism in the freshwater fish Murray cod (Maccullochella peelii peelii) deduced by the whole-body fatty acid balance method.

The whole-body fatty acid balance method was used to investigate the fatty acid metabolism in Murray cod (Maccullochella peelii peelii) fed diets containing canola (CO) or linseed oil (LO). Murray cod were able to elongate and desaturate both 18:2n-6 and 18:3n-3. In fish fed the CO diet, 54.4% of the 18:2n-6 consumed was accumulated, 38.5% oxidized and 6.4% elongated and desaturated to higher homologs. Fish fed the LO diet accumulated 52.9%, oxidized 37% and elongated and desaturated 8.6% of the consumed 18:3n-3. The overall roles of n-6 fatty acids appeared more important in Murray cod compared to other freshwater species. Murray cod also showed a preferential order of utilization of C18 fatty acid for energy production (18:3n-3 > 18:2n-6 > 18:1n-9). Moreover, it is demonstrated that an increase in dietary 18:3n-3 is directly responsible of increased desaturase activity and augmented saturated fatty acid accumulation in the fish body. The present study also suggests that, in the context of the possible maximization of the natural ability of fish to produce long chain polyunsaturated fatty acids, the whole-body approach can be considered well suited and informative and Murray cod is a suited candidate to fish oil replacement for its diets.

Animals↗
PubMed1984

Effects of reducing fatty acid metabolism on mechanical function in regionally ischemic hearts.

Fatty acids in excess impair mechanical function and electrical stability in ischemic hearts. The purpose of the present studies was to test whether oxfenicine, an agent capable of reducing fatty acid metabolism, can prevent these consequences and in so doing improve hemodynamic performance. Two groups of working swine hearts (n = 15), extracorporeally perfused with whole blood, were compared over 90 min of controlled coronary perfusion. An emulsion of triacylglycerols (Intralipid) with heparin were administered systemically to augment serum fatty acids threefold (0.30 to 0.92 mumol/ml). Labeled [U14C]palmitate was administered selectively into the left anterior descending coronary circulation to follow fatty acid oxidation. Coronary flow in this bed was decreased by 50% over the final 30 min of perfusion. Saline (n = 7) or oxfenicine (17-33 mg/kg, n = 8) was administered to placebo or treated animals at 30 min perfusion. 14CO2 production from labeled palmitate was decreased by 55% (P less than 0.025) at normal flows in oxfenicine-treated hearts and was reduced further during ischemia. Tissue levels of acyl carnitine were significantly reduced and acetyl CoA levels significantly increased in oxfenicine-treated hearts both in aerobic and ischemic myocardium. These changes were associated with an improvement in mechanical function. Left ventricular systolic and developed pressures and maximum left ventricular dP/dt were increased by 36 delta %, P less than 0.01; 46 delta %, P less than 0.025; and 41 delta %, P less than 0.025, respectively, at end ischemia as compared with placebo hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Studies of fatty acid metabolism with positron emission tomography in patients with cardiomyopathy.

Positron emission tomography (PET) permits in vivo as well as noninvasive study of fatty acid metabolism. Parameters of 11C-palmitate kinetics relate to the oxidation of fatty acids, and palmitic acid uptake is impaired in patients with coronary disease and cardiomyopathy. Normal myocardium shows homogeneous fatty acid metabolism and can resort to alternate substrates. Diseased myocardium exhibits regional heterogeneity in fatty acid uptake and utilization. In patients with cardiomyopathy, distinct patterns of fatty acid metabolism can be observed following changes of substrate availability by application of an oral glucose load. This intervention also enhances the heterogeneity of 11C-palmitic acid (CPA) uptake and clearance. Thus, PET studies with CPA permit the noninvasive demonstration of effects on substrate availability and may help to characterize patients with ventricular dysfunction on the biochemical level.

Adult↗
PubMedDate not supplied

[Effect of nonselective and cardioselective beta-adrenergic blockade on fatty acid metabolism in the myocardium].

Effects of beta-adrenoblocker obsidan and selective beta-adrenoblocker cordanum on metabolism of fatty acids in the rat myocardium were studied. Obsidan increased the concentration of triglycerides and decreased that of nonesterified fatty acids in the myocardial tissue, reduced the amounts of ketone bodies, beta-oxybutyrate and acetoacetate, accelerated oxidation of fatty acids by myocardial mitochondria. Cordanum produced no changes in beta-oxybutyrate concentration, decreased the concentrations of acetoacetate, induced accumulation of triglycerides. The drug reduced respiration control at the expense of an increase in controlled respiration rate. Thus, in contrast to total beta-adrenergic blockade induced by obsidan, cardioselective beta-adrenergic blockade by cordanum results in a decrease of myocardial oxygen consumption and a reduction of respiration controlled respiration rate.

Adenosine Triphosphate↗