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PubMed1989

Alkylthio acetic acids (3-thia fatty acids)--a new group of non-beta-oxidizable peroxisome-inducing fatty acid analogues--II. Dose-response studies on hepatic peroxisomal- and mitochondrial changes and long-chain fatty acid metabolizing enzymes in rats.

The activity of key enzymes involved in oxidation and esterification of long-chain fatty acids was investigated after male Wistar rats were treated with different doses of sulfur substituted fatty acid analogues, 1,10-bis(carboxymethylthiodecane) (BCMTD, non-beta-oxidizable and non-omega-oxidizable), 1-mono(carboxymethylthiotetradecane) (CMTTD, trivial name, alkylthio acetic acid, non-beta-oxidizable) and 1-mono(carboxyethylthiotetradecane) (CETTD trivial name, alkylthio propionic acid, beta-oxidizable). The sulfur substituted dicarboxylic acid and the alkylthio acetic acid induced in a dose-dependent manner the mitochondrial, microsomal and especially the peroxisomal palmitoyl-CoA synthetase activity, the mitochondrial and cytosolic palmitoyl-CoA hydrolase activity, the mitochondrial and especially the microsomal glycerophosphate acyltransferase activity and the peroxisomal beta-oxidation, especially revealed in the microsomal fraction. Morphometric analysis of randomly selected hepatocytes revealed that BCMTD and CMTTD treatment increased the number, size and volume fraction of peroxisomes and mitochondria. Thus, the observed changes in the specific activity of fatty acid metabolizing enzymes with multiple subcellular localization can partly be explained as an effect of changes in the s-values of the organelles as proliferation of mitochondria and peroxisomes occurred. The most striking effect of the alkylthio propionic acid was the formation of numerous fat droplets in the liver cells and enhancement of the hepatic triglyceride level. This was in contrast to BCMTD treatment which decreased the hepatic triglyceride content. In conclusion, the results provide evidence that administration of non-beta-oxidizable fatty acid analogues had much higher in vivo potency in inducing hepatomegaly and key enzymes involved in fatty acid metabolism, including proliferation of peroxisomes and mitochondria than is exhibited in the beta-oxidizable, alkylthio propionic acid. Moreover, the dicarboxylic acid was apparently three to six times more potent than the alkylthio acetic acid in inducing peroxisomal beta-oxidation and peroxisome proliferation when considered on a mumol/day basis. As palmitic acid and hexadecanedioic acid only marginally affected these hepatic responses, it is conceivable that the potency of the selected compounds as proliferators of peroxisomes and inducers of the associated enzymes depends on their accessibility for beta-oxidation.

Acetates↗
PubMed1997

Stearic acid, trans fatty acids, and dairy fat: effects on serum and lipoprotein lipids, apolipoproteins, lipoprotein(a), and lipid transfer proteins in healthy subjects.

To compare the effects on serum lipoproteins of stearic acid, trans fatty acids, and dairy fat, 80 healthy subjects consumed a dairy fat-based (baseline) diet for 5 wk, then an experimental diet high in either trans fatty acids (8.7% of energy; n = 40) or stearic acid (9.3% of energy; n = 40) for another 5 wk. All diets provided 32.2-33.9% of energy as fat, 14.6-15.8% as saturated plus trans fatty acids, 11.4-12.5% as cis-monounsaturated fatty acids, 2.9-3.5% as polyunsaturated fatty acids, and 200-221 mg cholesterol/10 MJ. Compared with the dairy fat diet, stearic acid and trans fatty acids decreased serum total cholesterol concentrations similarly (by 13% and 12%, respectively, P < 0.001) but the trans fatty acid diet decreased HDL cholesterol (17%) and apolipoprotein (apo) A-I (15%) significantly more than did the stearic acid diet (11% and 12%, respectively). Stearic acid but not trans fatty acids reduced concentrations of LDL cholesterol and apo B significantly (P < 0.001). The trans fatty acid diet increased the ratio of LDL to HDL cholesterol (19%) and of apo B to apo A-I (16%) more than did the dairy fat diet (P < 0.001) but the stearic acid diet had no effect. Lipoprotein(a) concentrations increased with both experimental diets, significantly more with trans fatty acids (30%) than with stearic acid (10%). In conclusion, high amounts of trans fatty acids had more adverse effects on lipoproteins than did equal amounts of stearic acid and dairy fat. Stearic acid reduced LDL cholesterol, did not affect the ratio of LDL to HDL cholesterol, and increased lipoprotein(a), although to a lesser extent than did trans fatty acids. Dietary fats low in both saturated fatty acids and trans fatty acids should be favored.

Adult↗
PubMed1987

Transport of Fe2+ across lipid bilayers: possible role of free fatty acids.

Fatty acids can form lipid-soluble complexes with Fe2+. Incorporation of fatty acids into phosphatidylcholine/cholesterol liposomes renders them permeable to Fe2+. Of several fatty acids tested, the most effective Fe2+ carriers were linoleic and oleic acids followed, in decreasing order of efficacy, by linolenic, myristic, arachidonic and palmitic acids. The initial Fe2+ transport rate for oleic acid depends on free Fe2+ in the medium which in turn shows a strong pH dependence above pH 7.0. The overall pH dependence of Fe2+ transport for several fatty acids shows an optimum near 6.9. Fe2+ transport catalysed by oleic acid can be inhibited by high NaCl concentrations but not 1 mM Co2+. It is suggested that free fatty acids may act as mediators of Fe2+ transport across biological membranes, particularly isolated intestinal brush-border membrane.

Ascorbic Acid↗
PubMedDate not supplied

[A catalogue of fatty acids].

Fatty acids structure and function is an area of renewed interest because of its effects on plasma lipids, biosynthesis of prostaglandins, leucotrienes and thromboxanes, and the obligatory demands of some fatty acids, especially for the newborn. Fatty acids are identified in three different ways: by the classical nomenclature, by its trivial name, and by the new methods also known as the omega system. These three different methods have created some confusion. The aim of this article is to revise fatty acids chemical structure and to compile a list of nutritional important fatty acids with the three different terminologies.

Fatty Acids↗
PubMed1980

High affinity of alpha-foetoprotein for arachidonate and other fatty acids.

Fatty acid analysis of purified bovine alpha-foetoprotein showed it to contain 2.7 mol of fatty acid/mol of alpha-foetoprotein. Purified alpha-foetoprotein focused at isoelectric point 4.8. Removal of bound ligands from alpha-foetoprotein by charcoal treatment changed its isoelectric point to 5.2. This change could be reversed by addition of exogenous fatty acids to the defatted alpha-foetoprotein. Albumin isolated from the same foetal calf serum source as alpha-foetoprotein contained 1.4 mol of fatty acid/mol of protein. alpha-Foetoprotein and albumin contained comparable amounts of fatty acids with 14 to 18 carbon atoms, but alpha-foetoprotein contained 16 times as much of the long-chain polyunsaturated fatty acids as albumin. alpha-Foetoprotein was found to have slightly higher affinity for palmitate and linoleate and severalfold higher affinity for arachidonate than albumin. These findings suggest that alpha-foetoprotein may play a role in the foetal metabolism of the long-chain polyunsaturated fatty acids.

Animals↗
PubMed1994

Peroxisome proliferator-activated receptor mediates induction of the mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase gene by fatty acids.

Fatty acids induce an increase in the transcription of the mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase gene, which encodes an enzyme that has been proposed as a control site of ketogenesis. We studied whether the peroxisome proliferator-activated receptor (PPAR) is involved in the mechanism of this transcriptional induction. We found that cotransfection of a rat mitochondrial HMG-CoA synthase promoter-chloramphenicol acetyltransferase reporter plasmid and a PPAR expression plasmid in the presence of the peroxisome proliferator clofibrate led to a more than 30-fold increase in chloramphenicol acetyltransferase activity, relative to the activity in the absence of both PPAR and inducer. Linoleic acid, a polyunsaturated fatty acid, increased this activity as potently as does clofibrate and more effectively than does monounsaturated oleic acid. We have identified, by deletional analysis, an element located 104 base pairs upstream of the mitochondrial HMG-CoA synthase gene, which confers PPAR responsiveness to homologous and heterologous promoters. This is the first example of a peroxisome proliferator-responsive element (PPRE) in a gene encoding a mitochondrial protein. This element contains an imperfect direct repeat that is similar to those described in the PPREs of other genes. Furthermore, gel retardation and cotransfection assays revealed that, as for other genes, PPAR heterodimerizes with retinoid X receptor and that both receptors cooperate for binding to the mitochondrial HMG-CoA synthase PPRE and subsequent activation of the gene. In conclusion, our data demonstrate that regulation of mitochondrial HMG-CoA synthase gene expression by fatty acids is mediated by PPAR, supporting the hypothesis that PPAR has an important role at the transcriptional level in the regulation of lipid metabolism.

Animals↗
PubMed1975

Z protein in hepatic uptake and esterification of long-chain fatty acids.

Fatty acids radioactivity was bound to Z protein in liver after administration of['3H]oleate to rats or to a perfused rat liver preparation. Pretreatment withflavaspidic acid (340 mumol/kg), a potent inhibitor of fatty acid binding to hepatic Zprotein in vitri, effectively reduced oleate radioactivity bound to Z by 90.2 plusor minus 4.3% and 85.0 plus or minus 6.2% in the intact rat and perfused liver, respectively. In spite of this effect, pretreatment of rats with flavaspidic acid did notalter plasma clearance, hepatic uptake, and esterification of ['3H]oleate. In contrast, in the perfused liver preparation, infusion of flavaspidic acid (340 mumol/kg)or bromosulphalein (360 mumol/kg) increased uptake of ['3H]oleate at least twofold,and oleate esterification was decreased by 15-30%. These results suggest that the binding of long-chain fatty acids to Z protein is not an obligatory step in their uptakeby the liver and that Z protein may be involved in fatty acid esterification.

Animals↗
PubMedDate not supplied

The use of iodinated free fatty acids for assessing fatty acid metabolism.

Free fatty acid is a major substrate fuel for normal myocardium. Cardiovascular disease is frequently associated with impairment of fatty acid oxidation. Therefore assessment of fatty acid metabolism may be an important tool for the early detection of myocardial abnormalities and may provide insight into pathologic heart conditions. Although carbon 11-labeled palmitate is a well-established tracer for probing myocardial fatty acid metabolism, a variety of iodinated fatty acid compounds have been introduced for assessing fatty acid metabolism, including straight-chain and branched-chain fatty acid compounds. Straight-chain fatty acid has advantages for measuring fatty acid oxidation on the basis of tracer clearance from the myocardium. Branched-chain fatty acid can be trapped in the myocardium without further washout and uptake in the myocardium may reflect fatty acid retention and some aspect of fatty acid metabolism. A long tracer retention period makes feasible the acquisition of single-photon emission computed tomographic images. This review examines the characteristics of both types of tracers and our recent clinical experience with beta-methyliodophenyl pentadecanoic acid, which has potential for detecting and characterizing both ischemic heart disease and cardiomyopathy.

Fatty Acids↗
PubMed2002

Sulfo-N-succinimidyl esters of long chain fatty acids specifically inhibit fatty acid translocase (FAT/CD36)-mediated cellular fatty acid uptake.

Sulfo-N-succinimidyl esters of LCFAs are a powerful tool to investigate the functional significance of plasmalemmal proteins in the LCFA uptake process. This notion is based on the following observations. First, sulfo-N-succinimidyl oleate (SSO) was found to inhibit the bulk of LCFA uptake into various cell types, i.e. rat adipocytes, type II pneumocytes and cardiac myocytes. Second, using cardiac giant membrane vesicles, in which LCFA uptake can be investigated in the absence of mitochondrial beta-oxidation, SSO retained the ability to largely inhibit LCFA uptake, indicating that inhibition of LCFA transsarcolemmal transport is its primary action. Third, SSO has no inhibitory effect on glucose and octanoate uptake into giant membrane vesicles derived from heart and skeletal muscle, indicating that its action is specific for LCFA uptake. Finally, SSO specifically binds to the 88 kDa plasmalemmal fatty acid transporter FAT, a rat homologue of human CD36, resulting in an arrest of the transport function of this protein. In addition to its inhibitory action at the plasma membrane level, evidence is presented for the lack of a direct inhibitory effect on subsequent LCFA metabolism. First, the relative contribution of oxidation and esterification to LCFA uptake is not altered in the presence of SSO. Second, isoproterenol-mediated channeling of LCFAs into oxidative pathways is not affected by sulfo-N-succinimidyl palmitate (SSP). As an example of its application, we used SSP to study the role of FAT/CD36 in contraction- and insulin-stimulated LCFA uptake by cardiac myocytes, showing that this transporter is a primary site of regulation of cellular LCFA utilization.

Animals↗