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PubMed2002

Insulin causes fatty acid transport protein translocation and enhanced fatty acid uptake in adipocytes.

Fatty acid uptake into 3T3 L1 adipocytes is predominantly transporter mediated. Here we show that, during 3T3 L1 adipocyte differentiation, expression of fatty acid transport proteins (FATPs) 1 and 4 is induced. Using subcellular membrane fractionation and immunofluorescence microscopy, we demonstrate that, in adipocytes, insulin induces plasma membrane translocation of FATPs from an intracellular perinuclear compartment to the plasma membrane. This translocation was observed within minutes of insulin treatment and was paralleled by an increase in long chain fatty acid (LCFA) uptake. In contrast, treatment with TNF-alpha inhibited basal and insulin-induced LCFA uptake and reduced FATP1 and -4 levels. Thus, hormonal regulation of FATP activity may play an important role in energy homeostasis and metabolic disorders such as type 2 diabetes.

3T3 Cells↗
PubMed2002

Suppression of fatty acid synthase promoter by polyunsaturated fatty acids.

Dietary polyunsaturated fat is known to suppress expression of fatty acid synthase (FAS), a central enzyme in de novo lipogenesis. The sterol regulatory element-binding protein (SREBP) has recently been shown to be involved in this suppression. We previously reported that the first 2.1 kb of the FAS promoter are sufficient for transcriptional induction by a high carbohydrate diet as well as suppression by polyunsaturated fat in transgenic mice. Here, we first examined the DNA sequences responsible for SREBP-mediated suppression of FAS promoter activity by polyunsaturated fatty acids (PUFA) in vivo. Feeding polyunsaturated fat prevented both the low-level activation of the -278 FAS promoter which contains the -150 sterol response element (SRE), as well as the maximal activation of the longer -444 FAS promoter. We observed that ectopic expression of the activated form of SREBP in liver prevented PUFA-mediated suppression of both the endogenous FAS and FAS promoter-reporter transgene expression. We also found that the promoter region required for PUFA suppression in vivo is located between -278 to -131, where SREBP functions. Using HepG2 cells, we further examined the specific FAS promoter elements required for PUFA suppression. We found that the -150 SRE, as well as the -65 E-Box, contribute to PUFA suppression of the FAS promoter, at least in vitro.

5' Untranslated Regions↗
PubMed2000

Binding of fatty acids and peroxisome proliferators to orthologous fatty acid binding proteins from human, murine, and bovine liver.

Liver-type fatty acid binding protein (L-FABP) has been proposed to be involved in the transport of fatty acids and peroxisome proliferators from the cytosol into the nucleus for interaction with the peroxisome proliferator-activated receptors (PPARs). On the basis of this premise, we investigated by isothermal titration calorimetry the binding of myristic, stearic, oleic, and docosahexaenoic acids to three orthologous L-FABPs and compared these results to those obtained for several xenobiotics [Wy14,643, bezafibrate, 5,8,11,14-eicosatetraynoic acid (ETYA), and BRL48,482] known for their peroxisome proliferating activity in rodents. Recombinant human, murine, and bovine L-FABPs were analyzed and the thermodynamic data were obtained. Our studies showed that fatty acids bound with a stoichiometry of 2:1, fatty acid to protein, with dissociation constants for the first binding site in the nanomolar range. With dissociation constants above 1 microM the drug peroxisome proliferators showed weaker binding, with the exception of arachidonate analogue ETYA, which bound with a similar affinity as the natural fatty acid. Some of the thermodynamic data obtained for fatty acid binding could be explained by differences in protein structure. Moreover, our results revealed that binding affinities were not determined by ligand solubility in the aqueous phase.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1981

Fatty acid accretion in fetal and neonatal liver: implications for fatty acid requirements.

The fatty acid content of liver was determined during the last trimester of infant growth and first 4 months of life in order to estimate fatty acid levels of developing liver and to assess minimal fatty acid requirements for tissue synthesis. Accretion rates were computed by regression analysis on fatty acid determinants of total liver lipid extracts from infants of varying developmental ages. During the last trimester of liver growth, accretion of most fatty acids paralleled increases in liver weight with the exception of C18:3, omega-3. This fatty acid remained at consistently low levels during the last trimester and represented less than 10% of total omega-3 fatty acids present in liver, even though significant accretion of longer chain omega-3 homologues occurred during the final trimester. For the term infants studied, significant increase in liver weight did not occur during the early weeks of life. However, liver levels of major fatty acids declined during the first five weeks of life apparently reflecting mobilization of saturated, omega-9 and omega-3 fatty acids from liver. During the first four months of life C18:2, omega-6 and total omega-6 fatty acid content of liver increased about 3.5- and 2-fold, respectively. After the initial 5 week lag net accretion of other fatty acid components also occurred in the developing liver. These developmental changes in fatty acid components of liver are quantitatively relevant to estimating the magnitude of the potential essential fatty acid reserve that may be present in liver of the developing human neonate.

Fatty Acids↗
PubMed2000

Cellular uptake of long-chain fatty acids: role of membrane-associated fatty-acid-binding/transport proteins.

The critical importance of long-chain fatty acids in cellular homeostasis demands an efficient uptake system for these fatty acids and their metabolism in tissues. Increasing evidence suggests that the plasma-membrane-associated and cytoplasmic fatty-acid-binding proteins are involved in cellular fatty acid uptake, transport and metabolism in tissues. These binding proteins may also function in the fine tuning of cellular events by modulating the metabolism of long-chain fatty acids implicated in the regulation of cell growth and various cellular functions. Several membrane-associated fatty-acid-binding/transport proteins such as plasma membrane fatty-acid-binding protein (FABPpm, 43 kDa), fatty acid translocase (FAT, 88 kDa) and fatty acid transporter protein (FATP, 63 kDa) have been identified. In the feto-placental unit, preferential transport of maternal plasma arachidonic and docosahexaenoic acids across the placenta is of critical importance for fetal growth and development. Our studies have shown that arachidonic and docosahexaenoic acids are preferentially taken up by placental trophoblasts for fetal transport. The existence of a fatty-acid-transport system comprising multiple membrane-binding proteins (FAT, FATP and FABPpm) in human placenta may be essential to facilitate the preferential transport of maternal plasma fatty acids in order to meet the requirements of the growing fetus. The preferential uptake of arachidonic and docosahexaenoic acids by the human placenta has the net effect of shunting these maternal plasma fatty acids towards the fetus. The roles of plasma membrane-associated binding/transport proteins (FABPpm, FAT and FATP) in tissue-specific fatty acid uptake and metabolism are discussed.

Animals↗
PubMed2004

Acute effects of monounsaturated fatty acids with and without omega-3 fatty acids on vascular reactivity in individuals with type 2 diabetes.

AIMS/HYPOTHESIS: We examined the acute postprandial effects of meals containing unsaturated fatty acids on flow-mediated dilation (FMD) of the brachial artery and triacylglycerols in individuals with type 2 diabetes. We hypothesised that consumption of omega-3 fatty acids would enhance vascular function. Saturated fat reduces FMD for several hours, but there is inconsistent evidence about whether foods containing unsaturated fats impair FMD acutely. Little is known about the acute effects of omega-3 fatty acids on vascular reactivity. METHODS: We measured FMD before and 4 h after 3 test meals (50 g fat, 2,615 kJ) in 18 healthy adults with type 2 diabetes. The monounsaturated fatty acids (MUFA) meal contained 50 g fat from high oleic safflower and canola oils. Two additional meals were prepared by replacing 7% to 8% of MUFA with docosahexaenoic acid and eicosapentaenoic acid from sardine oil or alpha-linolenic acid from canola oil. RESULTS: In the sample as a whole, FMD was increased 17% at 4 h vs. the fasting baseline. After the MUFA meal, subjects with the largest increases in triacylglycerols had the largest FMD decreases. The opposite pattern was observed after meals containing docosahexaenoic acid and eicosapentaenoic acid or alpha-linolenic acid. In subjects with high fasting triacylglycerols, meals containing 3 to 5 g of omega-3 fatty acids increased FMD by 50% to 80% and MUFA alone had no significant effects on FMD. CONCLUSIONS/INTERPRETATION: Endothelium-dependent vasodilation was not impaired 4 h after meals containing predominantly unsaturated fatty acids. The fatty acid composition of the meal and the metabolic status of the individual determine the vascular effects of a high-fat meal.

Blood Flow Velocity↗
PubMed2003

Sequence variation and genomic organization of fatty acid desaturase-2 (fad2) and fatty acid desaturase-6 (fad6) cDNAs in maize.

Increased levels of oleic acid may enhance the nutritional and functional value of corn. Corn oil is primarily composed of palmitic, stearic, oleic, linoleic and linolenic fatty acids. Delta-12 desaturase in plants converts oleic acid (18:1) to linoleic acid (18:2) by inserting a double bond at the delta-12 position. Fatty acid desaturase-2 (fad2) encodes delta-12 desaturase that functions in the endoplasmic reticulum while fatty acid desaturase-6 (fad6) encodes delta-12 desaturase that functions in plastids. Complementary DNA (cDNA) clones from putative maize homologs for fad2 and fad6 were identified and the entire clones DNA sequenced. The maize fad2 cDNAs showed an amino-acid identity of 67-77% to fad2 of Glycine, Arabidopsis and Brassica species. Our cDNA sequence comparisons suggested that more than one fad2 gene is transcribed in maize embryos. Two different fad2 cDNAs from an embryo cDNA library map to separate chromosomal positions, providing evidence consistent with two different isoforms of fad2 expressed in the embryo. The fad2 cDNAs from multiple tissue sources clustered into three groups on a phenogram, and map to different positions on chromosomes 4, 5 and 10, which suggests at least three different isoforms of fad2 may be expressed in the maize plant. The two maize fad6 cDNAs share 81% amino-acid identity with the Arabidopsis fad6 and map to chromosome 1. Northern analysis revealed that fad2 is transcribed in embryos at 14, 21, 28 and 35 days after pollination, with the highest level observed at day 14. None of the fad2 or fad6 clones mapped to maize chromosome bins associated with QTLs for the ratio of oleic/linoleic acid, notably bin 6.04 which contains the linoleic1 locus and the largest reported QTL for the oleic/linoleic ratio. This suggests, but does not prove, that some of the QTLs for the oleic/linoleic acid ratio do not involve allelic variants of fad2 or fad6 but rather involve other genes that may influence flux through the enzymes encoded by fad2 or fad6.

DNA, Complementary↗
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↗
PubMed2006

Protective effect of Arthrospira maxima on fatty acid composition in fatty liver.

BACKGROUND: Arthrospira maxima has been widely used for nutritional purposes. Additionally, A. maxima has shown immunomodulator, antiviral, antioxidant, vasomotor and hypolipidemic effects in laboratory and animal studies. A. maxima prevents fatty liver induced by either carbon tetrachloride (CCl4) or fructose-rich diet; however, the liver lipid composition in these models is not clearly known yet. The aim of this study was to evaluate the effects of A. maxima on the liver lipid profile in CCl4-induced steatohepatitis. METHODS: A single sublethal, intraperitoneal dose of CCl4 was administered to male Wistar rats fed a diet with or without 5% A. maxima. Liver lipids: total lipids, triacylglycerols, total cholesterol, free fatty acids, and thiobarbituric acid reactive substances were assessed 24 and 48 h after injury with CCl4. Additionally, triacylglycerols, total cholesterol and aspartate aminotransferase were evaluated in blood. RESULTS: Forty eight hours after CCl4 treatment, rats fed a diet without A. maxima had serum aspartate aminotransferase and liver triacylglycerols values that were, respectively, 2.2 and 1.4 times higher than those of animals receiving 5% A. maxima in their diet. The same pattern was observed for liver free fatty acids and thiobarbituric acid reactive substances. The groups fed a diet with A. maxima and treated with CCl4 showed a higher saturated fatty acid liver content than the groups without A. maxima in their diet. The percentage of unsaturated fatty acids increased 48 h after CCl4 treatment, but its value was 0.5 times lower in the group receiving A. maxima than in the group fed without A. maxima. In the liver, all animals receiving A. maxima showed a trend towards a lower percentage of unsaturated fatty acids, despite the mentioned increase 48 h after CCl4 treatment. CONCLUSIONS: The results suggest that, in the fatty liver induced by CCl4, the hepatoprotective effect of A. maxima involves (a) an antioxidant mechanism and (b) a lower unsaturation of the liver fatty acids. The preventive effect of A. maxima on the liver lipid changes induced by CCl4 could be partially explained by its antioxidant action and the ability to increase the synthesis/release of nitric oxide, but not by its soluble dietary fiber.

Animal Feed↗
PubMed1976

Biosynthesis of cyclopentenyl fatty acids. (2-Cyclopentenyl)carboxylic acid (aleprolic acid) as a special primer for fatty acid biosynthesis in Flacourtiaceae.

The biosynthesis of cyclopentenyl fatty acids from (2-cyclopentenyl)carboxylic acid (aleprolic acid) via chain-lengthening by C2-units was tested in seeds and leaves of Caloncoba echinata and Hydnocarpus anthelminthica of Flacourtiaceae and in various prepatations of higher plants other than Fla courtiaceae. Only tissues of Flacourtiaceae, where cyclopentenyl fatty acids are found naturally, were able to accept aleprolic acid as a starter molecule for the synthesis of cyclic fatty acids. Labelling patterns of straight chain and cyclic fatty acids, synthesized after incubation of Flacourtiaceae seeds with [1-(14)C[-acetate, indicated de novo synthesis of C16 fatty acids in either case, followed by elongation to higher homologs.

Acetates↗
PubMedDate not supplied

Dietary trans fatty acid.

Trans fatty acids are unsaturated fatty acids that contain at least one double bond in the trans configuration. In the diet they occur at relatively low levels in meat and dairy products as a by-product of fermentation in ruminant animals or in hydrogenated fats as a consequence of the hydrogenation process. In general, dietary hydrogenated fat/trans fatty acids have been reported to increase LDL cholesterol levels relative to oil in the natural state or cis fatty acids. In contrast, dietary hydrogenated fat/trans fatty acids have been reported have to have little effect or decrease HDL cholesterol levels, the later observation restricted to relatively high intakes of trans fatty acids. These two effects result in higher, therefore less favorable, total or LDL cholesterol/HDL cholesterol ratios. Significant increases in Lp(a) levels have been reported after consumption of diets relatively high in trans fatty acids compared with either unsaturated or saturated fatty acids. However, the magnitude of the change is for the most part small and the physiological significance of this observation has yet to be resolved. Data related to the mechanism by which hydrogenated fat/trans fatty acids alter serum lipid levels and other risk factors for cardiovascular disease are in the nascent stages. At this time it would appear prudent that public health recommendations should be aimed at encouraging the moderate consumption of products low in saturated fat or minimally hydrogenated. Trans fatty acids intake should not be stressed at the expense of saturated fat but should augment it.

Cardiovascular Diseases↗
PubMed1990

Effects of chronic administration of perfluorooctanoic acid on fatty acid metabolism in rat liver: relationship among stearoyl-coenzyme A desaturase, 1-acylglycerophosphocholine acyltransferase, and acyl composition of microsomal phosphatidylcholine.

Male and female rats were fed on a diet containing 0.01% (w/w) perfluorooctanoic acid (PFOA) for 2, 22, or 26 weeks and effect of PFOA on activities of microsomal 1-acylglycerophosphocholine acyltransferase, microsomal stearoyl-coenzyme A (CoA) desaturase, peroxisomal beta-oxidation and on acyl composition of microsomal phosphatidylcholine in liver were studied. The treatment of male rats with PFOA for 2 weeks caused increases in the activities of stearoyl-CoA desaturase, 1-acylglycerophosphocholine acyltransferase, and peroxisomal beta-oxidation. The elevated activities of microsomal 1-acylglycerophosphocholine acyltransferase and peroxisomal beta-oxidation were unchanging throughout the long-term treatment. The induced activity of microsomal 1-acylglycerophosphocholine acyltransferase was found to be highly correlated with the induced activity of peroxisomal beta-oxidation. In contrast to these two enzymes, the increased activity of stearoyl-CoA desaturase by the short-term treatment of rats with PFOA did not last for 26 weeks, although the activity in rats treated for the long-term was higher than that of age-matched controls. The treatment of male rats with PFOA caused great alterations in the acyl composition of microsomal phosphatidylcholine. The high correlation seen between proportion of 18:1 in the C-2 position of phosphatidylcholine and activities of both stearoyl-CoA desaturase and 1-acylglycerophosphocholine acyltransferase suggest that these two enzymes participate actively in the regulation of acyl composition of phosphatidylcholine in rat liver. The present results show that hepatic responses to PFOA remain consistent throughout the period of the administration, but the elevated activities of the hepatic enzymes and the altered acyl composition of microsomal phosphatidylcholine returned to control levels within 4 weeks after PFOA was withdrawn from the diet. Even after the chronic administration of PFOA, these parameters of female rats responded only slightly to the challenges by the chemical, which indicates a marked sex-related difference being still apparent in the response of rat liver to PFOA.

1-Acylglycerophosphocholine O-Acyltransferase↗
PubMed1991

Effect of low intake of n-3 fatty acids during development on brain phospholipid fatty acid composition and exploratory behavior in rats.

The effect of dietary restriction of n-3 fatty acids during development on brain phospholipid fatty acid composition and exploratory behavior has been studied in male Sprague Dawley rats. Female rats were fed semipurified diets containing either 5.5% safflower oil or 6% soybean oil for 6 wk prior to mating and throughout gestation and lactation. Control rats were maintained on laboratory chow. The male pups were weaned to the diets of the dams except for one group which was switched from safflower to soybean oil at weaning. Behavioral studies and brain phospholipid analyses were conducted at 16-18 wk of age. Rats fed safflower oil showed significantly lower levels of 22:6n-3 in phospholipids of synaptic membranes and myelin than rats fed soybean oil or chow. The decrease in 22:6n-3 was compensated for by an increase in 22:5n-6, the total content of polyunsaturated fatty acids remaining approximately constant. The brain phospholipid fatty acid composition of rats switched from safflower to soybean oil at weaning was similar to that of rats fed soybean oil throughout the experiment. There was no difference in spontaneous locomotor activity among the different dietary groups. However, rats raised on safflower oil displayed a significantly lower exploratory activity (horizontal movements and rearings) in a novel environment than rats fed soybean oil or chow. In contrast to the brain phospholipid fatty acid composition, there was no recovery of exploratory behavior in rats raised on safflower oil and switched to soybean oil at weaning suggesting a specific requirement of n-3 fatty acids during development.

Animals↗