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PubMed2005

Spillover of dietary fatty acids and use of serum nonesterified fatty acids for the synthesis of VLDL-triacylglycerol under two different feeding regimens.

The present study quantified dietary fatty acid flux in healthy men (n = 6) who were fed a liquid formula through a duodenal feeding tube (continuous feeding group) or who consumed the same formula in meals (meal feeding group). A triacylglycerol (TAG) stable isotope was added to the formula to determine the entry of dietary fatty acids into the serum and its clearance to the liver and resecretion into serum via VLDL. The contribution of dietary fatty acids to serum nonesterified fatty acids (NEFAs) was higher with meal feeding (24.4 +/- 2.6%) compared with continuous feeding (10.8 +/- 2.9%, P < 0.01) and, when multiplied by the NEFA concentration, resulted in similar absolute fatty acid spillover. Diet-derived NEFAs subsequently represented 10.6 +/- 1.2% and 4.7 +/- 1.3% of hepatic VLDL-TAG (meal feeding vs. continuous feeding, respectively, P = 0.004). Chylomicron remnant uptake by the liver contributed 9.3 +/- 1.9% of fatty acids to hepatic VLDL-TAG synthesis with meal feeding compared with continuous feeding (4.4 +/- 0.8%, P < 0.03). These data suggest that the extent of dietary fatty acid recycling via serum NEFAs and VLDL-TAG is determined by the rate of delivery of dietary fat to the intestine. The inefficient removal of dietary fat from the circulation may maintain VLDL-TAG production but may also result in prolonged postprandial lipemia.

Adult↗
PubMed1995

The effects of n-3 and n-6 polyunsaturated fatty acids on plasma lipids and fatty acids of treated phenylketonuric children.

Dietary-treated phenylketonuric patients (PKUs) display low levels of long-chain polyunsaturated fatty acids (PUFA) in plasma lipids. In a 6-month clinical trial we observed a decrease of triglycerides and an increase of n-3 long-chain PUFA in plasma of PKUs supplemented with fish oil, while no major differences in respect to the baseline values were found in a group supplemented with blackcurrant oil. A more complete source of long-chain PUFA of both the n-6 and n-3 series should be investigated for dietary supplementation of PKU patients.

Child↗
PubMed1977

Phytohaemagglutinin stimulation of human lymphocytes: effect of fatty acids on uridine uptake and phosphoglyceride fatty acid profile.

1. When added to cultures of human peripheral lymphocytes, saturated (palmitate, stearate, heptadecanoate) and unsaturated (oleate, linoleate, arachidonate) fatty acids bound to albumin at an acid-albumin ratio of 2:1, inhibited the phytohaemaegglutinin-stimulated uptake of [14C]-uridine. Uridine uptake in unstimulated cells was not affected by any of these fatty acids. 2. When saturated and unsaturated acids were present simultaneously in the incubation mixture the inhibit but relieved the inhibitory effects of both saturated and unsaturated fatty acids. 4. Stimulated and unstimulated cells incorporated exogenous fatty acids into membrane phosphoglycerides. Details of the fatty acid profiles are given. 5. Evidence is presented that the inhibition results, at least in part, from modification of phosphoglyceride fatty acid profile.

Dose-Response Relationship, Drug↗
PubMed2000

Long chain fatty acids inhibit and medium chain fatty acids activate mammalian cardiac hexokinase.

We investigated the effect of non-esterified fatty acids (FAs) on bovine heart hexokinase (type I: ATP: D-hexose 6-phosphotransferase, EC 2.7.1.1). Long chain FAs (C14 to C20) inhibited the enzyme in a way that correlated positively with both the chain length and the degree of unsaturation. Medium chain FA with 12 or less carbons activated hexokinase in a chain length dependent manner with the greater activation shown by laurate. The activation constant of laurate was 91.5 microM with a maximal activation of 60.3%. Oleate caused a maximal decrease in specific activity of 25% with an inhibition constant of 79 microM. Using the fluorescent probe cis-parinarate, we found a saturable binding site with K(d) of 3.5 microM. Oleate competed the fluorescent probe from the protein with a K(d) of 1.4 microM. Medium chain FAs did not compete the probe from HK. The binding of fatty acid to the protein appears to be entropically driven as indicated by an Arrhenius analysis (DeltaS=+231.6 J mol(-1) deg(-1)). The presence of oleate significantly increased the K(ATP)(m) from 0.47 mM to 0.89 mM while the K(glucose)(m) in the presence of the FA (0.026+/-0.003 mM) was not significantly different from the control (0.014+/-0.004 mM). A decrease in V(max) values in the presence of oleate indicated that a mixed allosteric inhibition was operating.

Adenosine Triphosphate↗
PubMed1983

Incorporation of cis-parinaric acid, a fluorescent fatty acid, into synaptosomal phospholipids by an acyl-CoA acyltransferase.

The cis-isomer of parinaric acid, a naturally occurring C-18 polyene fatty acid, was incubated with brain subcellular fractions and the polarization of fluorescence increased in a time dependent manner. Greatest increases occurred in synaptosomal and microsomal membranes. This increase in polarization of fluorescence was found with the cis, but not the trans, isomer of parinaric acid and required Mg2+ or Ca2+ and was stimulated by coenzyme A and ATP. Synaptosomes were incubated with cis-parinaric acid and lipids were extracted and examined by high performance liquid chromatography. The highest incorporations of cis-parinaric acid were found in phosphatidylcholine (71%) and phosphatidylethanolamine (20%) while only traces were found in phosphatidylserine and phosphatidylinositol. [3H]Oleic acid was also incorporated into membrane phospholipids and unlabeled oleic acid blocked incorporation of cis-parinaric acid. It is proposed that cis-parinaric acid, like fatty acids normally found in brain, is incorporated into membrane phospholipids by an acyl-CoA acyltransferase. The presence of this enzyme in nervous tissue may make it possible to easily introduce fluorescent fatty acid probes into membrane phospholipids and to thereby facilitate study of membrane-mediated processes.

Animals↗
PubMed2006

Methods for investigating placental fatty acid transport.

Fatty acids (FAs), especially essential fatty acids (EFAs) and their long chain polyunsaturated fatty acid (LCPUFAs) derivatives, are critical for proper fetal development. The fetus relies on the placental transfer of EFAs from the maternal circulation for development. In fact, fatty acid transfer is highly directional from the mother to the fetus. Significant changes in placental fatty acid transport and metabolism, the two primary processes that govern placental FA supply from mother to fetus, can subsequently result in aberrant fetal fatty acid/lipid homeostasis and dramatically increase the risk of abnormal fetal development. Besides passive diffusion, specific fatty acid transfer conferring proteins can actively mediate directional placental fatty acid uptake and transport. Enzymes for fatty acid beta-oxidation and synthesis and the ones participating PUFA metabolism, including cytochrome P450 (mainly CYP4A), cyclooxygenases (COXs), and lipooxygenases (LOXs), have also been identified in the placenta. Methods for studying functional placental fatty acid uptake/transport/metabolism are discussed, focusing on an in vitro placental trophoblast model and long chain unsaturated fatty acids. The relevant theory of FA transport pathways, kinetic data analysis (uptake rates, permeability, influx/efflux ratio, Km, and so on) and high-performance liquid chromatography identification are also discussed.

Animals↗
PubMed1995

Membrane fatty acids of breast carcinoma: contribution of host fatty acids and tumor properties.

To assess the part that host fatty-acid supply and tumor-specific fatty-acid utilization contribute to the membrane lipid composition of tumor tissue, intra-individual comparisons of membrane fatty acids were carried out between breast-carcinoma tissue and non-tumorous breast tissue adjacent to the tumor and taken as reference. Phospholipids were purified by thin-layer chromatography from tumor biopsies obtained from 59 patients with a localized presentation of breast cancer, and fatty acids analyzed by capillary gas chromatography. Elevated levels of palmitic, palmitoleic and arachidonic acids, along with a low level of linoleic acid, were observed in membrane phospholipids of tumors with poor histoprognostic grade. The level of mono-unsaturated fatty acids was higher, and the level of essential fatty acids was lower in the tumor than in the reference breast tissue. Fatty-acid-desaturating activity was not detectable in tumors. A positive relationship was observed among patients for most of the fatty acids between carcinoma and non-tumorous breast tissue, except for mono-unsaturated and essential fatty-acid levels, which were not correlated between both tissues. These data suggest that mechanisms specifically related to malignant transformation and tumor progression influence the membrane fatty-acid profile of breast carcinoma. Fatty acid supply to the tumor, possibly modified by metabolic conditions related to the host, also seems to play a decisive role in this composition.

Adult↗
PubMed2000

Nutritional status and intermediate chain-length fatty acids influence the conservation of essential fatty acids in the milk of northern Nigerian women.

The milk of 89 women in northern Nigeria was analyzed for the fatty acid composition of the total milk lipids, and assessed for the effect nutritional status has on the conservation of essential and non-essential fatty acids when the proportions of C(10)-C(14)fatty acids are increased. The women were stratified on the basis of their body mass index, and calculations were made to estimate the effects of a 3.3-fold increase in the proportion of C(10)-C(14)fatty acids on the proportion of alpha-linolenic acid, docosahexaenoic acid, linoleic acid and arachidonic in total milk lipids. In the well-nourished group (group III, body mass index >23 kg/m(2)), the critical n-3 and n-6 fatty acids were not conserved, while in poorly nourished women (group I, body mass index <19 kg/m(2)), marked conservation of alpha-linolenic acid, docosahexaenoic acid, arachidonic acid, and palmitic acid was seen. Poor nutritional status of the mother appears to promote selective retention of critical essential and non-essential fatty acids in the milk lipid fraction.

Adult↗
PubMedDate not supplied

Plasma free fatty acid and lipoproteins as sources of polyunsaturated fatty acid for the brain.

Polyunsaturated fatty acids (PUFA), which comprise 25-30% of the fatty acids in the human brain, are necessary for normal brain development and function. PUFA cannot be synthesized de novo and must be supplied to the brain by the plasma. It is necessary to know the PUFA content and composition of the various plasma lipids and lipoproteins in order to understand how these fatty acids are taken up and metabolized by the brain. Human plasma free fatty acid (FFA) ordinarily contains about 15% linoleic acid (18:2n-6) and 1% arachidonic acid (AA) (20:4n-6). Plasma triglycerides, phospholipids, and cholesterol esters also are rich in linoleic acid, and the phospholipids and cholesterol esters contain about 10% AA. These findings suggest that the brain probably can obtain an adequate supply of n-6 PUFA from either the plasma FFA or lipoproteins. By contrast, the plasma ordinarily contains only one-tenth as much n-3 PUFA, and the amounts range from 1% alpha-linolenic acid (18:3n-3) in the plasma FFA to 2% docosahexaenoic acid (22:6n-3, DHA) in the plasma phospholipids. The main n-3 PUFA in the brain is DHA. Therefore, if the plasma FFA is the primary source of fatty acid for the brain, much of the DHA must be synthesized in the brain from n-3 PUFA precursors. Alternatively, if the brain requires large amounts of preformed DHA, the phospholipids contained in plasma lipoproteins are the most likely source.

Animals↗
PubMed2003

Suppression of fatty acid synthase by dietary polyunsaturated fatty acids is mediated by fat itself, not by peroxidative mechanism.

This study examined the effect of dietary polyunsaturated fatty acids (PUFA) that were supplemented with vitamin E on lipid peroxidation, glutathione-dependent detoxifying enzyme system activity, and lipogenic fatty acid synthase (FAS) expression in rat liver. Male Sprague-Dawley rats were fed semipurified diets containing either 1% (w/w) corn oil or 10% each of beef tallow, corn oil, perilla oil, and fish oil for 4 wk. Alpha-tocopherol was supplemented in perilla oil (0.015%) and fish oil (0.019%). Hepatic thiobarbituric acid reactive substances, an estimate of lipid peroxidation, were not significantly different among the dietary groups. The glutathione peroxidase, glutathione reductase, and glutathione S-transferase activities were all elevated by the polyunsaturated fats, especially fish oil. The activity of FAS was reduced in the polyunsaturated fat-fed groups in the order of fish oil, perilla oil, and corn oil. The mRNA contents decreased in rats that were fed the 10% fat diets, particularly polyunsaturated fats, compared with the rats that were fed the 1% corn oil diet. Similarly, the inhibitory effect was the greatest in fish oil. These results suggest that lipid peroxidation can be minimized by vitamin E; PUFA in itself has a suppressive effect on lipogenic enzyme.

Animals↗
PubMed2004

Elongation of C16:0 to C18:0 fatty acids in methylotrophic yeast Hansenula polymorpha CBS 1976 and fatty acid auxotrophic mutants.

Fatty acid elongation defective mutant was isolated from the ethyl methanesulfonate treated Hansenula polymorpha based on the growth ability. Using biochemical and genetic approaches, the mutant was characterized. When compared with the fatty acid phenotype of the parental strain, the differences in profile and content of fatty acids in V1 mutant were found. In this V1 mutant, polyunsaturated fatty acids, linoleic and alpha-linolenic acids, could not be detected with a corresponding increase in the content of mono-unsaturated fatty acids. The ratio of C16/C18 fatty acids revealed that the accumulation of C16 fatty acids was increased significantly. The experiments on fatty acid supplementation indicated that the mutant required C18:0 for the proper growth. The results of genetic complementation with the elongase genes of Saccharomyces cerevisiae confirmed that the lesion was occurred at least in the extension of C16:0 to C18:0 of V1. The H. polymorpha mutant obtained in this work will be used as a useful tool for unraveling the pathway of fatty acid synthesis and the role of fatty acids on biological processes.

Acetyltransferases↗
PubMed1999

Fatty acids: links between genes involved in fatty acid and cholesterol metabolism.

Fatty acids are a major constituent of dietary fats and form an integral part of the cellular membrane and lipoproteins. The gene regulatory potential of fatty acids has long been recognized, but the precise regulatory mechanisms are unknown. The regulatory ability of fatty acids on the expression of a number of genes together with potential mechanisms and pathways of regulation are reviewed. In this review, we emphasize a key aspect of regulation mediated by the sterol regulatory element binding-protein, and its effects on sterol regulatory elements.

Animals↗
PubMed2003

Overexpression of sterol regulatory element-binding protein-1a in mouse adipose tissue produces adipocyte hypertrophy, increased fatty acid secretion, and fatty liver.

Sterol regulatory element-binding proteins (SREBPs) are a family of membrane-bound transcription factors that regulate cholesterol and fatty acid homeostasis. In mammals, three SREBP isoforms designated SREBP-1a, SREBP-1c, and SREBP-2 have been identified. SREBP-1a and SREBP-1c are derived from the same gene by virtue of alternatively spliced first exons. SREBP-1a has a longer transcriptional activation domain and is a more potent transcriptional activator than SREBP-1c in cultured cells and liver. Here, we describe the physiologic consequences of overexpressing the nuclear form of SREBP-1a (nSREBP-1a) in adipocytes of mice using the adipocyte-specific aP2 promoter (aP2-nSREBP-1a). The transgenic aP2-nSREBP-1a mice developed markedly enlarged white and brown adipocytes that were fully differentiated. Adipocytes isolated from aP2-nSREBP-1a mice had significantly increased rates of fatty acid synthesis and enhanced fatty acid secretion. The increased production and release of fatty acids from adipocytes led, in turn, to a fatty liver. Overexpression of the alternative SREBP-1 isoform, nSREBP-1c, in adipose tissue inhibits adipocyte differentiation; as a result, the transgenic nSREBP-1c mice develop a syndrome resembling human lipodystrophy, which includes a loss of peripheral white adipose tissue, diabetes, and fatty livers (Shimomura, I., Hammer, R. E., Richardson, J. A., Ikemoto, S., Bashmakov, Y., Goldstein, J. L., and Brown, M. S. (1998) Genes Dev. 12, 3182-3194). In striking contrast, nSREBP-1a overexpression in fat resulted in the hypertrophy of fully differentiated adipocytes, no diabetes, and mild hepatic steatosis. These results suggest that nSREBP-1a and nSREBP-1c have distinct roles in adipocyte fat metabolism in vivo.

Adipocytes↗
PubMed2005

Inhibition of hypothalamic fatty acid synthase triggers rapid activation of fatty acid oxidation in skeletal muscle.

Malonyl-CoA functions as a mediator in the hypothalamic sensing of energy balance and regulates the neural physiology that governs feeding behavior and energy expenditure. The central administration of C75, a potent inhibitor of the fatty acid synthase (FAS), increases malonyl-CoA concentration in the hypothalamus and suppresses food intake while activating fatty acid oxidation in skeletal muscle. Closely correlated with the increase in muscle fatty acid oxidation is the phosphorylation/inactivation of acetyl-CoA carboxylase, which leads to reduced malonyl-CoA concentration. Lowering muscle malonyl-CoA, a potent inhibitor of carnitine/palmitoyl-CoA transferase 1 (CPT1), releases CPT1 from inhibitory constraint, facilitating the entry of fatty acids into mitochondria for beta oxidation. Also correlated with these events are C75-induced increases in the expression of skeletal muscle peroxisome proliferator-activated receptor alpha (PPARalpha), a transcriptional activator of fatty acid oxidizing enzymes, and uncoupling protein 3 (UCP3), a thermogenic mitochondrial uncoupling protein. Phentolamine, an alpha-adrenergic blocking agent, prevents the C75-induced increases of skeletal muscle UCP3 and whole body fatty acid oxidation and C75-induced decrease of skeletal muscle malonyl-CoA. Thus, the sympathetic nervous system is implicated in the transmission of the "malonyl-CoA signal" from brain to skeletal muscle. Consistent with the up-regulation of UCP3 and PPARalpha is the concomitant increase in the expression of PGC1alpha, transcriptional coactivator of the UCP3 and PPARalpha-activated genes. These findings clarify the mechanism by which the hypothalamic malonyl-CoA signal is communicated to metabolic systems in skeletal muscle that regulate fatty acid oxidation and energy expenditure.

4-Butyrolactone↗
PubMed1994

Effects of dietary fatty acids on eicosanoid-generating capacity, fatty acid composition and chemotactic activity of rainbow trout (Oncorhynchus mykiss) leucocytes.

Rainbow trout, Oncorhynchus mykiss, were maintained on isocalorific diets in which either sunflower, menhaden or Fosol oils were used as the dietary source of fatty acids. At intervals over a period of 6 months, head kidney leucocytes were isolated and used for the analysis of their fatty acid composition and eicosanoid-generating capacity. Major changes in fatty acid composition were apparent within 4 weeks on the diets, with fish fed sunflower oil diets showing a 2.1-fold increase in total n-6 fatty acids and a 2.3-fold decrease in n-3 fatty acids, compared with the original basal levels. By week 8 the fatty acid composition changes were greater in the sunflower-fed fish, but thereafter remained relatively stable to the end of the experiment at week 24. Leucocytes from the fish maintained for > 8 weeks on the sunflower oil containing diet produced significantly lower percentages of 5-series lipoxygenase products derived from eicosapentaenoic acid including 12-hydroxyeicosapentaenoic acid, leukotriene B5 and lipoxin A5 compared with those cells from fish fed either menhaden or Fosol based diets. Unlike the fatty acid composition, differences in lipoxygenase product profiles between the dietary groups increased throughout the experiment and by week 24 the arachidonic acid/eicosapentaenoic acid derived product ratios were approx. 14:1 in the sunflower oil-fed fish compared with approx. 1:1.5 in the menhaden oil-fed fish. A functional consequence of these differing ratios was seen in the ability of supernatants containing these products to cause the in vitro locomotion of trout neutrophils. Supernatants from sunflower oil-fed fish were less chemo-attractive than supernatants from menhaden or Fosol oil-fed fish.

Animals↗
PubMed1995

Comparison of the effects on the diurnal blood pressure, glucose, and lipid levels of a diet rich in monounsaturated fatty acids with a diet rich in polyunsaturated fatty acids in type 2 diabetic subjects.

The influence on blood pressure, glucose metabolism, and lipid levels of an exchange of polyunsaturated fatty acids with monounsaturated fatty acids in the diet was compared in 16 Type 2 diabetic outpatients. In a cross-over study design the patients were randomly assigned to 3 weeks treatments with a diet containing 30% energy as monounsaturated fatty acids, or an isoenergetic diet with 30% energy as polyunsaturated fatty acids. The contents of total fat, saturated fatty acids, cholesterol, and fibre were similar in the two diets. On the last days of the two diet periods, 24-h ambulatory blood pressure was measured and the responses of glucose, hormones, and lipids to a carbohydrate rich test meal were measured. As compared with the polyunsaturated fatty acids diet, the monounsaturated fatty acids diet reduced 24-h systolic (129 +/- 11 vs 124 +/- 8 mmHg (mean +/- SD), p = 0.02) and diastolic blood pressure (76 +/- 11 vs 73 +/- 8 mmHg, p = 0.02). The two diets had similar, beneficial effects on glycaemic control, and cholesterol and lipoprotein concentrations. A diet rich in monounsaturated fatty acids has beneficial effects on the blood pressure, while similar effects on glucose and lipid levels are observed in normotensive Type 2 diabetic subjects.

Blood Glucose↗
PubMed2004

Effect of diet on the deposition of n-3 fatty acids, conjugated linoleic and C18:1trans fatty acid isomers in muscle lipids of German Holstein bulls.

This study examined the effects of feeding diets rich in either n-3 or n-6 polyunsaturated fatty acids (PUFA) on the fatty acid composition of longissimus muscle in beef bulls. Thirty-three German Holstein bulls were randomly allocated to either an indoor concentrate system or periods of pasture feeding (160 days) followed by a finishing period on a concentrate containing linseed to enhance the contents of n-3 PUFA and conjugated linoleic acids (CLA) in beef muscle. The relative proportion and concentration (mg/100 g fresh muscle) of n-3 fatty acids in the phospholipid and triglyceride fractions were significantly increased (p < or = 0.05) in muscle lipids of pasture-fed bulls. The pasture feeding affected the distribution of individual CLA isomers in the muscle lipids. The proportion of the most prominent isomer, CLA cis-9,trans-11, was decreased from 73.5 to 65.0% of total CLA in bulls fed on concentrate as compared to pasture. The second most abundant CLA isomers were CLA trans-7,cis-9 and CLA trans-11,cis-13 in bulls fed on concentrate and pasture, respectively. Diet had no effect on the concentration of C18:1 trans-11. In contrast, the concentration of the C18:1 trans-13/14, trans-15, and trans-16 isomers in the muscle lipids was up to two times higher in pasture-fed as compared to concentrate-fed bulls. Pasture feeding enhanced the concentration of n-3 fatty acids, but the diet had no effect on the concentration of CLA cis-9,trans-11.

Animals↗