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PubMed2005

Metabolism of amino acids by cultured rat Sertoli cells.

Sertoli cells support spermatogenesis both spatially and energetically; for this reason, these cells have important adaptations. The energetic metabolism of Sertoli cells was adapted to provide lactate and pyruvate to developing germ cells, because these substrates are essential for spermatocytes and spermatids. In this study, we investigated whether Sertoli cells use alanine, leucine, valine, and glycine as energetic substrates and whether the simultaneous addition of other nutrients, such as glucose and glutamine, might affect the metabolism of these amino acids. Alanine, leucine, valine, and glutamine are almost totally oxidized to CO2 by these cells. In contrast, glycine has been demonstrated to be a poor energetic substrate, being mainly incorporated into proteins, and their metabolism did not change in the presence of palmitic acid, glucose, and/or glutamine. The metabolism of the 3 other amino acids was modified by palmitic acid; besides, glucose changed alanine, leucine, and valine oxidation. Glutamine decreased the oxidation of alanine, leucine, and valine to CO2. Conversely, both alanine and leucine decreased the oxidation of glutamine. Our present findings show that Sertoli cells can adapt its energy metabolism to the oxidative substrates available to fulfill their role in spermatogenic energetic supply.

Alanine↗
PubMed1995

[Effect of free fatty acid on cholesterol nucleation in model bile].

We studied the effect of free fatty acids on cholesterol nucleation in model bile with a sensitive cholesterol crystal growth assay. Palmitic acid, oleic acid, linoleic acid and arachidonic acid were added to model biles in increasing concentrations from 0.5 to 20 umol/ml. The nucleation time of model bile with free fatty acids decreased to 30%-50% of control bile. The final crystal concentration increased with higher concentrations of palmitic acid. However, we found a decrease in the final crystal concentration with the unsaturated fatty acid-soleic acid, linoleic acid and arachidonic acid. The increase in the maximum crystal growth rate was marked in the model biles as linoleic acid was added. These findings show the effect of non-protein fraction in biles on gallstone formation and support the view that free fatty acids are pro-nucleating factors.

Bile↗
PubMed1986

Characterization of rat brain microsomal acyl-coenzyme A ligases: different enzymes for the synthesis of palmitoyl-coenzyme A and lignoceroyl-coenzyme A.

Palmitic acid solubilized with Triton WR-1339 was converted to palmitoyl-CoA by microsomal membranes but lignoceric acid solubilized with Triton WR-1339 was not an effective substrate even though the detergent dispersed the same amount of these fatty acids and was also not inhibitory to the enzyme [I. Singh, R. P. Singh, A. Bhushan, and A. K. Singh (1985) Arch. Biochem. Biophys. 236, 418-426]. This observation suggested that palmitoyl-CoA and lignoceroyl-CoA may be synthesized by two different enzymes. We have solubilized the acyl-CoA ligase activities for palmitic and lignoceric acid of rat brain microsomal membranes with Triton X-100 and resolved them into three separate peaks (fractions) by hydroxylapatite chromatography. Fraction A (palmitoyl-CoA ligase) had high specific activity for palmitic acid and Fraction C (lignoceroyl-CoA ligase) for lignoceric acid. Specific activity of palmitoyl-CoA ligase for palmitic acid was six times higher than in Fraction C and specific activity of lignoceroyl-CoA ligase for lignoceric acid was four times higher than in Fraction A. At higher concentrations of Triton X-100 (0.5%), lignoceroyl-CoA ligase loses activity whereas palmitoyl-CoA ligase does not. Lignoceroyl-CoA ligase lost 60% of activity at 0.6% Triton X-100. Palmitoyl-CoA ligase (T1/2 of 4.5 min) is more stable at 40 degrees C than lignoceroyl-CoA ligase (T1/2 of 1.5 min). The pH optimum of palmitoyl-CoA ligase was 7.7 and that of lignoceroyl-CoA ligase was 8.4. Similar to our results with intact membranes, palmitic acid solubilized with Triton WR-1339 was converted to palmitoyl-CoA by palmitoyl-CoA ligase whereas lignoceric acid when solubilized with Triton WR-1339 was not able to act as substrate for lignoceroyl-CoA ligase. Since solubilized enzyme activities for synthesis of palmitoyl-CoA and lignoceroyl-CoA from microsomal membranes can be resolved into different fractions by column chromatography and demonstrate different properties, we suggest that in microsomal membranes palmitoyl-CoA and lignoceroyl-CoA are synthesized by two different enzymes.

Acyl Coenzyme A↗
PubMed1990

The hemagglutinating glycoproteins of influenza B and C viruses are acylated with different fatty acids.

We present evidence that the hemagglutinin (HA) of influenza B virus and the glycoprotein of influenza C virus (HEF) are acylated. The fatty acid linkage is sensitive to treatment with hydroxylamine and mercaptoethanol, which points to a labile thioester-type linkage. The HA of influenza B virus contains mainly palmitic acid, whereas the HEF glycoprotein of influenza C virus is acylated with stearic acid which has not been observed before as the prevailing fatty acid in viral or cellular acyl proteins.

Acylation↗
PubMed1992

Dietary palmitic and oleic acids exert similar effects on serum cholesterol and lipoprotein profiles in normocholesterolemic men and women.

To compare the effects of dietary palmitic acid (16:0) vs oleic acid (18:1) on serum lipids, lipoproteins, and plasma eicosanoids, 33 normocholesterolemic subjects (20 males, 13 females; ages 22-41 years) were challenged with a coconut oil-rich diet for 4 weeks. Subsequently they were assigned to either a palm olein-rich or olive oil-rich diet followed by a dietary crossover during two consecutive 6-week periods. Each test oil served as the sole cooking oil and contributed 23% of dietary energy or two-thirds of the total daily fat intake. Dietary myristic acid (14:0) and lauric acid (12:0) from coconut oil significantly raised all the serum lipid and lipoprotein parameters measured. Subsequent one-to-one exchange of 7% energy between 16:0 (palm olein diet) and 18:1 (olive oil diet) resulted in identical serum total cholesterol (192, 193 mg/dl), low-density lipoprotein cholesterol (LDL-C) (130, 131 mg/dl), high-density lipoprotein cholesterol (HDL-C) (41, 42 mg/dl), and triglyceride (TG) (108, 106 mg/dl) concentrations. Effects attributed to gender included higher HDL in females and higher TG in males associated with the tendency for higher LDL and LDL/HDL ratios in men. However, both sexes were equally responsive to changes in dietary fat saturation. The results indicate that in healthy, normocholesterolemic humans, dietary 16:0 can be exchanged for 18:1 within the range of these fatty acids normally present in typical diets without affecting the serum lipoprotein cholesterol concentration or distribution. In addition, replacement of 12:0 + 14:0 by 16:0 + 18:1, but especially 16:0 or some component of palm olein, appeared to have a beneficial impact on an important index of thrombogenesis, i.e., the thromboxane/prostacyclin ratio in plasma.

Adult↗
PubMed1987

The uptake of phosphatidylcholine by brush-border membranes isolated from rabbit small intestine.

The uptake of [H3] dipalmitoyl phosphatidylcholine by isolated brush border membranes from rabbit small intestine was studied. The process was found to be stimulated by Ca2+ in a manner which was influenced by the protein -Ca2+ concentration ratio. At higher ratios the enhancement by divalent cation was diminished. Preincubation of the membranes with Ca2+ followed by their transfer to a Ca2+-free medium did not result in enhancement of uptake. The stimulation by Ca2+ could be seen only when this cation was present in the incubation medium. The uptakes of [1-14C] palmitic acid, and di-[1-14C] palmitoylglycerol were also examined and found to be comparable in extent to that of labelled phosphatidylcholine but more pronounced than that of 2-[1-14C] palmitoylglycerol. The incorporation of labelled palmitic acid, phosphatidylcholine or monoglyceride in brush border membranes prepared from jejunum and ileum was similar. The results indicate that brush border membranes are capable of incorporating a variety of exogenous lipids especially in the presence of Ca2+ and the possible consequences of such uptake on the structure and function of the membrane are discussed.

Animals↗
PubMed1988

Synthesis of phosphatidylcholines in ozone-exposed alveolar type II cells isolated from adult rat lung: is glycerolphosphate acyltransferase a rate-limiting enzyme?

Type II cells were exposed to ozone by gas diffusion through the thin Teflon bottom of culture dishes. The rate of phosphatidylcholine synthesis by type II cells, monitored by the incorporation of [Me-14C]choline, was impaired by ozone at concentrations that did not affect other cellular parameters. The enzymes choline kinase and cholinephosphate cytidylyltransferase were not susceptible to inactivation by ozone at concentrations at which the activity of glycerolphosphate acyltransferase was decreased. The enzyme activity of lactate dehydrogenase increased after ozone exposure. The specific activity of choline kinase in the cytosolic fraction of type II cells was fivefold that in whole lung. The metabolism of [Me-14C]choline was studied as a function of the choline concentration. Maximal rates of phosphatidylcholine synthesis were already attained at a concentration of 20 microM choline. Exposure of type II cells to ozone did not affect the recovery of label from [Me-14C]choline in choline phosphate and CDP choline. However, the maximal rate of phosphatidylcholine synthesis decreased after ozone exposure, which indicates that the decreased apparent activity of glycerolphosphate acyltransferase limits the supply of diacylglycerols and thereby the rate of phosphatidylcholine synthesis. If the flux through the diacylglycerol pathway was stimulated by the addition of palmitic acid, a higher maximal rate of phosphatidylcholine synthesis was observed. The uptake of [Me-14C]choline and the recovery of label in CDPcholine were not altered by the addition of different concentrations of palmitate. It is concluded that type II cells take up choline very efficiently, probably due to the high specific activity of choline kinase. At low choline concentrations the rate of phosphatidylcholine synthesis is determined by the supply of CDPcholine. At concentrations of choline in the upper physiological range, the rate of phosphatidylcholine synthesis is determined by the availability of diacylglycerols, which in turn is limited by the apparent activity of glycerolphosphate acyltransferase.

Acyltransferases↗
PubMed1996

Changes of fatty acid composition and oxidative metabolism of human neutrophils migrating into an inflammatory exudate.

The peripheral blood neutrophils and the neutrophils accumulated into a skin-window experimental exudate were compared for their ability to release superoxide anion (O2-) and for their fatty acid composition, determined by capillary gaschromatography. The basal O2- release and the phorbol myristate acetate (PMA)-induced O2- release were not significantly different in the two neutrophil populations, while in response to formyl-methionyl-leucyl-phenylalanine (fMLP) the exudate cells showed an activity that was two fold higher than that of blood cells. The most significant changes of fatty acid composition of exudate versus blood cells were the following: i) increase of C16:0 (palmitic acid) from 21.3 +/- 1.2% to 23.5 +/- 1.3% (+ 10.2%) of total fatty acids (p < 0.001),ii) increase of C18:2 (linoleic acid) from 9.3 +/- 1.7% to 11.0 +/- 2.1% (+ 18.3%) (p = 0.005), iii) decrease of C20:4 (arachidonic acid) from 12.8 +/- 1.6% to 10.6 +/- 1.2% (-17.3%) (p < 0.001), whereas C18:1 (oleic acid) did not change. The total content of saturated or unsaturated fatty acids did not change. In exudate cells, a strong negative correlation was found between palmitic acid content and O2- release in response to both fMLP and PMA (r = -0.52, p < 0.02 and r = -0.49, p < 0.05, respectively) whereas arachidonic acid correlated positively, but weakly, with O2- (r = 0.40, p = 0.07 and r = 0.47, p = 0.05, with fMLP and PMA as stimulants respectively). A positive correlation was also found between the arachidonic acid content of blood cells and the number of cells that migrated into the inflammatory exudate. These results indicate that the process of extravasation from blood into the exudate causes specific and consistent modifications of the fatty acid composition of neutrophils and suggest that these modifications have a role in the activation and the regulation of the O2- forming system.

Chemotaxis, Leukocyte↗
PubMed1980

Lipoprotein synthesis and secretion by cultured human intestinal mucosa.

We tested whether cultured human jejunal mucosa incorporates fatty acid into esterified lipids and whether organ culture can serve as a model system to study lipoprotein secretion by the human gut. Jejunal biopsies obtained from seven subjects were cultured for 24 h in medium containing 2 microCi of [3H]palmitic acid. More than 95% of the radioactivity incorporated by the tissue was found to be associated with esterified lipids: triglycerides, cholesterol esters and phospholipids, 7 . 8 +/- 1 . 2, 0 . 5 +/- 0 . 1 and 14 . 0 +/- 1 . 5 nmol/10 mg weight respectively. During the culture labelled triglycerides, phospholipids and cholesterol esters were secreted to the medium. Most of the newly synthesized esterified lipids in the medium were found in the d < 1 . 019 g/ml and d = 1 . 019--1 . 063 g/ml fractions. The majority of the newly synthesized triglycerides were found in the d < 1 . 019 g/ml fraction. Labelled cholesterol esters were enriched in the d = 1 . 063--1 . 21 g/ml fraction. Boiled biopsies adsorbed negligible amounts of radioactive palmitic acid and did not synthesize esterified lipids. The addition of puromycin to the culture medium and preincubation with colchicine resulted in decreased uptake of the labelled fatty acid and decreased secretion of esterified lipids to the medium. These experiments indicate that cultured human intestinal mucosa is a suitable model to study lipid synthesis and lipoprotein secretion by the human intestine.

Adolescent↗
PubMed1993

Modulation by fatty acids of Ca2+ fluxes in sarcoplasmic-reticulum vesicles.

The fatty acids palmitic (C16:0), stearic (C18:0), arachidic (C20:0) and arachidonic (C20:4) acids inhibit Ca2+ uptake and enhance Ca2+ efflux measured in vesicles derived from the sarcoplasmic reticulum of skeletal muscle. These effects of the fatty acids are impaired by the Ca(2+)-ATPase ligands Mg2+, Ca2+ and K+, and by drugs that block the leakage of Ca2+ through the Ca(2+)-ATPase such as Ruthenium Red, spermine [de Meis (1991) J. Biol. Chem. 266, 5736-5742] and thapsigargin [de Meis and Inesi (1992) FEBS Lett. 299, 33-35].

Adenosine Triphosphate↗
PubMed2000

Effect of triiodothyronine on the content of phospholipids in the rat liver nuclei.

The aim of the present study was to examine the effect of triiodothyronine (T3) on the content of phospholipids and on the incorporation of blood-borne palmitic acid into the phospholipid moieties in the nuclei of the rat liver. T3 was administered daily for 7 days, 10 microg x 100 g(-1). The control rats were treated with saline. Each rat received 14C-palmitic acid, intravenously suspended in serum. 30 min after administration of the label, samples of the liver were taken. The nuclei were isolated in sucrose gradient. Phospholipids were extracted from the nuclei fraction and from the liver homogenate. They were separated into the following fractions: sphingomyelin, phosphatidylcholine, phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine and cardiolipin. The content and radioactivity of each fraction was measured. It was found that treatment with T3 reduced the content of phosphatidylinositol and increased the content of cardiolipin in the nuclear fraction. In the liver homogenate, the content of phosphatidylinositol decreased and the content of phosphatidylethanolamine and cardiolipin increased after treatment with T3. The total content of phospholipids after treatment with T3 remained unchanged, both in the nuclear fraction and in the liver homogenate. T3 reduced the specific activity of phosphatidylcholine, phosphatidylserine, phosphatidylethanolamine and cardiolipin and had no effect on the specific activity of sphingomyelin and phosphatidylinositol both in the fraction of the nuclei and the liver homogenate. It is concluded that excess of triiodothyronine affects the content of phospholipids in the nuclei. The changes in the content of phospholipids in the nuclei largely reflect changes in their content in the liver.

Animals↗
PubMed1998

On the performance of a hollow-fiber bioreactor for acidolysis catalyzed by immobilized lipase

The present communication describes the chemical modification of anhydrous butterfat by interesterification with oleic acid catalyzed by a lipase of Mucor javanicus. Two reactor configurations were tested, a batch-stirred tank reactor containing suspended lipase and a batch-stirred tank reactor in combination with a hollow-fiber membrane module containing adsorbed lipase. The goal of this research was to assess the advantage of using a (hydrophobic) porous support to immobilize the lipase in attempts to engineer butterfat with increased levels of unsaturated fatty acid residues (oleic acid) at the expense of medium-to-long chain saturated fatty acids (myristic and palmitic acids). Reactions were carried out at 40 degrees C in the absence of solvent under controlled water activity, and were monitored by chromatographic assays for free fatty acids. The results obtained indicate that the rate of interesterification using the proposed reactor configuration is enhanced by a factor above 100 relative to that using suspended lipase, for the same protein mass basis. Although hydrolysis of butterfat occurred to some degree, the enzymatic process that uses the hollow-fiber reactor was technically superior to the stirred tank system. Copyright 1998 John Wiley & Sons, Inc.

Journal Article↗
PubMed2003

Triacylglycerol and phospholipid fatty acids of the silverleaf whitefly: composition and biosynthesis.

The identification and composition of the fatty acids of the major lipid classes (triacylglycerols and phospholipids) within Bemisia argentifolii Bellows and Perring (Homoptera: Aleyrodidae) nymphs were determined. Comparisons were made to fatty acids from the internal lipids of B. argentifolii adults. The fatty acids, as ester derivatives, were analyzed by capillary gas chromatography (CGC) and CGC-mass spectrometry (MS). All lipid classes contained variable distributions of eight fatty acids: the saturated fatty acids, myristic acid (14:0), palmitic acid (16:0), stearic acid (18:0), arachidic acid (20:0); the monounsaturated fatty acids, palmitoleic acid (16:1), oleic acid (18:1); the polyunsaturated fatty acids, linoleic acid (18:2), linolenic acid (18:3). Fourth instar nymphs had 5-10 times the quantities of fatty acids as compared to third instar nymphs and 1-3 times the quantities from adults. The fatty acid quantity differences between fourth and third instar nymphs were related to their size and weight differences. The percentage compositions for fatty acids from each lipid class were the same for the pooled groups of third and fourth instar nymphs. For nymphs and adults, triacylglycerols were the major source of fatty acids, with 18:1 and 16:0 acids as major components and the majority of the polyunsaturated fatty acids, 18:2 and 18:3 were present in the two phospholipid fractions, phosphatidylethanolamine and phosphatidylcholine. Evidence was obtained that whiteflies indeed synthesize linoleic acid and linolenic acid de novo: radiolabel from [2-(14)C] acetate was incorporated into 18:2 and 18:3 fatty acids of B. argentifolii adults and CGC-MS of pyrrolidide derivatives established double bonds in the Delta(9,12) and Delta(9,12,15) positions, respectively.

Animals↗
PubMed2005

Role of adiponectin in the protective action of dietary saturated fat against alcoholic fatty liver in mice.

The protective effect of dietary saturated fatty acids against the development of alcoholic liver disease has long been known, but the underlying mechanism is not completely understood. We examined the involvement of the adipocyte hormone adiponectin. Circulating adiponectin levels were significantly elevated by chronic ethanol administration to mice consuming a diet high in saturated fat. The increase in circulating adiponectin was associated with the activation a set of hepatic signaling pathways mediated through AMP-activated protein kinase, PPAR-alpha, and PPAR-gamma coactivator alpha, which in turn led to markedly increased rates of fatty acid oxidation, prevention of hepatic steatosis, and alleviation of liver enzyme changes. Furthermore, treatment of rat 3T3-L1 adipocytes with saturated fatty acids (palmitic or stearic acids) in the presence of ethanol increased secretion of adiponectin and enhanced activity of a mouse adiponectin promoter. In conclusion, the protective action of saturated fat against the development of alcoholic fatty liver in mice is partially mediated through induction of adiponectin. The present findings suggest a novel paradigm for dietary fatty acids in the pathogenesis of alcoholic liver disease and provide a promising therapeutic strategy-nutritional modulation of adiponectin-in treating human alcoholic fatty liver disease.

3-Hydroxybutyric Acid↗
PubMed1990

Lipoxin A4 and lipoxin B4 stimulate the release but not the oxygenation of arachidonic acid in human neutrophils: dissociation between lipid remodeling and adhesion.

The profiles of actions of lipoxin A4 (LXA4) and lipoxin B4 (LXB4), two lipoxygenase-derived eicosanoids, were examined with human neutrophils. At nanomolar concentrations, LXA4 and LXB4 each stimulated the release of [1-14C]arachidonic acid from esterified sources in neutrophils. Lipoxin-induced release of [1-14C]arachidonic acid was both dose- and time-dependent and was comparable to that induced by the chemotactic peptide f-met-leu-phe. Time-course studies revealed that lipoxin A4 and lipoxin B4 each induced a biphasic release of [1-14C]arachidonic acid, which was evident within seconds (5-15 sec) in its initial phase and minutes (greater than 30 sec) in the second phase. In contrast, the all-trans isomers of LXA4 and LXB4 did not provoke [1-14C]AA release. Lipoxin-induced release of arachidonic acid was inhibited by prior treatment of the cells with pertussis toxin but not by its beta-oligomers, suggesting the involvement of guaninine nucleotide-binding regulatory proteins in this event. Dual radiolabeling of neutrophil phospholipid classes with [1-14C]arachidonic acid and [3H]palmitic acid showed that phosphatidylcholine was a major source of lipoxin-induced release of [1-14C]arachidonic acid. They also demonstrated that lipoxins rapidly stimulate both formation of phosphatidic acid as well as phospholipid remodeling. Although both LXA4 and LXB4 (10(-8)-10(-6) M) stimulated the release of [1-14C]arachidonic acid, neither compound evoked its oxygenation by either the 5- or 15-lipoxygenase pathways (including the formation of LTB4, 20-COOH-LTB4, 5-HETE, or 15-HETE). LXA4 and LXB4 (10(-7) M) each stimulated the elevation of cytosolic Ca2+ as monitored with Fura 2-loaded cells, albeit to a lesser extent than equimolar concentrations of FMLP. Neither lipoxin altered the binding of [3H]LTB4 to its receptor on neutrophils. In addition, they did not stimulate aggregation or induce adhesion of neutrophils to human endothelial cells. Results indicate that both LXA4 and LXB4 stimulate the rapid remodeling of neutrophil phospholipids to release arachidonic acid without provoking either aggregation or the formation of lipoxygenase-derived products within a similar temporal and dose range. Together they indicate that LXA4 and LXB4 display selective actions with human neutrophils and suggest that these eicosanoids possess unique profiles of action which may regulate neutrophil function during inflammation.

Arachidonic Acids↗
PubMed1994

Analysis of lung surfactant in the metamorphosing bullfrog (Rana catesbeiana).

In bullfrog (Rana catesbeiana) tadpoles, the lung begins to function at an advanced stage of metamorphosis. As a preliminary step for investigation of the mechanisms involved in lung maturation, pulmonary surfactant was prepared from tadpoles at advanced stages of metamorphosis and its biochemical properties were analyzed. Surfactant phospholipid analysis revealed that the major constituent was phosphatidylcholine (PC), as examined in the animals at late climax (stage 24). Other detectable phospholipids were phosphatidylethanolamine, phosphatidylserine, sphingomyelin, and phosphatidylglycerol, a marker lipid in mammalian surfactant. As in mammals, PC in the surfactant was rich in saturated fatty acids, about 50% of fatty acid moieties being palmitic acid. The content of surfactant PC in the lung increased moderately around mid-climax and markedly at the end of climax. The effect of antiserum against bullfrog prolactin (PRL) on the pulmonary surfactant was studied in climactic tadpoles. The content of surfactant PC in the lung of the antiserum-treated larvae was lower than that in the lung of the normal rabbit serum-injected larvae, whereas the content of PC in the whole lung did not differ between the antiserum-treated and control groups. The results suggest that synthesis of surfactant in the amphibian lung is enhanced as metamorphosis progresses and that PRL is involved in lung maturation.

Animals↗
PubMed1994

[The effect of zinc deficiency on heart and brain lipids in rats force-fed with coconut oil or fish oil diets].

The present study investigated the effect of zinc deficiency on lipid concentrations and fatty acid composition of heart and brain in force-fed rats receiving either a diet with coconut oil and safflower oil (86:14, w/w) or a diet with fish oil and safflower oil (91:9, w/w). Four groups of growing male Sprague-Dawley rats were fed 11.6 g of a semisynthetic diet containing either 0.8 mg Zn/kg or 111 mg Zn/kg with either coconut oil and safflower oil or fish oil and safflower oil per day by gastric tube for 10 days. Concentrations of lipids in heart as well as fatty acid composition of heart phospholipids and brain total lipids were determined. Zinc deficient rats fed the coconut oil diet had higher concentrations of triglycerides (16.3 mg/g vs. 9.21 mg/g) and total fatty acids (29.3 mg/g vs. 21.8 mg/g) in heart than control rats fed coconut oil diet, whereas concentrations of phospholipids and total cholesterol were not different between zinc deficient and control rats. Concentrations of lauric acid (12:0), myristic acid (14:0), palmitic acid (16:0), palmitoleic acid (16:1), and oleic acid (18:1) were by 65 to 192% higher in hearts of zinc deficient rats fed coconut oil diet than in control rats fed coconut oil diet. In contrast, concentrations of triglycerides, phospholipids, total cholesterol, and total fatty acids in heart were similar in zinc deficient rats and control rats fed fish oil diet. The fatty acid composition of heart phospholipids was only slightly influenced by zinc deficiency in the rats fed both types of dietary fat. The level of arachidonic acid in phospholipids which may represent desaturation activity was not different in the zinc deficient rats and control rats fed coconut oil diet, and was only slightly reduced in zinc deficient rats fed fish oil diet compared to control rats fed fish oil diet. This finding suggests that zinc deficiency does not impair delta-5 and delta-6 desaturation of linoleic acid in heart. Concentrations of fatty acids in brain as well as fatty acid composition of brain total lipids was only slightly influenced by zinc deficiency. This suggests that short-term zinc deficiency does not affect fatty acid metabolism of brain.

Alkaline Phosphatase↗
PubMed1989

[Distribution and elimination of medium- and long-chain fatty acids of a fat emulsion in lipoproteins of severely injured patients following bolus injection].

A fat emulsion containing 20% fat as medium chain triglycerides (MCT) and long chain triglycerides (LCT) (1:1) was injected as a bolus in an amount of 0.2g fat per kg body weight to six patients, three to five days after a serious injury. Triglyceride concentrations increased within two min in lipoprotein fractions d less than 0.95 g/ml (Chylomicrons), d less than 1.006 g/ml (VLDL), d less than 1.063 g/ml (LDL) and d less than 1.21 g/ml (HDL). Sixty minutes after injection triglyceride concentrations had again reached preexperimental values in all lipoprotein fractions. Cholesterol values did not change. According to the composition of the fat emulsion, linoleic acid content increased in triglycerides of all lipoprotein fractions, whereas octanoic and decanoic acid did so only in triglyceride-rich lipoproteins (d less than 1.006). Half-life values of elimination of octanoic acid (3.3 min) and decanoic acid (3.9 min) in triglycerides of lipoprotein fraction d less than 1.006 were nearly half as short as that of long chain fatty acids (linoleic acid, 6.4 min; oleic acid, 6.5 min; palmitic acid, 7.5 min). Thus in contrast to LCT, MCT are only found in triglyceride-rich lipoproteins (d less than 1.006) and are also eliminated more rapidly.

Fat Emulsions, Intravenous↗