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PubMed1975

Cell membrane-binding properties of group A streptococcal lipoteichoic acid.

Lipoteichoic acid (LTA) was extracted from group A streptococci, previously treated with hot HCl, by the phenol method. The extracted LTA was loaded on an isoelectric (IE) focusing column and two fractions were collected; one at pH 4.65 and the other at pH 2.95. Chemical analysis demonstrated that the unfractionated LTA contained alanine and glycerolphosphate at molar ratio of 1:10, and ester-linked lipids, but no detectable sugars or amino-sugars. The two IE fractions contained lipids but lacked alanine. The LTA and its IE fractions spontaneously adsorbed to human erythrocytes (sensitization) causing them to agglutinate in the presence of rabbit anti-LTA. The RBC-sensitizing and antigenic activities of IE fractions were equal to, or greater (for IE fraction at pH 4.65) than the unfractionated LTA, indicating that alanine is not involved in the sensitizing activity of LTA. Mild ammonia-hydrolysis abolished the RBC-sensitizing activity of LTA and its IE fractions. Chloroform-methanol-soluble material of the ammonia-hydrolysate lacked antigenic activity but blocked sensitization of erythrocytes by LTA. The water-soluble material of the hydrolyzed LTA retained antigenic activity, was not able to block sensitization by LTA, and its sensitizing activity was restored after esterification with fatty acids. These experiments indicate that ester-linked fatty acids (palmitic acid being the major one) are involved in the spontaneous adsorption of LTA to erythrocytes. The LTA, its lipid moiety, and anti-LTA blocked adherence of group A streptococci to human epithelial cells, suggesting that small amounts of LTA may reside on the streptococcal surface to mediate attachment and colonization of these organisms on mucosal surfaces in vivo.

Ammonia↗
PubMed2000

Correlation between DNA or protein adducts and benzo[a]pyrene diol epoxide I-triglyceride adduct detected in vitro and in vivo.

In this study, we demonstrated the in vitro and in vivo formation of carcinogen-lipid adduct and its correlation with DNA or protein adducts. The lipids from serum or hepatocyte membranes of Sprague-Dawley rats, human serum and standard major lipids were in vitro reacted with benzo[a]pyrene (B[a]P) and B[a]P metabolites. 7, 8-Dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene(BPDE-I), an ultimate carcinogenic form of B[a]P, was covalently bound to triglyceride (TG). BPDE-I-TG adducts isolated by thin-layer chromatography (TLC) were further detected by high-performance liquid chromatography. TGs, including triolein, tripalmitin and tristearin, showed positive reactions with BPDE-I. However, cholesterol, phospholipids (phosphatidylcholine, phosphatidyl-ethanolamine, phosphatidyl-inositol and sphingomyelin) and non-esterified fatty acids (palmitic acid, oleic acid, linoleic acid and stearic acid) did not react with BPDE-I. In addition, other B[a]P metabolites (B[a]P-phenols and -diols) did not react with TG. TG appeared to be the most reactive lipid yet studied with respect to its ability to form an adduct with BPDE-I. There was a clear-cut dose-related formation of [1,3-(3)H]BPDE-I-lipid adducts in vitro between TG and [1,3-(3)H]BPDE-I. In an animal study, BPDE-I-TG was also formed in the serum of rats orally treated with B[a]P (25 mg/rat). Also, obvious correlations between [(3)H]B[a]P related-biomolecule adducts (DNA or protein) or lipid damage and the BPDE-I-TG adducts were obtained in various tissues of mice i.p. treated with [(3)H]B[a]P. These data suggest that TG can form an adduct with BPDE-I, as do other macromolecules (DNA, RNA and protein). Therefore, a carcinogen-lipid adduct would be a useful biomarker for chemical carcinogenesis research and cancer risk assessment.

Adult↗
PubMed2004

Dietary fatty acids regulate acyl-CoA:cholesterol acyltransferase and cytosolic cholesteryl ester hydrolase in hamsters.

To investigate the effects of dietary fatty acids on acyl-CoA:cholesterol acyltransferase (ACAT) and cytosolic cholesteryl ester hydrolase (cCEH), male Syrian hamsters (F(1)B hybrid) were fed a modified version of the NIH-07 open formula, cereal-based rodent diet enriched with one of the following 4 dietary fatty acids: palmitic acid (16:0), trans fatty acids (18:1t), oleic acid (18:1c), or linoleic acid (18:2). Hamsters fed 16:0 and 18:1t had significantly higher plasma non-HDL cholesterol concentrations compared with those fed 18:1c and 18:2. However, differences in plasma apolipoprotein (apo)B(100) concentration, hepatic cCEH mRNA abundance, and hepatic ACAT activity between 16:0- and 18:1t-fed hamsters suggest that the hypercholesterolemic effects are achieved by different mechanisms. Specifically, an increase in ACAT activity by 16:0 may induce enrichment of cholesteryl esters in apoB(100)-containing particles, whereas 18:1t may increase the number of the particles. Hepatic cholesteryl esters accumulated in the 18:1c- and 18:2-fed groups with no differences in hepatic ACAT activity and cCEH mRNA abundance among hamsters fed unsaturated fatty acids (i.e., 18:1t, 18:1c, and 18:2). Considering the lack of change in free cholesterol concentration and increased cholesteryl esters in the liver, the hypocholesterolemic effect of 18:1c and 18:2 compared with 18:1t may be attributed to decreased production of apoB(100)-containing particles. ACAT-1 was expressed in all the tissues examined; in contrast, ACAT-2 was highly expressed in the liver and small intestine. Hepatic ACAT activity was disproportionate to the levels of ACAT-1 and ACAT-2 mRNA and protein, indicating post-transcriptional regulation of ACAT by dietary fatty acids. The data suggest that cholesterolemic effects of individual dietary fatty acids can be achieved through their independent modulation of pathways regulating assembly and secretion of apoB(100)-containing particles.

Animals↗
PubMed1995

Serum fatty acids and the risk of coronary heart disease.

To examine the relation between serum fatty acids and coronary heart disease (CHD), the authors conducted a nested case-control study of 94 men with incident CHD and 94 men without incident CHD who were enrolled in the Usual Care group of the Multiple Risk Factor Intervention Trial between December 1973 and February 1976. After confirming the stability of the stored serum samples, the authors measured serum fatty acid levels by gas-liquid chromatography and examined their association with CHD. In all multivariate models, levels of the cholesterol ester saturated fatty acid palmitic acid (16:0) were directly associated with CHD risk (standardized odds ratio = 1.68; 95% confidence interval 1.10-2.55 in the model that adjusted for total plasma cholesterol level). Levels of the phospholipid omega-3 fatty acid docosapentaenoic acid (22:5) were inversely associated with CHD risk in the two multivariate models that controlled for the effects of total plasma cholesterol level or high density lipoprotein cholesterol to total plasma cholesterol ratio (standardized odds ratio = 0.58; 95% confidence interval 0.38-0.89 in the first model that controlled for total plasma cholesterol level). In contrast to the first two multivariate models, levels of the docosahexaenoic acid (22:6) were inversely associated with CHD risk in a third multivariate model that controlled for the effects of high density lipoprotein cholesterol to low density lipoprotein cholesterol ratio (standardized odds ratio = 0.57; 95% confidence interval 0.36-0.90). These findings are consistent with other evidence indicating that saturated fatty acids are directly correlated with CHD and that omega-3 polyunsaturated fatty acids are inversely correlated with CHD. Because these associations were present after adjustment for blood lipid levels, other mechanisms, such as a direct effect on blood clotting, may be involved.

Adult↗
PubMed1982

Effect of unsaturated fatty acids and Ca2+ on phosphatidylinositol synthesis and breakdown.

CDP-diglyceride : inositol transferase was inhibited by unsaturated fatty acids. The inhibitory activity decreased in the following order: arachidonic acid greater than linolenic acid greater than linoleic acid greater than oleic acid greater than or equal to palmitoleic acid. Saturated fatty acids such as myristic acid, palmitic acid, and stearic acid had no effect. Calcium ion also inhibited the activity of CDP-diglyceride : inositol transferase. In rat hepatocytes, arachidonic acid inhibited 32P incorporation into phosphatidylinositol and phosphatidic acid without any significant effect on 32P incorporation into phosphatidylcholine, phosphatidylethanolamine and phosphatidylserine. Ca2+ ionophore A23187 also inhibited 32P incorporation into phosphatidylinositol. However, 32P incorporation into phosphatidic acid was stimulated with Ca2+ ionophore A23187. Phosphatidylinositol-specific phospholipase C was activated by unsaturated fatty acids. Polyunsaturated fatty acids such as arachidonic acid and linolenic acid had a stronger effect than di- and monounsaturated fatty acids. Saturated fatty acids had no effect on the phospholipase C activity. The phospholipase C required Ca2+ for activity. Arachidonic acid and Ca2+ had synergistic effects. These results suggest the reciprocal regulation of phosphatidylinositol synthesis and breakdown by unsaturated fatty acids and Ca2+.

Animals↗
PubMed2003

Fatty acids and glucose increase neutral endopeptidase activity in human microvascular endothelial cells.

Neutral endopeptidase (NEP), a membrane-bound metallopeptidase enzyme that degrades neuropeptides, bradykinin, atrial natriuretic factor, enkephalins, and endothelin may regulate response to injury. We have previously demonstrated increased NEP localization and enzyme activity in diabetic wounds and skin compared with normal controls. We hypothesized that hyperlipidemia and hyperglycemia associated with type 2 diabetes mellitus may induce excessive NEP activity and thereby diminish normal response to injury. Human microvascular endothelial cells were treated with five different fatty acids (40 microM) with varying degrees of saturation, including oleic acid, linoleic acid, palmitic acid, stearic acid, and linolenic acid and/or glucose (40 mM) for 48 h. The effect of the antioxidative agents vitamin E and C on NEP enzyme activation was determined by treating the cultured cells with alpha-tocopherol succinate and/or L-ascorbic acid. Cell membrane preparations were assayed for NEP activity by incubation with glutaryl-Ala-Ala-Phe-4-methoxy-beta naphthylamide to generate a fluorescent degradation product methoxy 2 naphthylamine. High glucose or fatty acid concentration upregulated NEP activity. The highest NEP activity was observed with combined elevated glucose, linoleic acid, and oleic acid (P < 0.05). Antioxidant vitamin E and C treatment significantly reduced NEP enzyme activity after fatty acid exposure (P < 0.05). Thus, hyperglycemia and hyperlipidemia associated with type 2 diabetes mellitus may increase endothelial cell NEP activity and thereby decrease early pro-inflammatory responses. The modulator effect of vitamin E and C on NEP membrane enzyme activity after exposure to fatty acid stimulation suggests that lipid oxidation may activate NEP.

Antioxidants↗
PubMed2003

Aeromicrobium marinum sp. nov., an abundant pelagic bacterium isolated from the German Wadden Sea.

An obligately salt-dependent Gram-positive bacterium, designated strain T2(T), was isolated from surface waters of the German Wadden Sea. The organism exhibited optimum growth at salt concentrations similar to that of sea water. On the basis of phenotypic, chemotaxonomic and phylogenetic differences, it is concluded that strain T2(T) (=DSM 15272(T)=LMG 21768(T)) is the first marine species of the genus Aeromicrobium to be identified, for which the name Aeromicrobium marinum is proposed. It is also the first described marine bacterium within the family Nocardioidaceae. Strain T2(T) is a rod-shaped, aerobic, heterotrophic bacterium containing LL-diaminopimelic acid in the peptidoglycan and MK-9(H(4)) as the major menaquinone. The bacterium is characterized by high proportions of the fatty acids palmitic acid, oleic acid, tuberculostearic acid and hydroxypalmitic acid. DNA-DNA hybridization analysis showed the marine bacterium to display 29.1 % relatedness with Aeromicrobium fastidiosum DSM 10552(T) and 44.4 % relatedness with Aeromicrobium erythreum DSM 8599(T). A. marinum was demonstrated to be an abundant member of the pelagic bacterial community in the German Wadden Sea since it represented about 1 % of the total bacterial population as revealed by dot-blot hybridization and most-probable-number counts.

DNA, Bacterial↗
PubMed1969

Environmentally-induced changes in the Fatty acids of chlorella.

Qualitative and quantitative analyses were made of the major fatty acids of Chlorella fusca, Shihira and Krauss, in both autotrophic and heterotrophic culture. Cells grown heterotrophically were subjected to CO(2) concentrations as great as 40%-in-air.The major fatty acids of autotrophic cells grown under a 1% environmental concentration of CO(2), in order of concentration were 16:0, 18:3, 16:4, 18:2, 18:1, and 16:3. The analysis of heterotrophic cells at 1% CO(2), by comparison, indicated a complete absence of 16:4, reduced amounts of 18:3, and increased amounts of the other major acids.An increase in the environmental concentration of CO(2) (from 1%-30%) over the heterotrophic cultures produced a 40% increase in total lipids and nearly a 50% increase in fatty acids. Palmitic acid (16:0) and 18:1 largely account for the fatty acid change by increasing from 12 mg to 33 mg/g dry wt and 8 mg to 17 mg/g dry wt respectively. Possible explanations for this enhanced synthesis of fatty acids are suggested.

Journal Article↗
PubMed2005

Unsaturated fatty acids induce calcium influx into keratinocytes and cause abnormal differentiation of epidermis.

Abnormal follicular keratinization is involved in comedogenesis in acne vulgaris. We recently demonstrated that calcium influx into epidermal keratinocytes is associated with impaired skin barrier function and epidermal proliferation. Based on these results, we hypothesized that sebum components affect calcium dynamics in the keratinocyte and consequently induce abnormal keratinization. To test this idea, we first observed the effects of topical application of sebum components, triglycerides (triolein), saturated fatty acids (palmitic acid and stearic acid), and unsaturated fatty acids (oleic acid and palmitoleic acid) on hairless mouse skin. Neither triglyceride nor saturated fatty acids affected the skin surface morphology or epidermal proliferation. On the other hand, application of unsaturated fatty acids, oleic acid, and palmitoleic acid induced scaly skin, abnormal keratinization, and epidermal hyperplasia. Application of triglycerides and saturated fatty acids on cultured human keratinocytes did not affect the intracellular calcium concentration ([Ca(2+)](i)), whereas unsaturated fatty acids increased the [Ca(2+)](i) of the keratinocytes. Moreover, application of oleic acid on hairless mouse skin induced an abnormal calcium distribution in the epidermis. These results suggest that unsaturated fatty acids in sebum alter the calcium dynamics in epidermal keratinocytes and induce abnormal follicular keratinization.

Acne Vulgaris↗
PubMed2006

The in situ physiology of Skermania piniformis in foams in Australian activated sludge plants.

The in situ physiology of the filamentous bacterium Skermania piniformis frequently seen in activated sludge foams in Australia was investigated. An oligonucleotide probe, Spin1449, targeting the 16S rRNA of S. piniformis was designed for its identification by fluorescence in situ hybridization (FISH), validated with pure cultures and applied successfully to foam samples from two geographically distant Australian plants. While filaments of this bacterium appeared to be comparatively hydrophobic, the organism had no clear preference for hydrophobic or hydrophilic substrates. In both foams examined using microautoradiography (MAR), filaments selectively took up substrates under aerobic and anoxic (NO(3) (-)) but not anaerobic or anoxic (NO(2) (-)) conditions. Skermania piniformis assimilated oleic acid, palmitic acid, glycerol and glycine. Ectoenzyme activities detected suggest that S. piniformis has an ability to assimilate a greater range of substrates than might be concluded from the MAR data obtained here. Based on the substrate uptake data presented here, an anaerobic selector may work for controlling S. piniformis in activated sludge systems.

Actinobacteria↗
PubMed1988

Regulation of gamma-aminobutyric acid/barbiturate receptor-gated chloride ion flux in brain vesicles by phospholipase A2: possible role of oxygen radicals.

Preincubation of brain membranes with phospholipase A2 (PLA2) has been shown previously to affect the binding characteristics of various recognition sites associated with the gamma-aminobutyric acid (GABA) receptor complex. In the present study, we have investigated the effects of PLA2 (from Naja naja siamensis venom) on the functional activity of the GABA receptor/chloride ion channel. PLA2 (0.001-0.02 U/mg protein) preincubation decreased pentobarbital-induced 36Cl- efflux and muscimol-induced 36Cl- uptake in rat cerebral cortical synaptoneurosomes. The effect of PLA2 was prevented by EGTA and two nonselective PLA2 inhibitors, mepacrine and bromophenacyl bromide. The removal of free fatty acids by addition of bovine serum albumin both prevented and reversed the effect of PLA2. Products of the catalytic activity of PLA2, such as the unsaturated free fatty acids, arachidonic and oleic acids, mimicked the effect of PLA2. However, the saturated fatty acid, palmitic acid, and lysophosphatidyl choline had no effect on pentobarbital-induced 36Cl- efflux. Because unsaturated free fatty acids are highly susceptible to peroxidation by oxygen radicals, the role of oxygen radicals was investigated. Xanthine plus xanthine oxidase, a superoxide radical generating system, mimicked the effect of PLA2, whereas the superoxide radical scavenger, superoxide dismutase, diminished the effects of PLA2 and arachidonic acid on pentobarbital-induced 36Cl- efflux. Similarly, the effect of PLA2 was also inhibited by methanol (1 mM), a scavenger of the hydroxyl radical, and by catalase. These data indicate that exogenously added PLA2 induces alterations in membrane phospholipids, possibly promoting the generation of oxygen radicals and fatty acid peroxides which can ultimately modulate GABA/barbiturate receptor function in brain.

Acetophenones↗
PubMed1993

Arachidonic acid and other unsaturated fatty acids alter membrane potential in PC12 and bovine adrenal chromaffin cells.

The action of arachidonic acid and other fatty acids on membrane potential in PC12 and bovine chromaffin cells was investigated using a membrane potential-sensitive fluorescent dye. Arachidonic acid (1-40 microM) provoked dose-dependent membrane hyperpolarization, thereby reducing hyperpolarization induced by the K(+)-selective ionophore valinomycin. Other cis-unsaturated fatty acids, but not lipoxygenase products or the saturated fatty acid palmitic acid, also affected membrane potential. Tetraethylammonium blocked the arachidonic acid-induced hyperpolarization. These data suggest that cis-unsaturated fatty acids alter membrane potential in PC12 and bovine chromaffin cells by modulating K+ conductances. Valinomycin-generated hyperpolarization had no effect on agonist-induced Ca2+ influx into bovine chromaffin cells, whereas preincubation with arachidonic acid and other cis-unsaturated fatty acids blocked Ca2+ influx and secretion. We propose a model where internally generated fatty acids act as a feedback to desensitize the stimulated cell via inhibition of receptor-dependent Ca2+ influx and induction of membrane hyperpolarization.

Animals↗
PubMed1979

Purification and characterization of smooth and rough lipopolysaccharides from Brucella abortus.

In an attempt to obtain pure and well characterized smooth lipopolysaccharide (S-LPS) and rough lipopolysaccharide (R-LPS), smooth and rough strains of Brucella abortus were extracted by two different modifications of the phenol-water method. S-LPS was obtained in the phenol phase, and R-LPS was obtained in the aqueous phase. Further purification was accomplished by treatment with enzymes, detergents, NaI as a chaotropic agent to separate non-covalently bound contaminants, and by gel filtration. The degree of purity of the molecules was determined by chemical and immunological analysis and by electrophoresis in sodium dodecyl sulfate-polyacrylamide gels. Lipid identification by gas-liquid chromatography showed seven major fatty acids. Palmitic acid accounts for about 50%, stearic acid accounts for about 10%, and hydroxylated fatty acids account for less than 5% of total fatty acids. 2-Keto-3-deoxyoctonate but not heptose was detected in the sugar analysis. Protein was found to be firmly bound to S-LPS but not to R-LPS.

Antigens, Bacterial↗
PubMed1990

Unusual fatty acid substitution in lipids and lipopolysaccharides of Helicobacter pylori.

Cellular fatty acids, phospholipid fatty acids, and lipopolysaccharide fatty acids of four strains of Helicobacter pylori were analyzed by gas-liquid chromatography. The presence of myristic acid, palmitic acid, stearic acid, oleic acid, linoleic acid, 19-carbon cyclopropane fatty acid, beta-hydroxypalmitic acid, and beta-hydroxystearic acid was confirmed. In phospholipids, myristic acid and 19-carbon cyclopropane fatty acid were the major fatty acids. Hydroxy fatty acids and unsaturated fatty acids were not detected or occurred only in small amounts. The major fatty acids of lipopolysaccharides were stearic acid, beta-hydroxypalmitic acid, and beta-hydroxystearic acid. Unsaturated fatty acids and 19-carbon cyclopropane fatty acid were not found. The unusual compositions of H. pylori phospholipid and lipopolysaccharide fatty acids may have important implications for the taxonomy, physicochemical membrane properties, and biological activity of lipopolysaccharides.

Campylobacter↗
PubMed1991

Iso- and anteiso-fatty acids in bacteria: biosynthesis, function, and taxonomic significance.

Branched-chain fatty acids of the iso and anteiso series occur in many bacteria as the major acyl constituents of membrane lipids. In addition, omega-cyclohexyl and omega-cycloheptyl fatty acids are present in several bacterial species. These two types of fatty acids are synthesized by the repeated condensation of malonyl coenzyme A with one of the branched-chain and cyclic primers by the same enzyme system. The pathway of de novo branched-chain fatty acid synthesis differs only in initial steps of synthesis from that of the common straight-chain fatty acid (palmitic acid) present in most organisms. The cell membranes composed largely of iso-, anteiso-, and omega-alicyclic acids support growth of bacteria, which inhabit normal as well as extreme environments. The occurrence of these types of fatty acids as major cellular fatty acids is an important criterion used to aid identification and classification of bacteria.

Bacteria↗
PubMed1996

Docosahexaenoic acid reduces GABA response in substantia nigra neuron of rat.

.1. The effects of docosahexaenoic acid (DHA) on gamma-aminobutyric acid (GABA) response (IGABA) were investigated on the neuron acutely dissociated from rat substantia nigra (SN), with the use of patch recordings in a whole cell mode. 2. DHA (5 x 10(-6) M) reduced bicuculline-sensitive GABA (10(-4) M) current by 50.3 +/- 13.1% (mean +/- SE) at a holding potential (Vh) of -40 mV under voltage clamp. 3. The GABA concentrations for the half-maximum and threshold of IGABA were not altered by the presence or absence of 5 x 10(-6) M DHA in the external solution. 4. The decrease of 10(-4) M IGABA, following the peak during GABA application, was more rapid in the presence of 5 x 10(-6) M DHA than in its absence. The time constants for IGABA decay were significantly different between the two conditions. 5. DHA reduced the IGABA and the glycine-induced response (Igly) in a concentration-dependent manner. On the contrary, DHA potentiated the aspartate-induced response (Iasp) in a concentration-dependent manner, suggesting that DHA influences the activity of chloride channels but does not exhibit a nonspecific blocking effect on any ionic channel. 6. The application of thimerosal did not affect the reduction of IGABA by DHA, suggesting it unlikely that DHA reduces the IGABA by binding to phospholipids or triglycerides and altering the lipid environment around the chloride channel. 7. Arachidonic acid (AA) also reduced the IGABA in a manner similar to DHA. Docosapentaenoic acid (DPA) reduced the IGABA less potently than DHA. Other polyunsaturated and saturated fatty acids, such as docosatrienoic acid, docosatetraenoic acid, palmitic acid, and oleic acid, had very little or no effect on the IGABA. 8. DHA, as well as AA, may play an important role in modulating neuronal excitability by reducing the IGABA and Igly, and potentiating N-methyl-D-aspartate receptor-mediated responses in the SN.

Animals↗
PubMed1994

Feeding trans fatty acids to rats has no effect on the intestinal uptake of glucose, fatty acids or cholesterol.

Trans fatty acids are produced in the manufacture of margarine, and these hydrogenated fatty acids may have a deleterious effect on the reduction in fasting levels of serum cholesterol anticipated from the feeding of cis polyunsaturated fatty acids. We undertook this study in rats to test the effect of feeding trans fatty acids on the intestinal uptake of glucose, fatty acids and cholesterol. Adult female Wistar rats were fed for 2 weeks semisynthetic, isocaloric diets containing no oleic acid (18:1), cis 18:1 or trans 18:1. There was no difference between the three dietary groups in the animals' food consumption or body weight gain. Rats fed trans 18:1 had an approximately 20% decline in the total weight of the ileum as compared with controls fed no 18:1, and therefore there was also a decline in the percentage of the ileal tissue comprised of mucosa. When comparing rats fed trans 18:1 with those fed cis 18:1 or no 18:1, there was no difference in the uptake of varying concentrations of D-glucose when expressed as nmol.100 mg tissue-1.min-1 or nmol.100 mg mucosal-1.min-1 for jejunum or for ileum. Also, there was no difference in the value of the maximal transport rate (Vmax), Michaelis constant (Km), or the contribution of passive uptake of glucose assessed with L-glucose. There was no diet-associated change in the jejunal or ileal uptake of a medium-chain length fatty acid (lauric acid), a long-chain length saturated fatty acid (palmitic acid), a monounsaturated fatty acid (oleic acid), two polyunsaturated fatty acids (linoleic and linolenic acids), or cholesterol. Thus, we conclude that 2 weeks' feeding of trans fatty acid to rats has no influence on the jejunal or ileal uptake of glucose, fatty acids or cholesterol.

Absorption↗
PubMed1993

Lung surfactant phospholipids associate with polymerizing fibrin: loss of surface activity.

Intraalveolar fibrin formation is a hallmark of many acute and chronic lung inflammatory processes. We investigated the influence of fibrin polymerization on biochemical and biophysical properties of a calf lung surfactant extract (CLSE) used for therapy of neonatal distress syndrome. Thrombin-induced coagulation of human fibrinogen (range, 0.04 to 4 mg/ml) in the presence of CLSE (2 mg/ml phospholipids) resulted in progressive loss of surface tension-lowering properties and adsorption facilities of this surfactant preparation; the CLSE-inhibitory capacity of desAABB-fibrin surpassed that of fibrinogen by more than two orders of magnitude. In parallel with the loss of surface activity, association of the predominant surfactant phospholipid dipalmitoylphosphatidylcholine (DPPC) (14C-labeled, admixed to 2 mg/ml CLSE) with polymerizing desAABB-fibrin occurred. A volume of 0.3 mg/ml insoluble fibrin effected a approximately 50% loss, and 0.6 mg/ml a > 90% loss, of DPPC from the aqueous phase. Dioleoylphosphatidylcholine, dipalmitoylphosphatidic acid, stearic acid, palmitic acid, and arachidonic acid, admixed to CLSE as labeled compounds, as well as total CLSE phospholipids were retained in polymerizing desAABB-fibrin with dose-effect curves superimposable to that of DPPC; no fibrin association was noted for 14C-glycerol-3-phosphate. Polymerizing desAA-fibrin, generated by incubation of CLSE-fibrinogen mixtures with arvin, captured DPPC and resulted in loss of surface properties at even lower concentrations, compared with desAABB-fibrin. In contrast, CLSE incubation with preformed desAABB- and desAA-fibrin polymers did not cause substantial phospholipid coupling with the clot material or loss of surface properties. Microtiter plate-immobilized fibrinogen and desAABB- and desAA-fibrinomonomers did not bind CLSE phospholipids enriched with 14C-DPPC.(ABSTRACT TRUNCATED AT 250 WORDS)

1,2-Dipalmitoylphosphatidylcholine↗