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PubMed1984

Linoleic acid and arachidonic acid metabolism in human peripheral blood leucocytes: comparison with the rat.

Peripheral blood leucocytes from human male volunteers and from male rats were incubated in vitro in the presence of 14C-labelled linoleic acid [( 14C]LA) or 3H-labelled arachidonic acid [( 3H]AA). The time-course of [14C]LA and [3H]AA incorporation into human leucocyte total lipids was maximal at 80-90% of the initial dose within 20-30 min of dosing the cells. Compared with mixed leucocytes, isolated polymorphonuclear leucocytes were only marginally different in the differential incorporation of [14C]LA and [3H]AA into total lipids. In human leucocytes, [14C]LA was incorporated initially into triglycerides but predominantly into phosphatidylcholine thereafter. In the rat, [14C]LA remained as the free acid (63%), with lesser amounts entering the phospholipids (9%), monoglycerides-diglycerides (12%) and triglycerides (less than 1%). Utilization of [14C]LA by the delta 6-desaturase was only a minor route of its metabolism in both human and rat leucocytes. 3H-labelled prostaglandins E2 and F2 alpha accounted for up to 30% of the radioactivity released into the incubation medium from human leucocytes incubated with [3H]AA for 60 min. Stimulation of phagocytosis in the human leucocytes with latex beads or with unopsonized zymosan did not alter the differential incorporation of [14C]LA or [3H]AA into the leucocyte lipid fractions.

Adult↗
PubMedDate not supplied

Intracellular Ca2+ and cytotoxicity.

Following injury or activation in some immune cell lines, elevation of intracellular Ca2+ concentration (Cai2+) is an early and major event that precedes cell death. Agents shown to elevate Cai2+ and to result subsequently in the death of some cells include human immunodeficiency virus (HIV) (in T4+ cells), 25-hydroxy cholesterol, tumor necrosis factor (TNF), cyclosporine, dexamethasone, alpha-interferon, and Ca2+ ionophores. The effects of these agents, both on Cai2+ and on cytotoxicity, are additive. This type of Ca2+-related cytotoxicity may be associated with either accelerated synthesis of triglycerides (TNF), accelerated synthesis of cholesterol ester (25-hydroxy cholesterol), or cholesterol (HIV) and terminally with declining synthesis of structural phospholipid. Agents that can lower Cai2+ (e.g., phorbol esters, diglycerides, lipoproteins [LDL], oleic acid, or serum) under appropriate conditions ameliorate the Ca2+-induced cytotoxicity. Metabolism of other divalent metals, i.e., Zn2+ and Cd2+, also become altered with cell injury, e.g., glucocorticoids elevate Cai2+, but block uptake of Zn2+. These observations support the idea that chronic elevation of Cai2+ by many chemically unrelated agents leads to cell death by creating imbalance both in cell biosynthetic mechanisms--especially in those controlling lipid metabolism--as well as creating imbalances in metabolism of other trace metals, especially Zn2+.

Animals↗
PubMed1996

Is phospholipase in vinegared oysters a casual agent for human poisoning?

In this survey, lipid metabolism and activities of the lipolytic enzymes diglyceride lipase (DLase) and phospholipase A (PLase A) in the oyster digestive glands (ODGs), with 4% added acetic acid (the same acid concentration as vinegar) and incubated at 37 degrees C for 3 h, were investigated. Significant decreases in triglyceride, phosphatidycholine, and phosphatidylethanolamine and increases in monoglyceride, lysophosphatidylcholine, and lysophosphatidylethanolamine were observed in the acetic acid-treated ODGs. Changes in ODGs treated with PBS were smaller than in the acetic acid-treated ones but larger than in the nontreated ones. Both PLase A1, and PLase A2 in ODGs were activated by addition of acetic acid and incubated at 37 degrees C for 3 h. PLase A1 activities were higher than those of PLase A2, in all experimental ODGs. Addition of formic acid also induced activation of PLase A at pH 2. On the other hand, DLase in ODGs decreased remarkably with acetic acid treatment. These data showed that the increase in lipid metabolites such as free fatty acids and lysophospholipids in the acetic acid-treated ODGs might be due to catabolism of PLase A, which was activated by the acid treatment at 37 degrees C.

Acetates↗
PubMed1993

Effects of high-fat diet on incidence of spontaneous tumors in Wistar rats.

In a 2.5-year carcinogenicity study, two groups, both including male and female Wistar rats, were fed two different diets with 4% and 16% fat. In addition to 4% soybean oil, the high-fat diet contained 12% mono- and diglycerides, of which 85% was stearic acid and 13% palmitic acid. There was no difference in food consumption, body weight, weight gain, and longevity between the two groups. A statistically significant increase in the incidence of tumors in the high-fat group was seen in fibroadenoma of the mammae (female, p = 0.05). No statistically significant difference was seen when the incidence of benign mammary tumors (adenomas and fibroadenomas) was combined, just as the overall incidence of mammary tumors (adenomas, fibroadenomas, and adenocarcinomas) was not significantly different between the groups. A statistically significant decrease in the incidence of tumors in the high-fat group was seen in adenoma of the parathyroid gland (male, p = 0.04) and medullary carcinoma of the adrenal gland (male, p = 0.04). Combining the incidence of benign and malignant tumors of the adrenal medulla led to a further increase in the level of significance (p = 0.02). The present study showed that a high-fat diet influenced the tumor incidence in certain organs of rats. However, the overall differences in tumor incidence between rats fed the low- and the high-fat diet are considered marginal. Therefore we were not able to confirm or deny the hypothesis that a high-fat diet promotes the development of cancer. It should be noted that, in our study, fat accounted for about 30% of the total energy in the high-fat diet. This is much below the amount of fat normally found in the western diet but corresponds well to the level recommended for human intake. In addition, the rats fed the high-fat diet did not gain more weight, even though no difference was recorded in food consumption (g/kg body wt) between the groups.

Adenofibroma↗
PubMed2002

Irish National Food Ingredient Database: application for assessing patterns of additive usage in foods.

Patterns of food additive usage in the Irish food supply and changes in patterns of usage between 1995-97 and 1998-99 were assessed by means of an Irish National Food Ingredient Database (INFID). Of the 300 additives permitted for use according to the European Union food additives Directives, some 54% were recorded in foods in INFID. Colours, emulsifiers and acids were the most frequently used additive categories, representing 18, 13 and 12% of the total additives used, respectively. Colours were most commonly recorded in sauces (n = 182 brands, 26% of sauces), emulsifiers were most commonly recorded in biscuits (n = 181 brands, 47% of biscuits) and acids were most commonly recorded in sauces (304 brands, 43% of sauces). Carotenes (E160a), Annatto (E160b), mono- and diglycerides of fatty acids (E471) and citric acid (E330) were the most commonly used colour, emulsifier and acid, respectively. All diet soft drinks (n = 37), low-fat spreads (n = 25) and liver pâtés (n = 10) recorded the use of at least one additive. When expressed in terms of the number of brands that contain additives, sauces (n = 522, 73% of sauces), biscuits (n = 323, 84% of biscuits) and preserves (n = 321, 85% of preserves) were ranked highest. For most categories of additive (n = 24), there appeared to be a minimal change in qualitative additive usage between 1995-97 and 1998-99. However, there was a significant increase in the frequency of use of emulsifiers (p < 0.001), acids (p < 0.01), sweeteners (p < 0.05) and acidity regulators (p < 0.05), and a significant decrease in the frequency of use of antioxidants (p < 0.05) during the period 1998-99 compared with 1995-97. Despite changes in additive usage patterns, it appeared that changes in the types of brands on sale between both periods were more apparent than actual changes in qualitative ingredient formulations across brands, as some 17% of brands that were on sale in 1995-97 were no longer on sale in 1998-99.

Databases, Factual↗
PubMed1999

Changes in the components of dry-fermented sausages during ripening.

Several chemical changes occur during the ripening of dry-fermented sausages that determine the flavor and odor of the end product. The phenomena that take place during fermentation, that is, both acidification of the sugars by lactic acid bacteria and reduction of nitrates and nitrites to nitric oxide by micrococci have been known for several years. However, the chemical changes involved in this process, and, particularly, the agents responsible have not yet been established, although they have been attributed to changes in the majority components (proteins and lipids) and to the ingredients added (spices and condiments) in the preparation of the original mixture. The typical flavor and odor of dry-fermented sausages cannot be attributed to volatile substances alone, but to a large number of volatile and nonvolatile compounds present in the product in suitable proportions. Microbial growth in the sausage together with activity of the meat endogenous enzymes are undoubtedly partially responsible for the development of a number of aromatic and sapid compounds. However, lipid autooxidation reactions are also an important source of these substances, and it is not yet known which of these processes is more important in sausage ripening. Much research has focused on the break up of triglycerides into free fatty acids, diglycerides, and monoglycerides during ripening and the progressive increase in the amounts of different carbonyl oxidation products. Carbonyl compounds probably play a significant role in determining the flavor because, in general, these have very low perception thresholds, in the ppm and ppb range. Similarly, the protein breakdown to yield peptides and amino acids has been studied extensively, the latter being substrates of several microbial and chemical reactions that generate many flavor compounds.

Animals↗
PubMed2004

Efficient gene delivery with serum into human cancer cells using targeted anionic liposomes.

Success of human gene therapy depends upon the development of delivery vehicles or vectors, which can selectively deliver therapeutic genes to target cells with efficiency and safety. Previous studies have shown an efficient, systemic trans-gene expression in many cell lines (in vitro) by using an anionic liposomal vector, based on the composition of retroviral envelopes (artificial viral envelopes, AVEs). The AVE-liposomes and their complexes with plasmid (DNA) were characterized according to zeta potential measurements and transmission electron microscopy (TEM). We successfully demonstrated that AVE liposomes, dispersed in 10% serum-containing growth medium, efficiently delivered plasmid DNA to HuH-7 (human hepatoma cell line) cells. We assessed the utility of liver-targeted vesicles as a drug/gene delivery system for the treatment of liver diseases. We found that small unilamellar AVE vesicles containing 15 mol% digalactosyl diglyceride (DGDG) are efficiently targeted to the liver via the hepatic asialoglycoprotein receptor.

Carbohydrates↗
PubMed2001

Final report on the safety assessment of Lecithin and Hydrogenated Lecithin.

Lecithin is a naturally occurring mixture of the diglycerides of stearic, palmitic, and oleic acids, linked to the choline ester of phosphoric acid, commonly called phosphatidylcholine. Hydrogenated Lecithin is the product of controlled hydrogenation of Lecithin. Bilayers of these phospholipids in water may form liposomes, a spherical structure in which the acyl chains are inside and not exposed to the aqueous phase. Lecithin and Hydrogenated Lecithin are used in a large number of cosmetic formulations as skin conditioning agents-miscellaneous and as surfactant-emulsifying agents. Hydrogenated Lecithin is also used as a suspending agent-nonsurfactant. Historical data on concentration of use of Lecithin reveals that 0.1% to 1.0% is the concentration range most frequently seen, with concentrations up to 50% reported for two moisturizing products. A solution of 65% Lecithin is currently reported to be used at concentrations up to 3% in cosmetics. Nonocclusive application of Lecithin-containing liposomes to murine skin resulted in 30% penetration to the subdermis. In piglet skin, the same application resulted in 99% accumulating in the stratum corneum. In general, liposomes are considered effective in capturing other compounds inside their spherical structure and delivering any such captured compound through the skin barrier. As a result, caution should be exhibited in formulating cosmetic products that contain these ingredients in combination with other ingredients whose safety is based on their lack of absorption or where dermal absorption is a concern. Lecithin is virtually nontoxic in acute oral studies, short-term oral studies, and subchronic dermal studies in animals. Lecithin is not a reproductive toxicant, nor is it mutagenic in several assays. In an oral carcinogenicity study, brain neoplasms were found in mice exposed to Lecithin. In a subcutaneous carcinogenicity study, no neoplasms were found in mice and rats exposed to Lecithin. Adverse reactions to Lecithin in a metered-dose inhaler have been reported. Lecithin and Hydrogenated Lecithin were generally nonirritating and nonsensitizing in animal and human skin. Based on the available data, Lecithin and Hydrogenated Lecithin are safe as used in rinse-off cosmetic products; they may be safely used in leave-on products at concentrations up to 15%, the highest concentration tested in clinical irritation and sensitization studies; but the safety of use could not be substantiated in cosmetic products likely to be inhaled. Because of the possibility of formation of nitrosamines, these ingredients should not be used in cosmetic products in which N-nitroso compounds may be formed.

Administration, Inhalation↗
PubMed1987

Two G-proteins act in series to control stimulus-secretion coupling in mast cells: use of neomycin to distinguish between G-proteins controlling polyphosphoinositide phosphodiesterase and exocytosis.

Provision of GTP (or other nucleotides capable of acting as ligands for activation of G-proteins) together with Ca2+ (at micromolar concentrations) is both necessary and sufficient to stimulate exocytotic secretion from mast cells permeabilized with streptolysin-O. GTP and its analogues, through their interactions with Gp, also activate polyphosphoinositide-phosphodiesterase (PPI-pde generating inositol 1,4,5-trisphosphate and diglyceride [DG]). We have used mast cells labeled with [3H]inositol to test whether the requirement for GTP in exocytosis is an expression of Gp activity through the generation of DG and consequent activation of protein kinase C, or whether GTP is required at a later stage in the stimulus secretion sequence. Neomycin (0.3 mM) inhibits activation of PPI-pde, but maximal secretion due to optimal concentrations of guanosine 5'-O-(3-thiotriphosphate) (GTP-gamma-S) can still be evoked in its presence. When ATP is also provided the concentration requirement for GTP-gamma-S in support of exocytosis is reduced. This sparing effect of ATP is nullified when the PPI-pde reaction is inhibited by neomycin. We argue that the sparing effect of ATP occurs as a result of enhancement of DG production and through its action as a phosphoryl donor in the reactions catalyzed by protein kinase C.

Animals↗
PubMed1971

Fine structural localization of acyltransferases. The monoglyceride and -glycerophosphate pathways in intestinal absorptive cells.

A study of the fine structural localization of the acyltransferases of the monoglyceride and alpha-glycerophosphate pathways for triglyceride synthesis in the intestinal absorptive cell is reported. Glutaraldehyde-fixed tissue was found to synthesize diglyceride and triglyceride from monopalmitin and palmityl CoA, and parallel morphological studies showed the appearance of lipid droplets in the smooth endoplasmic reticulum of the absorptive cell. Glutaraldehyde-fixed tissue also synthesized triglyceride from alpha-glycerophosphate, although this enzyme system was more susceptible to fixation than the monoglyceride pathway acyltransferases. Cytochemical methods for the localization of free CoA were based (a) on the formation of the insoluble lanthanium mercaptide of CoA and (b) on the reduction of ferricyanide by CoA to yield ferrocyanide which forms an insoluble precipitate with manganous ions. By these methods the monoglyceride pathway acyltransferases were found to be located mainly on the inner surface of the smooth endoplasmic reticulum. The alpha-glycerophosphate pathway acyltransferases were localized mainly on the rough endoplasmic reticulum. Activity limited to the outer cisternae of the Golgi membranes occurred with both pathways. The possible organization of triglyceride absorption and chylomicron synthesis is discussed in view of these results.

Absorption↗
PubMed1981

Metabolism and intracellular localization of a fluorescently labeled intermediate in lipid biosynthesis within cultured fibroblasts.

In this paper we report on the uptake and distribution of an exogenously supplied fluorescent phosphatidic acid analogue by Chinese hamster fibroblasts. Under appropriate in vitro incubation conditions, 1-acyl-2-(N-4-nitrobenzo-2-oxa-1,3-diazole)-aminocaproyl phosphatidic acid was rapidly and preferentially transferred from phospholipid vesicles to cells at 2 degrees C. However, unlike similar fluorescent derivatives of phosphatidylcholine and phosphatidylethanolamine that remain restricted to the plasma membrane under such incubation conditions (Struck, D. K., and R. E. Pagano. 1080. J. Biol. Chem. 255:5405--5410), most of the phosphatidic acid-derived fluorescence was localized at the nuclear membrane, endoplasmic reticulum, and mitochondria. This was shown by labeling cells with rhodamine-containing probes specific for mitochondria or endoplasmic reticulum, and comparing the patterns of intracellular NBD and rhodamine fluorescence. Extraction and analysis of the fluorescent lipids associated with the cells after treatment with vesicles at 2 degrees or 37 degrees C revealed that a large fraction of the fluorescent phosphatidic acid was converted to fluorescent diglyceride, phosphatidylcholine, and triglyceride. Our findings suggest that fluorescent phosphatidic acid may be useful in correlating biochemical studies of lipid metabolism in cultured cells and studies of the Intracellular localization of the metabolites by fluorescence microscopy. In addition, this compound provides a unique method for visualizing the endoplasmic reticulum in living cells.

Animals↗
PubMed2004

Hepatolipidemic effects of naringenin in high cornstarch- versus high coconut oil-fed rats.

The effects of naringenin (Nar) on hepatic neutral and polar lipids were examined in rats that were fed either a high (27.98%) cornstarch (CornS) or a high (19.05%) coconut oil (CocoO) diet, with or without supplementation with 0.60% NAR, for 40 days. Liver weights and total, neutral, and polar lipids were significantly increased following the feeding of CocoO (P <.01) when compared with the CornS-fed rats. Furthermore, significant elevations in liver weight and total neutral lipids were observed (P <.01) with the CornS-Nar compared with the CornS diet; cholesterol esters (CE), CE:cholesterol (CE:C) ratio, triglycerides (TG), and phosphatidylethanolamine (PE) were significantly increased (P <.01). When Nar was added to the CocoO diet, liver protein, total lipids, and total neutral and polar lipids were significantly decreased (P <.01). Of the neutral lipids, CE, CE:C ratio, TG, free fatty acids (FFA), mono- and diglycerides (P <.01), and C (P <.05) were significantly decreased. CE and TG were more significantly decreased than C, while FFA decreased most markedly (P <.01). Of the hepatic polar lipids, lysophosphatidylcholine, sphingomyelin, phosphatidylcholine, phosphatidylserine and -inositol, PE, and phosphatidic acid were significantly elevated (P <.001) following the feeding of the high CocoO diet compared with the high CornS diet. When Nar was added to the CornS diet, PE was significantly elevated (P <.01), and the outer membrane to inner membrane lipids ratio was significantly decreased (P <.01). When Nar was added to the CocoO diet, all of the polar lipids examined were significantly decreased when compared with the CocoO diet (P <.01). Dietary Nar supplementation significantly reduced both hepatic neutral and polar lipids in rats fed a high CocoO diet, but not in the CornS-fed rats.

Animals↗
PubMed1996

Coupling of the thrombin receptor to G12 may account for selective effects of thrombin on gene expression and DNA synthesis in 1321N1 astrocytoma cells.

In 1321N1 astrocytoma cells, thrombin, but not carbachol, induces AP-1-mediated gene expression and DNA synthesis. To understand the divergent effects of these G protein-coupled receptor agonists on cellular responses, we examined Gq-dependent signaling events induced by thrombin receptor and muscarinic acetylcholine receptor stimulation. Thrombin and carbachol induce comparable changes in phosphoinositide and phosphatidylcholine hydrolysis, mobilization of intracellular Ca2+, diglyceride generation, and redistribution of protein kinase C; thus, activation of these Gq-signaling pathways appears to be insufficient for gene expression and mitogenesis. Thrombin increases Ras and mitogen-activated protein kinase activation to a greater extent than carbachol in 1321N1 cells. The effects of thrombin are not mediated through Gi, since ribosylation of Gi/Go proteins by pertussis toxin does not prevent thrombin-induced gene expression or thrombin-stimulated DNA synthesis. We recently reported that the pertussis toxin-insensitive G12 protein is required for thrombin-induced DNA synthesis. We demonstrate here, using transfection of receptors and G proteins in COS-7 cells, that G alpha 12 selectively couples the thrombin receptor to AP-1-mediated gene expression. This does not appear to result from increased mitogen-activated protein kinase activity but may reflect activation of a tyrosine kinase pathway. We suggest that preferential coupling of the thrombin receptor to G12 accounts for the selective ability of thrombin to stimulate Ras, mitogen-activated protein kinase, gene expression, and mitogenesis in 1321N1 cells.

Animals↗
PubMed2003

Association of the Golgi UDP-galactose transporter with UDP-galactose:ceramide galactosyltransferase allows UDP-galactose import in the endoplasmic reticulum.

UDP-galactose reaches the Golgi lumen through the UDP-galactose transporter (UGT) and is used for the galactosylation of proteins and lipids. Ceramides and diglycerides are galactosylated within the endoplasmic reticulum by the UDP-galactose:ceramide galactosyltransferase. It is not known how UDP-galactose is transported from the cytosol into the endoplasmic reticulum. We transfected ceramide galactosyltransferase cDNA into CHOlec8 cells, which have a defective UGT and no endogenous ceramide galactosyltransferase. Cotransfection with the human UGT1 greatly stimulated synthesis of lactosylceramide in the Golgi and of galactosylceramide in the endoplasmic reticulum. UDP-galactose was directly imported into the endoplasmic reticulum because transfection with UGT significantly enhanced synthesis of galactosylceramide in endoplasmic reticulum membranes. Subcellular fractionation and double label immunofluorescence microscopy showed that a sizeable fraction of ectopically expressed UGT and ceramide galactosyltransferase resided in the endoplasmic reticulum of CHOlec8 cells. The same was observed when UGT was expressed in human intestinal cells that have an endogenous ceramide galactosyltransferase. In contrast, in CHOlec8 singly transfected with UGT 1, the transporter localized exclusively to the Golgi complex. UGT and ceramide galactosyltransferase were entirely detergent soluble and form a complex because they could be coimmunoprecipitated. We conclude that the ceramide galactosyltransferase ensures a supply of UDP-galactose in the endoplasmic reticulum lumen by retaining UGT in a molecular complex.

Animals↗
PubMed1999

Perturbations in the control of cellular arachidonic acid levels block cell growth and induce apoptosis in HL-60 cells.

Our previous studies demonstrated that inhibitors of arachidonate-phospholipid remodeling [i.e. the enzyme CoA-independent transacylase (CoA-IT)] decrease cell proliferation and induce apoptosis in neoplastic cells. The goal of the current study was to elucidate the molecular events associated with arachidonate-phospholipid remodeling that influence cell proliferation and survival. Initial experiments revealed the essential nature of cellular arachidonate to the signaling process by demonstrating that HL-60 cells depleted of arachidonate were more resistant to apoptosis induced by CoA-IT inhibition. In cells treated with CoA-IT inhibitors a marked increase in free arachidonic acid and AA-containing triglycerides were measured. TG enrichment was likely due to acylation of arachidonic acid into diglycerides and triglycerides via de novo glycerolipid biosynthesis. To determine the potential of free fatty acids to affect cell proliferation, HL-60 cells were incubated with varying concentrations of free fatty acids; exogenously provided 20-carbon polyunsaturated fatty acids caused a dose-dependent inhibition of cell proliferation, whereas oleic acid was without effect. Blocking 5-lipoxygenase or cyclooxygenases had no effect on the inhibition of cell proliferation induced by arachidonic acid or CoA-IT inhibitors. An increase in cell-associated ceramides (mainly in the 16:0-ceramide fraction) was measured in cells exposed to free arachidonic acid or to CoA-IT inhibitors. This study, in conjunction with other recent studies, suggests that perturbations in the control of cellular arachidonic acid levels affect cell proliferation and survival.

Acyltransferases↗
PubMed1995

Chemotaxonomic characterization of yeast cells.

Yeast species are analyzed on the basis of their lipid composition to evaluate if chemotaxonomic classification of different species is feasible. The cell walls of samples of Baker's and Brewer's yeast are disrupted by smashing the cells with glass beads at low temperatures. The liberated lipids are extracted with chloroform-methanol. Fractionation of the extract into simple lipids and complex lipids (phospholipids) is performed by column chromatography on silica gel. Elution with methanol produces the simple lipids fraction, whereas elution with methanol-chloroform-ammonium hydroxide produces the phospholipid fraction. The latter fraction is analyzed by high-performance liquid chromatography with light-scattering detection. High-temperature capillary gas chromatography of the simple lipids fraction permits the separation of waxes, sterols, squalene, sterol esters, free fatty acids, monoglycerides, diglycerides, and triglycerides.

Cell Wall↗
PubMed1986

Human milk kills Giardia lamblia by generating toxic lipolytic products.

This study supports our previous hypotheses that normal human milk kills Giardia lamblia trophozoites in vitro and that this killing is due to the release of free fatty acids (FFAs) from milk triglycerides by action of the bile salt-stimulated lipase (BSL) of human milk. Heat-stable killing of G. lamblia was generated when normal human milk was preincubated with sodium cholate, which activates BSL. Moreover, both the skim-milk (containing BSL) and cream (containing mainly triglycerides) fractions were required to kill G. lamblia. We measured the toxicity of FFA and other products of lipolysis to G. lamblia. cis-Unsaturated FFAs (LD50 less than 12 microM), three of four monoglycerides, and four of five lysophosphatidylcholines were toxic to the parasites (LD50 less than 100 microM). In contrast, the parasites were not harmed by the corresponding diglycerides, phosphatidylcholines, triolein, or glycerol. Thus, products of lipid hydrolysis in the normal digestive tract are toxic to G. lamblia. We also demonstrated that albumin and conjugated bile salts, which bind FFA, partially protected trophozoites from killing by oleic acid.

Bile Acids and Salts↗
PubMed1980

Lymph fatty acid composition during constant infusion of saturated fats of different chain lengths in the rat.

The fatty acid composition of intestinal lymph in the rat was determined during constant intraduodenal infusion of a single saturated fatty acid with chain length ranging from C8 to C18 in the form of mixed mono- and diglycerides. The appearance of the infused fatty acid in lymph triglycerides depended on the chain length with the optimum at 14 and 16. Fatty acids with chain length less than 14 were not significantly incorporated into lymph phospholipid and cholesterol ester. Lymph phospholipids had the highest specificity toward stearic acid and cholesterol esters toward palmitic acid. Feeding hydrogenated coconut oil to the rat diminished the essential fatty acids and induced eicosatrienoic acid (20:3 omega 9) present in lymph lipids with no change in the appearance of infused saturated fatty acids except an increase in the infused lauric acid in lymph triglyceride. This study also suggested that the rat intestine probably could synthesize and export triglycerides containing almost entirely myristic and palmitic acids, but unsaturated fatty acids apparently were required for the synthesis of other lipoprotein lipids to transport saturated fatty acids via the lymphatic pathway.

Animals↗