Composition ofO-alkyl andO-alk-1-enyl moieties in the glycerolipids of the human adrenal

A comparison of human adult and fetal adrenals with respect to their levels of glyceryl ether lipids and other lipid components is reported. Fetal glands contained significantly lower levels of alk-1-enyl phosphoglycerides and of cholesterol. Neutral glyceryl ether diesters, and ethanolamine and choline phosphoglycerides were isolated from adult adrenal tissue. The composition of theO-alkyl glycerol groups in these lipid fractions was obtained by means of gas chromatography of the trimethylsilyl ethers and diacetyl derivatives;O-alk-1-enyl glycerols were analyzed as their diacetates. About one-half of the alkyl and alk-1-enyl glycerol moieties present in glyceryl ether diesters contained hydrocarbon side chains with 20, 22, or 24 carbon atoms. Long hydrocarbon chains (C_19–24) were also found in theO-alkyl glycerol moieties present in the total lipids of fetal adrenals.     

Apoproteins in association with intralipid incubations in rat and human plasma

Intralipid was incubated with rat and human plasma and examined for changes in lipid and apoprotein composition. Upon incubation in rat plasma, Intralipid acquired an apoprotein complement similar to that found in chylomicrons following plasma incubation or in chylomicrons after alimentary lipemia. Since the apoproteins of lipoproteins probably govern their metabolism, these results suggest that Intralipid and chylomicrons undergo similar metabolic fates. This pattern is characterized by a predominance of Apo E (the arginine-rich apoprotein) and Apo C. Incubation of Intralipid with human plasma showed the uptake of Apo A-I and Apo A-IV as well. Density fractionation of the plasma into separate lipoprotein classes facilitated identification of high density lipoprotein as the major apoprotein donor to the Intralipid. When rat lipoprotein-free plasma (δ>1.21) was incubated with Intralipid, a different apoprotein pattern appeared in the particles of S_f>400 depending on whether the entire Intralipid preparation or only the S_f>400 fraction alone was incubated. The difference consisted of a virtual total absence of the arginine-rich protein on the S_f>400 particles in whole Intralipid incubations. Density fractionation of the S_f<400 particles of Intralipid and recombination of these fractions with the S_f>400 fraction before incubation revealed the major inhibitory fraction to be δ<1.006 (S_f 20–400).     

Effects of dietary triacylglycerol structure on triacylglycerols of resultant chylomicrons from fish oil- and seal oil-fed rats

We investigated the influence of the intramolecular fatty acid distribution of dietary triacyl-sn-glycerols (TAG) rich in n-3 polyunsaturated fatty acids (PUFA) on the structure of chylomicron TAG. Fish oil and seal oil, comparable in fatty acid compositions but with different contents of major n-3 PUFA esterified at thesn-2 position (20:5n-3, 46.6%, and 5.3%; 22:6n-3, 75.5%, and 3.8%, respectively), were fed to rats. Mesenteric lymph was collected and the chylomicrons were isolated by ultracentrifugation. The fatty acid composition of chylomicrons largely reflected the fatty acid composition of the oils administered. The intramolecular fatty acid distributions of the TAG fed were reflected in the chylomicron TAG as the fraction of the total contents observed in thesn-2 position of 20:5n-3 were 23.6 and 13.3%, and of 22:6n-3 were 30.6 and 5.4% for resultant chylomicrons following fish oil and seal oil administration, respectively. Thus, after seal oil administration, significant higher load of n-3 PUFA was esterified in thesn-1,3 positions of chylomicron TAG compared with fish oil administration (P<0.05).     

Effect of dietary cholesterol oxidation products on the plasma clearance of chylomicrons in the rat

Oxidized cholesterols in the diet have been shown to exacerbate arterial cholesterol deposition and the development of atherosclerosis in animal models. Dietary oxidized cholesterols are absorbed through the intestine and incorporated into lymph chylomicrons. The aim of this study was to investigate the effect of oxidized cholesterols on the metabolism of nascent chylomicrons in vivo. It was shown that oxidized cholesterols markedly delay the clearance of chylomicrons from plasma compared to rats given TG alone. However, there was no difference in the clearance of chylomicrons containing oxidized cholesterols vs. purified cholesterol, although the presence of oxysterols did appear to exacerbate the removal of these particles from circulation. The impaired clearance of chylomicrons containing oxidized cholesterols was not due to impaired lipolysis and slower conversion to the remnant form. Moreover, the incorporation of oxidized cholesterols did not alter the hepatic or splenic uptake of chylomicrons compared to chylomicrons isolated from rats given purified cholesterol or TG alone. Collectively, the results of this study suggest that the exacerbated delay in clearance of chylomicron remnants enriched with oxysterols may be due to impaired uptake by tissues other than the liver and spleen. Apolipoprotein (apo) analysis showed that oxysterol incorporation reduced the apoE content and altered the apoC phenotype of chylomicrons, which may have an impact on the removal of chylomicron remnants from plasma. In conclusion, dietary oxysterols appear to have the potential to adversely affect chylomicron metabolism. Therefore, further investigations in humans are required to determine whether dietary oxidized cholesterols found in cholesterol-rich processed foods delay the clearance of postprandial remnants, which may contribute to and exacerbate the development of atherosclerosis.     

Comparison of the clearances of serum chylomicron triglycerides enriched with eicosapentaenoic acid or oleic acid

Rat mesenteric lymph chylomicrons containing triglycerides enriched with either [¹⁴C]oleic acid (OA) or [¹⁴C]-eicosapentaenoic acid (EPA) were prepared by ultracentrifugation of lymph samples collected for 6 hr after a single duodenal infusion of an emulsion containing either fatty acid. These chylomicrons were injected into the jugular vein of recipient rats and, at various time intervals, blood was drawn and serum was assayed for radioactivity. In separate animals, serum lipoprotein fractions were separated by ultracentrifugation, and the redistribution of labeled fatty acid among circulating lipoproteins was determined by liquid scintillation spectrometry. When the early disappearance rates (10 min) of either total serum radioactivity or specifically the chylomicron fraction were compared, there were no differences between the groups receiving OA-or EPA-enriched chylomicrons. However, disappearance rates of EPA-enriched chylomicrons were slower than those of OA-enriched chylomicrons from 25 to 90 min. The small but significant differences in the disappearance rates for the longer time periods cannot be ascertained without further studies. At 5 min after injection of either type of chylomicron, the d<1.006 g/ml lipoprotein fraction of serum chylomicrons and very low density lipoproteins contained almost 90% of the original radioactivity. By 240 min, when less than 2% of the radioactivity remained, this radioactivity in the d<1.006 g/ml fraction was 43–46%, with concomitant increases in the low and high density lipoprotein fractions and in the lipoprotein-free serum. Deceased.     

Measurement of human chylomicron triglyceride clearance with a labeled commercial lipid emulsion

Human chylomicron triglyceride (TG) kinetics has been difficult to determine directly owing to technical limitations. This report describes a new method for studying chylomicron metabolism. Healthy volunteers (n=10) sipped a drink providing 175 mg fat·kg⁻¹·h⁻¹ for 7.5 h to produce a steady-state chylomicronemia. A commercial 10% intravenous lipid emulsion was labeled with [³H]triolein, purified by high-performance liquid chromatography, and sterilized. A trace amount of labeled emulsion was injected intravenously 30 min before (i.e., in the fasting state) and 5, 6, and 7 h after sipping began (i.e., triplicate determinations in the fed state). Chylomicron half-lives were calculated from the monoexponential decay curves, and apparent distribution volumes were estimated by back-extrapolation to time zero. Plasma and estimated chylomicron TG concentrations increased from 89±13 and 0.8±0.3 to 263±43 and 91±39 mg/dL (mean±SEM), respectively, with feeding. Tracer-determined chylomicron TG half-lives were 5.34±0.58 and 6.51±0.58 min during the fasting and fed states, respectively (P<0.01). The apparent distribution volume during the fasting state was 24% greater than plasma volume (4515±308 vs. 3630±78 mL, P<0.02), consistent with significant margination of lipid emulsion particles to endothelial binding sites. Margination was reduced during the fed state, suggesting that native chylomicrons competed with lipid emulsion particles for endothelial lipoprotein lipase. The results indicate that a radiolabeled commercial lipid emulsion is metabolized in a fashion similar to native chylomicron TG, and thus can be used to study chylomicron TG kinetics.     

Metabolism of fatty acid,glycerol and a monoglyceride analogue by rat cardiac myocytes and perfused hearts

Studies have been conducted on the uptake and metabolism of unesterified fatty acid, free glycerol and 1-hexadecyl glyceryl ether by rat cardiac myocytes, and of fatty acid, intact triglyceride and the glyceryl ether by perfused rat hearts. Cardiac myocytes efficiently extracted, oxidized and esterified oleic acid, but demonstrated little ability to utilize free glycerol. Although the glyceryl ether was efficiently extracted by myocytes, it was neither hydrolyzed or esterified. The perfused heart also extracted and metabolized unesterified fatty acid, and the fatty acid released during lipolysis of circulating lipoprotein triglyceride. The glyceride glycerol, however, was largely recovered (90%) in the perfusate suggesting inefficient myocardial utilization of either free glycerol or partial glycerides. Myocardial extraction of glyceryl monoether was demonstrated, but the monoglyceride analogue was also unmetabolized by intact heart tissue. The results suggest that if monoglycerides are produced by the action of lipoprotein lipase on circulating triglycerides, reutilization of intact monoglycerides for higher glyceride synthesis is not a major fate of these products.     

Effect of marginal zinc deficiency on the apolipoprotein-B content and size of mesenteric lymph chylomicrons in adult rats

To investigate the mechanisms underlining the impaired intestinal absorption of lipids in zinc deficiency, the apo-B content and chemical composition of chylomicrons from marginally zinc-deficient rats fed 2.8 ppm of dietary zinc (ZD) were compared with those from pair-fed (PF) and ad libitum control (CT) groups fed an adequate level (30.8 ppm) of zinc. Chylomicrons, obtained by cannulating the mesenteric lymph, were isolated by ultracentrifugation at 1.3×10⁶ g/min at 12 C and purified by 2% agarose column chromatography. Apolipoprotein- (apo) B was separated by the method of isopropanol precipitation. The apo-B concentration of chylomicrons was lowered significantly in ZD group. The apo-B contents of chylomicrons in ZD, PF and CT rats, as expressed as % chylomicron protein, were 8.7±0.1, 11.5±0.5 and 10.7±0.7%, respectively. No significant differences were noted between ZD and PF groups in total protein (TP), phospholipid (PL), triglyceride (TG) and cholesterol (CH), although there was a slight decrease in TG and an increase in CH in CT rats compared with ZD and PF groups. The ratio of the core to surface constituents, as determined by TG/(TP+PL), was significantly higher in ZD group relative to the controls, suggesting that chylomicrons from ZD rats were larger. This finding was consistent with the appearance of larger chylomicron particles in the lacteal of the intestinal mucosa following lipid ingestion. These findings suggest that the intestinal synthesis of apo-B may be defective in zinc-deficient rats and may explain in part the impaired absorption of dietary lipids observed in zinc deficiency. Presented in an abstract form at the 70th annual meeting of the Federation of American Societies for Experimental Biology: Fed. Proc. 45, 974, 1986.     

Carbohydrate content of apolipoprotein B-48 from rat chylomicrons of varying density

Monosaccharide composition was determined in apolipoprotein B-48 (apoB) of chylomicrons of rat mesenteric lymph. Chylomicrons were separated into three fractions based on density. Triglyceride and apolipoprotein content were determined in each. ApoB was isolated and quantified using precipitation with isopropanol. Chylomicrons were collected in lymph under normal conditions, and with Poloxalene 2930 when chylomicron secretion was inhibited. Most of the triglyceride was carried in the least dense fraction, while the highest apoB content was in the most dense fraction under normal conditions. Mannose and galactosamine contents of apoB were similar in all fractions while contents of both glucosamine and galactose were highest in the least dense fraction. When chylomicron secretion was inhibited by Poloxalene, the amount of triglyceride recovered in the least dense fraction was significantly reduced. Despite the inhibition of lipid transport in the least dense fraction of chylomicrons by Poloxalene, there was little change in apoB recoveries and in the relative content of various monosaccharides in the apoB from each of the three fractions as compared to results obtained during lipid absorption under normal conditions. In conclusion, carbohydrate composition of apoB of chylomicrons is heterogeneous and varies with chylomicron density.     

Hydrocarbon transport in chylomicrons and high-density lipoproteins in rat

A lipoprotein system is described that transports gut hydrocarbons of low polarity in chylomicrons of intestinal lymph and plasma to plasma high density lipoproteins (HDL) in rat. Four highly lipophilic aryl and alkyl hydrocarbons [benzo(α)pyrene; 1,1,1-trichloro-2,2-bis(p-chlorophenol)ethane (DDT), hexadecane and octadecane] were selected to give a graded range of polarity. Chylomicrons were labeled doubly with radioisotopes in triacylglycerol and a single hydrocarbon by feeding [³H]-glycerol and [¹⁴C]hydrocarbon. All hydrocarbons were transported in the triacylglycerol oil phase of chylomicrons. Injected chylomicron triacylglycerol and 3 of 4 hydrocarbons were cleared simultaneously from plasma consistent with lipoprotein-lipase dependent hydrocarbon clearance but DDT was cleared more rapidly. HDL was the major plasma acceptor of all labeled hydrocarbons. Plasma chemical fluxes were measured for octadecane and DDT and both showed net fluxes from chylomicrons to HDL. HDL selectively concentrated chylomicron hydrocarbons from chylomicron triacylglycerol. Lipoprotein lipase stimulation by intravenous heparin significantly increased transfer of alkanes from chylomicrons to HDL. These results indicate that (a) chylomicrons transport gut-derived hydrocarbons with a wide range of structure and polarity as triacylglycerol solutes; (b) HDL are a major plasma acceptor of all these hydrocarbons, demonstrating both selective solute uptake from triacylglycerol and net chemical uptake for the 2 hydrocarbons studied and (c) efflux of these chylomicron hydrocarbons from plasma and into HDL is regulated partly by hydrolysis of chylomicron triacylglycerol.     

Ultracentrifugal isolation of serum chylomicron-containing fractions with quantitation by infrared spectrometry and NCH elemental analysis

An ultracentrifugal method for isolating chylomicron-containing fractions from serum by flotation, using either standard Spinco swinging-bucket rotors or a specially fabricated swinging-bucket rotor, is described. Lower limits of the S_f rates of the chylomicron fractions are evaluated using a computer technique to define lipoprotein flotation over a nonlinear NaCl density gradient. The latter is prepared by a special overlayering technique. Quantitation within a 9–50 μg region of mass assay is accomplished by both infrared spectrometry and elemental analysis for N, C and H. Results indicate that the chylomicron concentration in serum for a small population of nonfasting male adults ranges from approximately 0–50 mg %. Associated with the Bio-Medical Research Division, Lawrence Radiation Laboratory, Livermore, California     

Rat Small Intestinal Mucosal Epithelial Cells Absorb Dietary 1,3‐Diacylglycerol Via Phosphatidic Acid Pathways

Compared with triacylglycerol (TAG), dietary 1,3‐diacylglycerol (1,3‐DAG) is associated with reduced serum lipid and glucose levels. We investigated the metabolism of 1,3‐DAG by assaying its intermediate metabolites during digestion and absorption in the rat small intestine. After gavage with TAG emulsion, TAG was digested mainly to 2‐monoacylglycerol (2‐MAG) and unesterified fatty acid (FFA) in the rat small intestinal lumen. 2‐MAG was directly absorbed into the small intestinal epithelial cells and esterified to 1,2(2,3)‐DAG, and further esterified to TAG. After gavage with 1,3‐DAG emulsion, 1,3‐DAG was digested mainly to 1(3)‐MAG and FFA in the rat small intestinal lumen with subsequent significant increase of 1‐MAG and 1,3‐DAG concentrations in small intestinal mucosal epithelial cells, and the 2‐MAG, 1,2(2,3)‐DAG, and TAG concentrations in mucosal epithelial cells were not significantly different after 1,3‐DAG than after TAG gavage, suggesting that the metabolic pathway of 1,3‐DAG is different from that of TAG. In intestinal mucosal epithelial cells, we further assayed enzyme levels and gene expression of proteins in the phosphatidic acid (PtdOH) pathway. The glycerol kinase, phosphatidate phosphatase, and diacylglycerol acyltransferase‐2 expression and the relative expression of mRNA of enzymes were significantly increased in the 1,3‐DAG group compared with the TAG group, suggesting that TAG synthesis from dietary 1,3‐DAG was mainly via PtdOH pathways, which may partially account for the effect of dietary DAG on postprandial serum TAG.     

Digestion and assimilation features of dietary DAG in the rat small intestine

Several recent studies have demonstrated that dietary DAG oil rich in 1,3-species suppresses the postprandial increase of serum TAG level and decreases body fat accumulation, compared with TAG oil. To clarify the mechanisms underlying the beneficial effects of DAG, we investigated the metabolic features of DAG in the small intestine with regard to the digestion pathway in the lumen and the TAG-synthesis pathway in the mucosa. When intraduodenally infused as an emulsion, TAG was digested to 1,2-DAG, 2-MAG, and FFA, whereas 1,3-DAG was digested to 1(3)-MAG and FFA. When assessed by the incorporation of [1-¹⁴C]linoleic acid in lipids, the mucosal TAG-synthesis was significantly reduced by DAG infusion compared with TAG infusion. However, the mucosal 1,3-DAG synthesis was remarkably increased in the DAG-infused rats. The total amount of mucosal 1,3-DAG was also increased (4.5-fold) after DAG infusion compared with that after TAG infusion. Next, we examined the synthesis pathway of 1,3-DAG. In cultures of the everted intestinal sacs, 1,3-DAG production required the presence of 1-MAG, suggesting that the 1,3-DAG synthesis was due to acylation of 1(3)-MAG in the DAG-infused rats. Furthermore, measurements of DAG acyltransferase activity indicated that 1,3-DAG was little utilized in TAG synthesis. These findings suggest that features of 1,3-DAG digestion and assimilation in the intestine may be responsible for the reduction of the postprandial serum TAG level by dietary DAG.     

Atherogenesis in swine fed several types of lipid-cholesterol diets

Eighteen-month-old Nebraska strain minipigs were fed diets containing 2% cholesterol and 20% corn oil, lard, or coconut oil for 12 to 18 months. Concentrations of serum total lipid, total cholesterol, and total phospholipid increased 200 to 300% with each diet. Changes in serum concentrations of S_f 20+ and S_f 0–20 lipoproteins varied with diets fed. Serum concentration of high density lipoprotein was increased in all cases. Intima concentration of S_f 0–20 lipoprotein fraction was elevated by feeding the corn oil diet. There was no development of atherosclerosis as a result of feeding the corn oil-cholesterol diet, but there was an increase in atherosclerosis as a result of feeding the lard or coconut oil diet. There were no correlations between fatty acid patterns of several lipid fractions from serum and corresponding lipid fractions from aortic intima of corn oil fed animals. Deceased.     

Metabolities of dietary triacylglycerol and diacylglycerol during the digestion process in rats

The present study investigated the metabolic fate of dietary TAG and DAG and also their digestion products in the stomach and small intestine. A diet containing 10% TAG or DAG oil, enriched in 1,3-DAG, was fed to Wistar rats ad libitum for 9 d. After 18 h of fasting, each diet was re-fed ad libitum for 1 h. The weights of the contents of the stomach and small intestine were measured, and the acylglycerol and FFA levels were analyzed by GC at 0, 1, and 4 h after the 1-h re-feeding. The amounts of re-fed diet ingested and the gastric and small intestinal content were not different between the two diet groups. In the TAG diet group, the main products were TAG and DAG, especially 1(3),2-DAG. In addition, 1,3-DAG and 1(3)-MAG were present in the stomach, and the 1,3-DAG levels increased over time after the re-feeding period. In the DAG diet group, the main products in the stomach were DAG, MAG, FFA, and TAG. There were significantly greater amounts of 1,3-DAG, 1(3)-MAG, and FFA in the DAG diet group in the stomach compared with the TAG diet group. The amount of FFA in the stomach relative to the amount of ingested TAG plus DAG in the DAG diet group was higher than that in the TAG diet group. Acylglycerol and FFA levels were considerably lower in the small intestine than in the stomach. These results indicate that, in the stomach, where acyl migration might occur, the digestion products were already different between TAG and DAG oil ingestion, and that DAG might be more readily digested by lingual lipase compared with TAG. Furthermore, almost all of the dietary lipid was absorbed, irrespective of the structure of the acylglycerol present in the small intestine.     

Effects of a Single and Short-Term Ingestion of Diacylglycerol on Fat Oxidation in Rats

This study examines the effect of diacylglycerol (DAG) oil consisting mainly of 1,3-species on fat oxidation as a possible mechanism for anti-obesity. We examined the following: (1) the long-term (23-week) effects of a DAG oil diet on the development of obesity; (2) the effect of a single ingestion of DAG oil on fat oxidation; and, (3) the short-term (2-week) effect of a DAG oil diet on fat metabolism in rats. Rats fed a DAG oil diet accumulated significantly less body fat compared to rats fed a triacylglycerol (TAG) oil diet, each oil possesses a similar fatty acid composition. More ¹⁴C-CO₂ was expired and less ¹⁴C-radioactivity was incorporated into visceral fat after administration of a tracer emulsion containing 1,3-[oleoyl-1-¹⁴C] diolein compared to [carboxyl-¹⁴C] triolein. Indirect calorimetry showed respiratory quotients were significantly lower in the DAG oil diet group than in the TAG oil diet group. More ¹⁴C-CO₂ was expired and less ¹⁴C-radioactivity was incorporated into visceral fat in the DAG oil diet group than in the TAG oil diet group after a single intragastric administration of [carboxyl-¹⁴C] triolein. These results suggest the following. (1) DAG oil has an inhibitory effect on diet-induced fat accumulation. (2) 1,3-DAG, a major component of DAG oil, is more susceptible to oxidation. (3) A short-term ingestion of DAG oil increases fat utilization at the whole body level and results in increased oxidation of dietary fat. The stimulated fat oxidation might be one explanation for the anti-obesity effect of long-term DAG oil ingestion.     

Production of specific structured lipids by enzymatic interesterification: optimization of the reaction by response surface design

Rapeseed oil and capric acid were interesterified in solvent-free media catalyzed by Lipozyme IM from Rhizomucor miehei to produce specific-structured lipids (SSLs). The process was optimized by response surface design concerning the effects of acyl migration and the byproducts of diacylglycerols (DAGs). A five-factor response surface design was used to evaluate the influences of five major factors and their relationships. The five factors were water content (W_c, wt-% based on enzyme used), reaction temperature (T_e, °C), enzyme load (E_l, wt-% based on substrates), reaction time (T_r, h) and substrate ratio (S_r, rapeseed oil/capric acid, mol/mol), varied at three levels together with two star point levels. The net incorporation [Δ(I_f–M_f), in which I_f represents incorporation (1,3-positions) and M_f acyl migration (2-position), and the contents of DAGs were analyzed and calculated. All parameters had strong influence on the net incorporation, and the experimental and predicted values were close. The best fitting quadratic model was determined by regression and backward elimination. The coefficients of determination (R²) of the models were 0.971 for net incorporation and 0.938 for DAG content. Thus, we conclude that the quadratic response models adequately expressed the reaction. Based on the models, the reaction was optimized for the maximum net incorporation and minimum DAG content. The reaction and the control of water content or water activity (Aw) was also discussed.     

Absorption of dietary cholesterol oxidation products and incorporation into rat lymph chylomicrons

Cholesterol oxidation products (oxysterols) induce macrophage lipid loading and accumulate in early arterial fatty streaks. The origin of lesion oxysterols has not been elucidated. The absorption of oxysterols from the diet and transport to the arterial wall by postprandial lipoprotein remnants may be a significant source. This study aimed to investigated the extent of oxysterol absorption and the effect on chylomicron composition. Cholesterol was heat-treated, causing 30% oxidation; the major oxidation products were 7β-hydroxycholesterol, 7-ketocholesterol, 5α,6α-epoxycholesterol, and 5β,6β-epoxycholesterol. Conscious lymph-cannulated rats were given a bolus gastric infusion of 50 mg oxidized cholesterol or 50 mg purified cholesterol in a vehicle of triglyceride. In the rats given the oxidized cholesterol, 6% of the oxysterol load was absorbed and incorporated into lymph chylomicrons. Rats given pure cholesterol had no increase in oxysterols above baseline levels. The incorporation of oxysterols into lymph chylomicrons differed over time with 7β-hydroxycholesterol, having peak absorption at 3 h, followed by 7-ketocholesterol at 4 h and 5α,6α-epoxycholesterol at 5 h. The absorption of oxysterols in animals given the oxidized cholesterol gastric infusate was associated with lymph chylomicron compositional changes at 2–4 h. The oxidized cholesterol-treated group has a twofold increase in the cholesterol (890±84 μg vs. 440±83 μg at 3 h) and triglyceride content (19.76±3.4 μg vs. 8.49±3.8 μg at 3 h). This led to a doubling of chylomicron size over this postprandial period, with particles having a mean diameter of 294 nm in the oxidized cholesterol-treated animals, compared to 179 nm in the purified cholesterol group. In conclusion, dietary oxysterols appear to influence postprandial lipoprotein particle size and composition. These changes may have effects on the clearance of chylomicrons from plasma, arterial delivery of oxysterols, and possible deposition in arterial lesions.     

Effect of medium-chain fatty acid positional distribution in dietary triacylglycerol on lymphatic lipid transport and chylomicron composition in rats

The present study was carried out to examine if the positional distribution of medium-chain fatty acid (MCF) in dietary synthetic fat influences lymphatic transport of dietary fat and the chemical composition of chylomicrons in rats with permanent cannulation of thoracic duct. Four types of synthetic triacylglycerol were prepared: (i) sn-1(3) MCF-sn 2 linoleic acid, (ii) interesterified sn-1(3) MCF-sn 2 linoleic acid, (iii) sn-2 MCF-sn-1(3) linoleic acid, and (iv) interesterified sn-2 MCF-sn-1(3) linoleic acid. A purified diet composed of equal amounts of the synthetic fat and cocoa butter was given to rats with permanent lymph duct cannulation. The positional distribution of MCF in the dietary fat had no significant effect on the lymph flow, triacylglycerol output, phospholipid output, lipid composition of chylomicrons, or the particle size. The positional distribution of MCF in the synthetic triacylglycerol was maintained in the chylomicron triacylglycerol. These results showed that MCF in the dietary triacylglycerol is transported into lymphatics and the positional distribution is well preserved in chylomicron triacylglycerol.     

Metabolism of alkyl glyceryl ethers in the rat

The metabolism of¹⁴C- and³H-labeled alkyl glyceryl ethers after intraperitoneal injections was examined in the liver and intestine of the rat. Additionally, in vitro experiments were conducted with intestinal homogenates and intetinal contents. From these investigations it was concluded that the liver and the intestine metabolize the alkyl glyceryl ethers very differently. Intestinal contents can alter α-batyl alcohol, as indicated by preliminary experiments, and intestinal cells contain enzyme systems which convert the alkyl glyceryl ethers to the mono- and di-acyl derivatives. Very little esterified glyceryl ethers were found in the liver lipids. The intestine contains an enzyme system which, although it has a greater specificity for chain length and for isomeric position of the ether than that of the liver system, does cleave the glyceryl ethers. From in vivo studies, of intestinal tissue it was concluded that all of the injected glyceryl ethers were converted intact the ethanolamine, serine, and choline alkyl glyceryl ether phospholipids; with the use of α-batyl alcohol, the phosphatidyl ethanolamine fraction, contained most of the labeled glyceryl ether phospholipid with β-batyl alcohol, α-chimyl, and β-chimyl alcohols, the phosphatidyl, choline fraction contained most of the labeled alkyl glyceryl ether phospholipid. No significant amount (<1%) of labeled alkyl glyceryl ether phospholipids was found in any of the rat-liver lipids. Predoctoral trainee supported by Public Health Service Training Grant 5TI-GM-404-04 from the National Institute of General Medical Sciences, National Institutes of Health. Work done in partial fulfillment of the Ph.D. in the Department of Biochemistry at the University of North Carolina.