bluuebunny/crossref_metadata_2025_split huggingface dataset:
Response of hypercholesterolemic subjects to administration of tocotrienols
Authors: Qureshi A. A. , Bradlow B. A. , Brace L. , Manganello J. , Peterson D. M. , Pearce B. C. , Wright J. J. K. , Gapor A. , Elson C. E. 
Published: November 2006

AbstractThe cholesterol‐suppressive actions of Palmvitee and γ‐tocotrienol were assessed in hypercholesterolemic subjects after acclimation to the American Heart Association Step 1 dietary regimen for four and eight weeks, respectively. The four‐week dietary regimen alone elicited a 5% decrease (P<0.05) in the cholesterol level of the 36 subjects. Subjects continuing on the dietary regimen for a second four‐week period experienced an additional 2% decrease in their cholesterol levels. Dietary assessments based on unanticipated recalls of 24‐h food intake records suggest that significant reductions in energy and fat, predominantly in saturated fat, intakes are responsible. The subjects experienced significant Palmvitee‐ and γ‐tocotrienol‐mediated decreases in cholesterol. The group of subjects acclimated to the dietary regimen for four weeks responded to Palmvitee (a blend of tocols providing 40 mg α‐tocopherol, 48 mg α‐tocotrienol, 112 mg γ‐tocotrienol, and 60 mg δ‐tocotrienol/day for four weeks) with a 10% decrease in cholesterol (P<0.05). Dietary assessments showed no further change in energy and fat intakes. α‐Tocopherol attenuates the cholesterol‐suppressive action of the tocotrienols. The second group of subjects, acclimated to the dietary regimen for eight weeks, received 200 mg‐γ‐tocotrienol/d for four weeks. The cholesterol‐suppressive potency of this α‐tocopherol‐free preparation was calculated to be equivalent to that of the mixture of tocotrienols (220 mg) used in the prior study. Cholesterol levels of the 16 subjects in the second group decreased 13% (P<0.05) during the four‐week trial. Plasma apolipoprotein B andex vivo generation of thromboxane B2 were similarly responsive to the tocotrienol preparations, whereas neither preparation had an impact on high density lipoprotein cholesterol and apolipoprotein A‐I levels.
Antioxidant effects of tocotrienols in patients with hyperlipidemia and carotid stenosis
Authors: Tomeo A. C. , Geller M. , Watkins T. R. , Gapor A. , Bierenbaum M. L. 
Published: November 2006

AbstractAntioxidants may have a role in the prevention of atherosclerosis. In the present trial, we investigated the antioxidant properties of Palm Vitee, a γ‐tocotrienol‐, and α‐tocopherol enriched fraction of palm oil, in patients with carotid atherosclerosis. Serum lipids, fatty acid peroxides, platelet aggregation, and carotid artery stenosis were measured over an 18‐month period in fifty patients with cerebrovascular disease. Change in stenosis was measured with duplex ultrasonography. Ultrasound scans were done at six months, twelve months, and yearly thereafter. Bilateral duplex ultrasonography revealed apparent carotid atherosclerotic regression in seven and progression in two of the 25 tocotrienol patients, while none of the control group exhibited regression and ten of 25 showed progression (P<0.002). Serum thiobarbituric acid reactive substances, anex vivo indicator of maximal platelet peroxidation, decreased in the treatment group from 1.08±0.70 to 0.80±0.55 μM/L (P<0.05) after 12 mon, and in the placebo group, they increased nonsignificantly from 0.99±0.80 to 1.26±0.54 μM/L. Both tocotrienol and placebo groups displayed significantly attenuated collagen‐induced platelet aggregation responses (P<0.05) as compared with entry values. Serum total cholesterol, low density lipoprotein cholesterol, and triglyceride values remained unchanged in both groups, as did the plasma high density lipoprotein cholesterol values. These findings suggest that antioxidants, such as tocotrienols, may influence the course of carotid atherosclerosis.
Distribution of cholesterol among its carriers in the bile of male and female hamsters
Authors: Mikami Takahiro , Cohen Bertram I. , Mikami Yasuko , Ayyad Nariman , Mosbach Erwin H. 
Published: November 2006

AbstractThe distribution of cholesterol among its carriers was studied in the bile of male and female hamsters. Sasco hamsters (Sasco Inc., Omaha, NE) were fed a semipurified diet with 0.0% cholesterol and 4% butterfat (group 1, males; group 4, females); a semipurified diet with 0.3% cholesterol and 1.2% plamitic acid (group 2, males; group 5, females); and a semipirified diet with 0.3% cholesterol and 4% safflower oil (group 3, males; group 6, females). At the end of six weeks, gallstones were found only in male hamsters receiving both cholesterol and dietary fat (fatty acid) (incidence of cholesterol stones: 90% in group 2; 22% in group 3). The biliary cholesterol carriers were separated and isolated from the bile of the hamsters by gel filtration chromatography, using the method of Pattinson [Pattinson, N.R., Willis, K.E., and Frampton, C.M. (1991)J. Lipid Res. 32, 205–214]. In those male hamsters that formed cholesterol gallstones, significant amounts of cholesterol were present in the void volume which contained large cholesterol phospholipid vesicles (void volume vesicles) (23% in group 2 and 15% in group 3). Smaller cholesterol/phospholipid vesicles were eluted next (fractions 30–45) and contained 15% of biliary cholesterol in group 2 and 21% in group 3. The remainder of the cholesterol was associated with mixed cholesterol/phospholipid/bile salt micelles. The cholesterol/phospholipid ratio was larger in both the void volume vesicles and small vesicles (2.40 and 1.48 in group 2; 2.56 and 1.33 in group 3, respectively) compared to the micelles (about 0.3 in groups 2 and 3). In contrast, the bile of the female hasmters contained few vesicles (3% small vesciles in group 5) and the cholesterol/phospholipid ratio of these vesicles was lower (0.94). Hamsters fed cholesterol‐free diets (groups 1 and 4) had no biliary cholesterol/phospholipid vesilces; and cholesterol was present in micelles. The results suggest that both the gender and the diet of the hamsters affected the distribution of biliary cholesterol between vesicles and micelles. The development of cholelithiasis in this animal model appears to depend on the rapid nucleation of cholesterol‐rich phospholipid vesicles in bile.
Evidence that palmitic acid is absorbed assn‐2 monoacylglycerol from human milk by breast‐fed infants
Authors: Innis Sheila M. , Dyer Roger , Nelson Carolanne M. 
Published: November 2006

AbstractMilk fatty acids consist of about 20–25% palmitic acid (16∶0), with about 70% of 16∶0 esterified to thesn‐2 position of the milk triacylglycerols. Hydrolysis of dietary triacylglycerols by endogenous lipases producessn‐2 monoacylglycerols and free fatty acids, which are absorbed, reesterified, and then secreted into plasma. Unesterified 16∶0 is not well absorbed and readily forms soaps with calcium in the intestine. The positioning of 16∶0 at thesn‐2 position of milk triacylglycerols could explain the high coefficient of absorption of milk fat. However, the milk lipase, bile salt‐stimulated lipase, has been suggested to complete the hydrolysis of milk fat to free fatty acids and glycerol. These studies determined whether 16∶0 is absorbed from human milk assn‐2 monopalmitin by comparison of the plasma triacylglycerol total andsn‐2 position fatty acid composition between breast‐fed and formula‐fed term gestation infants. The human milk and formula had 21.0 and 22.3% of 16∶0, respectively, with 54.2 and 4.8% 16∶0 in the fatty acids esterified to the 2 position. The plasma triacylglycerol total fatty acids had 26.0±0.6 and 26.2±0.6% of 16∶0, and thesn‐2 position fatty acids had 23.3±3.3 and 7.4±0.7% of 16∶0 in the three‐month‐old exclusively breast‐fed (n=17) and formula‐fed (n=18) infants, respectively. Marked differences were found in the plasma total and the 2 position phospholipid percentage of 20∶4ω6, i.e., 11.6±0.3 and 6.9±0.6 (total), 17.7±1.4 and 9.7±0.6 (sn‐2 position) and percentage of 22∶6ω3, 4.6±0.3 and 2.1±0.3 (total), 5.6±0.6 and 2.0±0.2 (sn‐2 position) for the breast‐fed and formula‐fed infants, respectively. These studies provide convincing evidence that 16∶0 is absorbed from human milk assn‐2 monoacyl‐glycerol. The metabolic significance of the differences in positional distribution of fatty acids in the plasma lipids of breast‐fed and formula‐fed infants is not known.
In vitro activation of mouse skin protein kinase C by fatty acids and their hydroxylated metabolites
Authors: Lo Herng‐Hsiang , Bartek Gwendolyn A. , Fischer Susan M. 
Published: November 2006

AbstractTo understand how dietary fatty acids differentially modulate mouse skin tumorigenesis, the ability of specific fatty acids and their derivatives to activate murine epidermal protein kinase C (PKC)in vitro was investigated. Total PKC from untreated female SSIN mouse skin was partially purified and incubated with specific fatty acids at concentrations up to 300 μM in the presence of Ca2+ and phosphatidylserine. Thecis‐unsaturated fatty acids tested, ranging from 16∶1 to 22∶6, stimulated PKC activity in a similar dose‐dependent manner with an approximate threefold maximum increase over control. Neither the number ofcis‐double bonds nor the chainlength of these fatty acids affected their relative ability to activate PKC.trans‐Fatty acids, with the exception of linoelaidic acid (t,t‐18∶2n−6), exhibited about half of the potency of their correspondingcis‐isomers in stimulating PKC at the plateau concentration (200 μM) or lower. Substitutions close to the double bond oncis‐fatty acids abolished their ability to activate PKC. The hydroxylated metabolites of arachidonic acid (20∶4n−6) and linoleic acid (c,c‐18∶2n−6), i.e., the hydroxyeicosatetraenoic acids (HETE) and hydroxyoctadecadienoic acids (HODE), also activated mouse skin PKCin vitro, but only about half as effectively as did the respective parent fatty acids. The results suggest that both hydroxyl substitution andtrans‐configuration of HETE and HODE are responsible for their reduced ability to activate PKC. Overall the data suggests that the reduced skin tumor yield observed in mice fed diets high inc,c‐18∶2n−6 is not likely to be due to differences in the ability ofc,c‐18∶2n−6 or 20∶4n−6, or their matabolites, to activate PKC.
Lymphatic absorption of oxidized cholesterol in rats
Authors: Osada Kyoichi , Sasaki Eiji , Sugano Michihiro 
Published: November 2006

AbstractThe absorption of cholesterol and of cholesterol oxidation products (oxidized cholesterols) was compared in lymph‐cannulated rats. We found that the lymphatic absorption of an intragastrically administered, emulsified lipid meal containing 25 mg of cholesterol or 25 mg of oxidized cholesterols, within 24 h, was approximately 67 and 30%, respectively. The absorption rate of individual oxidized cholesterols differed considerably and was approximately 30% for 7α‐hydroxycholesterol, 42% for 7β‐hydroxycholesterol, 32% for 5β‐epoxycholesterol, 28% for 5α‐epoxycholesterol, 15% for cholestanetriol and 12% for 7‐ketocholesterol. Moreover, cholesterol oxidation products delayed the absorption of oleic acid as triolein. Approximately 35 and 48% of cholesterol was recovered in chylomicrons (CM) and very low density lipoprotein (VLDL), respectively. In contrast, 54 and 40% of the oxidized cholesterols was recovered in CM and VLDL, respectively, although there was a significant difference in the distribution of individual oxidized cholesterols. The results of the present study indicate that oxidized cholesterols are absorbed to a lesser extent than is cholesterol, that they disturb fat absorption and that they distribute differently between lymphatic lipoproteins.
Effects of n−3 and n−6 fatty acids on the activities and expression of hepatic antioxidant enzymes in autoimmune‐prone NZB×NZW F1 mice
Authors: Venkatraman Jaya T. , Chandrasekar Bysani , Kim Jong Dai , Fernandes Gabriel 
Published: November 2006

AbstractMenhaden fish oil (FO) containing n−3 fatty acids dramatically extends the life span and delays the onset and progression of autoimmune disease in (NZB×NZW)F1 (B/W) female mice as compared to those fed corn oil (CO) rich in n−6 lipids. As an inefficient antioxidant defense system has been linked to autoimmune diseases, the present study was undertaken to determine whether the protective action of n−3 lipids is mediated through their antioxidant defense system. Weanling B/W mice were fed a nutritionally adequate, semipurified diet containing CO or krill oil (KO) or FO at 10% level (w/w)ad libitum until the mice were 6.5 months old. All diets contained the same level of vitamin E (21.5 mg/100 g diet). We compared the effects of feeding n−6 and n−3 lipids on survival, kidney disease, hepatic microsomal lipid composition, peroxidation, and on the activity and mRNA expression of the antioxidant enzymes catalase, glutathione peroxidase (GSH‐Px) and superoxide dismutase (SOD) in 6.5‐month‐old B/W mice. The results showed that when compared to livers from CO‐fed mice, livers from KO‐ and FO‐fed mice showed: (i) significantly higher (P<0.001) activities and expression of CAT, GSH‐Px and SOD; (ii) significantly lower (P<0.001) arachidonic acid (20∶4n−6) and linoleic acid (18∶2n−6) and higher (P<0.001) eicosapentaenoic acid (20∶5n−3) and docosahexaenoic acid (22∶6n−3) levels in hepatic microsomes; and (iii) significantly lower (P<0.001) estimated peroxidation indices and thiobarbituric acid reactive substances generation. The data indicate that one of the mechanisms through which the n−3 lipids delay the onset of autoimmune diseases in B/W mice may be through maintenance of higher activities and expression of hepatic antioxidant enzymes.
Serum fatty acid profiles in cystic fibrosis patients and their parents
Authors: Christophe A. B. , Warwick W. J. , Holman R. T. 
Published: November 2006

AbstractFatty acid compositions of the major serum lipid classes from 43 cystic fibrosis (CF) homozygotes (CF patients), 36 obligate heterozygotes (parents of CF patients) and 34 controls were determined by capillary gas chromatography. Fatty acid compositions of the homozygote CF patients were skewed in the direction of relative essential fatty acid deficiency in comparison with the controls. Less pronounced, but similar deviations from normal, were observed in the heterozygotes. Homozygotes with normal fatty acid compositions and heterozygotes with considerably disturbed fatty acid profiles were found.
A microprecipitation technique suitable for measuring α‐lipoprotein cholesterol
Authors: Puppione Donald L. , Charugundla Sarada 
Published: November 2006

AbstractA semi‐automated method has been developed for determining α‐lipoprotein cholesterol values. Precipitation of apolipoprotein B containing lipoproteins takes place in wells of microtiter plates after 100 μL of serum are mixed with 20 μL of a heparin/MnCl2 solution. A Beckman (Fullerton, CA) Biomek 1000 work station is used to transfer sera, supernatants and reagents between tubes and microtiter plates. Supernatant cholesterol is determined enzymatically, and absorbances are read at 490 nm using a Molecular Devices Corporation (Palo Alto, CA) plate reader. Values obtained on both fresh and frozen serum samples agreed with corresponding data obtained at the Centers for Disease Control (CDC; Atlanta, GA). For the fresh samples, the average bias was 2.87%. The within‐run coefficients of variations were between 2.2 and 0.6% for the data obtained on CDC frozen control pools. The results indicate that the semi‐automated method is suitable for obtaining accurate and precise data for α‐lipoprotein cholesterol. The method lends itself to the analysis of large numbers of samples and is particularly suited for the study of lipoproteins of small mammals.
The effects of dietary fish oil on alveolar type II cell fatty acids and lung surfactant phospholipids
Authors: Baybutt Richard Carleton , Smith John Edgar , Yeh Yu‐Yan 
Published: November 2006

AbstractThe purpose of this study was to determine the responsiveness of alveolar type II cells to dietary fish oil and the consequent effects on alveolar and lung surfactant. Rats were fed a corn oil or a fish oil diet for four weeks. Dietary n−3 fatty acids were readily incorporated into the type II cell phospholipids as indicated by higher levels of eicosapentaenoic acid (2.77±0.10%) and docosahexaenoic acid (1.63±0.10%) in the group receiving the fish oil diet. The elevated levels of n−3 fatty acids were accompanied by concomitant reduction in arachidonic acid and linoleic acid. Neither eicosapentaenoic acid nor docosahexaenoic acid was incorporated into type II cell triacylglycerols. Feeding a fish oil containing diet increased surfactant phospholipids, particularly 1,2‐disaturated acyl phosphatidylcholines in whole lung compared to a corn oil diet. However, the amount of surfactant found in the alveolus was not different between the two diet treatment groups. The results suggest that dietary n−3 fatty acids stimulate synthesis and/or inhibit degradation of lung surfactant without altering surfactant secretion in alveoli.
Turnover of cholesterol and dipalmitoyl phosphatidylcholine in surfactant of adult rat lung
Authors: Jones Michael E. , Barr Heather A. , Nicholas Terence E. 
Published: November 2006

AbstractIn order to compare the turnover of two major surfactant components, [1α,2α(n)‐3H]cholesterol and [methyl14C choline] dipalmitoyl phosphatidylcholine (DPPC) were introduced as lamellar bodiesvia the trachea into lightly anesthetized rats which were then allowed to recover. The radiotracers were assumed to have entered the alveolar surfactant pool and to have subsequently recycled in part into the lamellar bodies of alveolar type II cells. For DPPC, the specific activityvs. time curves of tubular myelin rich (alv‐1) and tubular myelin poor (alv‐2) alveolar lavage fractions were similar, and there was a plausible precursor‐product relationship between lamellar bodies and either (or both) of these compartments. In contrast, however, the specific activities of alv‐1 and alv‐2 for cholesterol were quite different, allowing us to reject the hypothesis of a precursor‐product relationship between classical lamellar bodies and alv‐2. The estimated turover time for DPPC in alv‐1 was 240 or 206 min, depending on which subfraction of lamellar bodies one takes to be the precursor. For cholesterol it was 583 or 624 min. These longer turnover times for cholesterol should lead to a greater than twofold increase in the relative concentration of cholesterol in the putative product compartment. Such an increase was not found. We interpret this as reflecting either noncompartmental behavior of the alveolar surfactant pool, or multiple pools of lamellar bodies with different turnover times. We conclude that two major components of pulmonary surfactant, cholesterol and DPPC, are handled differently, and that for at least one of these substances, the widely accepted scenario of a compartmental precursor‐product relationship between lamellar bodies and alveolar surfactant must be rejected.
Hypolipidemic effects of β‐cyclodextrin in the hamster and in the genetically hypercholesterolemic rico rat
Authors: Riottot Michel , Olivier Philippe , Huet Anne , Caboche Jean‐Jacques , Parquet Michel , Khallou Jamila , Lutton Claude 
Published: November 2006

AbstractThe effect of increasing amounts of a cyclic oligosaccharide, β‐cyclodextrin (BCD), included in the diet on plasma cholesterol and triglycerides, was investigated in two animal models, namely in male genetically hypercholesterolemic Rico rats and in male Syrian hamsters. The distribution of bile acids in the gastrointestinal tract and in the feces of hamsters was also determined. In the Rico rats and hamsters, plasma cholesterol and triglycerides decreased linearly with increasing doses of BCD. In these two species, 20% BCD as compared to control diet lowered cholesterolemia (−35%) and triglyceridemia (−70%). In the hamster, the BCD diet caused a marked decrease in cholesterol and triglycerides in chylomicrons and very low density lipoprotein, and in high density lipoproteins cholesterol. Composition and amounts of bile acids were modified in the gastrointestinal tract of hamsters receiving 10% BCD as compared to the control group. The total bile acid content of the gallbladder of treated hamsters was fourfold higher than in the control group, and the bile contained a large amount of hydrophilic bile acids. This trend was also observed in the small intestine, in which percentages and total quantities of cholic plus deoxycholic acids (cholic pathway) were higher than those of chenodeoxycholic plus ursodeoxycholic plus lithocholic acids (chenodeoxycholic pathway). The bile acid contents of the cecum and colon of treated hamsters were 2.7‐fold higher than those of control animals, but the bile acid composition was similar in the two groups of hamsters. Fecal excretion of bile acids was 3.3‐fold higher in the treated group than in the control group, and the percentage of lithocholic acid was markedly increased and close to that observed in the colon. The turnover of the chenodeoxycholic pool was twice as fast in treated hamsters as in control hamsters, whereas that of cholic acid was not significantly modified. These results suggest that BCD does not alter the microbial degradation of bile acids, but rather stimulates their synthesis and increases their pool size. BCD prevents the intestinal absorption of lithocholic acid and washes this cytotoxic bile acid from the colon. The hypocholesterolemic effect of BCD appears to be due to stimulation of bile acid synthesis.
Human platelets release a paf‐acether: Acetylhydrolase similar to that in plasma
Authors: Korth Ruth , Bidualt Jocelyne , Palmantier Remi , Benveniste Jacques , Ninio Ewa 
Published: November 2006

AbstractIntact washed human platelets aggregated in response to paf‐acether (paf) and did not metabolize [3H]paf at concentrations up to 10 nM. However, when platelets were lysed by exposure to pH 9.5, resulting in 37.5±2.5% (mean ±SD, n=3) lactic dehydrogenase (LDH) release, 20.5±5.7% of the radioactivity was detected as labeled lyso paf and 5.7±3.1% as labeled alkylacylglycerophosphocholine. When platelets were aggregated with 0.5 IU/mL thrombin or high concentrations of paf (100 nM), they released a part of their acetylhydrolase without releasing LDH. In supernatants obtained from aggregated platelets, 21±2% or 10±2% (n=3), respectively, of the total platelet acetylhydrolase activity was detectedvs. none in supernatants of resting cells. The release of acetylhydrolase was concentration‐and time‐dependent and paralleled the release of PF 4, a marker for α‐granules. The acetylhydrolase affinity for paf (Km) measured in sonicates of resting and thrombin‐activated platelets was 8.3±1.5 μMvs. 10.6±1.5 μM, n=5, n.s. in a “Mann Whitney” test. The latter Km was slightly but significantly different (P<0.05, n=5) from that of the thrombin‐released acetylhydrolase (7.9 ±1.5 μM) and that of the latter was itself different from plasma acetylhydrolase (5.3±0.5,P<0.05, n=5). Addition of plasma (acid‐treated to inactivate acetylhydrolase) decreased the Km value of supernatant acetylhydrolase to 6.1±1.4 μM. All preparations of acetylhydrolase exhibited similar pH requirements and sensitvity to various inhibitors. Thus paf and thrombin cause release of acetylhydrolase from platelets in parallel with release of the α‐granule marker PF4. This phenomenon might represent a protective mechanism against paf‐mediated effects in thrombotic and cardiovascular diseases.