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1.
Arne T. Høstmark Øystein Spydevold Einar Lystad Eva Kristensen Ida Goffeng Bay 《Lipids》1982,17(7):489-499
The effect of varying the dietary sunflower oil/sucrose (SO/SU) ratio on rat plasma lipid concentration and lipoprotein distribution
was studied. Four groups of 10 rats were fed for 4 weeks diets with varying SO/SU ratios. Lipoprotein components were then
estimated in whole plasma and after cumulative density ultracentrifugation. Whole plasma triacylglycerol (TG), total cholesterol
(TC) and free cholesterol (FC) decreased with increasing SO/SU ratio; the CE/FC ratio increased, because CE remained virtually
unaltered. Plasma TG-lowering was due to a decrease in VLDL and LDL-TG. Protein, CE and FC in d=1.063–1.100 g/ml (HDL2b) and d=1.100–1.125 g/ml (HDL2a) lipoproteins decreased upon increasing the SO/SU ratio. In contrast, in d=1.125–1.200 g/ml (HDL3) lipoproteins, there was a concomitant increase in these components. Although increasing the SO/SU ratio effected more protein
and CE transportation in HDL3 and less in HDL2, the total amount of these components in high density lipoproteins (d=1.063–1.200 g/ml) remained constant. Apo A-I and apo
C-III decreased in HDL2 but increased in HDL3 upon increasing the SO/SU ratio. Also, HDL2 apo E, and the apo C-II/apo C-III and small apo B/large apo B ratios in VLDL and LDL were lowered by increasing the SO/SU
ratio. The hepatic VLDL-TG output during isolated liver perfusion was lowest in rats fed the diet with the highest SO/SU ratio.
In perfusate, like in plasma, the VLDL and LDL apo C-II/apo C-III ratio, as well as the small apo B/large apo B ratio, decreased
upon increasing the dietary SO/SU ratio. The results indicate that there can be appreciable diet-dependent variations in plasma
HDL subgroup distribution in spite of unchanged total HDL levels. 相似文献
2.
While it is known that the transfer of cholesteryl ester (CE) from high density lipoprotein (HDL) to the apo B-containing
lipoproteins is increased in patients with diabetes, the extent to which the various lipoprotein fractions engage in neutral
lipid exchange and the magnitude to which triglyceride (TG) is translocated is not known. To examine in greater detail neutral
lipid net mass transfer in diabetes, the HDL subfractions and the apo B-containing lipoproteins were separated, and the net
mass transfer of CE and TG was compared to that of control subjects. In both groups, bidirectional transfer of CE from HDL3 to very low density lipoprotein (VLDL) + low density lipoprotein (LDL) and of TG from VLDL+LDL to HDL3, took place, but this process was significantly greater (P<.01) in insulin-dependent diabetes mellitus (IDDM). In contrast, CE and TG accumulated in HDL2 to a similar degree in normal and IDDM subjects. In recombination experiments with each of the apo B-containing lipoproteins,
IDDM VLDL had a greater capacity to facilitate the exchange of core lipids from both IDDM and control HDL3: on the other hand, LDL from IDDM and control subjects both donated TG and CE to HDL2 and affected little change in HDL3. These findings indicate that all the major plasma fractions normally participate in the trafficking of CE and TG among the
lipoproteins during neutral lipid transfer and show that the principal perturbation in cholesteryl ester transfer in IDDM
involves altered interaction between VLDL and the HDL3 subfraction. 相似文献
3.
Both tumor necrosis factor-α (TNF-α) and EFA deficiency (EFAD) have been established as causes of marked perturbations in
lipid and lipoprotein metabolism. Excessive levels of circulating TNF-α can coexist with EFAD in various clinical disorders
such as cystic fibrosis and type I diabetes. The present study therefore aimed to investigate their combined effects on lipid
profile and lipoprotein composition by administering TNF-α to EFAD rats. Lipoprotein lipase (LPL), the ratelimiting enzyme
in TG catabolism, was also measured in epididymal adipose tissue. EFAD, after a 4-wk period, induced significant increases
in plasma TG (80%, P<0.001), total cholesterol (TC, 27%, P<0.025), and HDL-cholesterol (HDL-C, 62%). Two hours after the administration of TNF-α, a further rise in TG (43%, P<0.05) was noted in controls, but not EFAD animals. TC and HDL-C were unaffected by TNF-α treatment. In addition, TNF-α modified
lipoprotein-lipid composition. VLDL and HDL2 derived from EFAD rats were depleted in apolipoprotein (apo) E and apo A-II, and enriched in apo A-12 h after TNF-α administration.
Finally, TNF-α decreased adipose tissue LPL activity in both control and EFAD animals. The TNF-α-induced inhibition was more
marked in EFAD rats. The present results demonstrated that TNF-α can amplify or antagonize the effects of EFAD on lipid profile,
lipoprotein composition, and LPL activity. These data also suggest that the host's nutritional status is a determining factor
for the modulating effect of TNF-α on lipid metabolism. 相似文献
4.
Frank T. Lindgren Gerald L. Adamson Virgie G. Shore Gary J. Nelson Perla C. Schmidt 《Lipids》1991,26(2):97-101
The effects of n−3 fatty acids on plasma lipids, lipoproteins and apoproteins have usually been studied in humans after feeding
of purified fish oil. This study describes the effect of a natural diet, containing salmon as the source of n−3 fatty acids,
on these parameters as compared to a diet very low in n−3 fatty acids. The subjects were nine normolipidemic, healthy males
who were confined to a nutrition suite for 100 days. During the first 20 days of the study the participants were given a stabilization
diet consisting of 55% carbohydrates, 15% protein, and 30% fat. The n−3 content of this diet was less than 1%, and it contained
no 20- or 22-carbon n−3 fatty acids. After the stabilization period the men were split into two groups, one group continued
on the stabilization diet while the other received the salmon diet that contained approximately 2.1 energy percent (En%) of
calories from 20- and 22-carbon n−3 fatty acids. Both diets contained equal amounts of n−6 fatty acids. This regime continued
for 40 days, then the two groups switched diets for the remainder of the study. Plasma triglycerides were lowered significantly
(p<0.01) and high density lipoprotein cholesterol (HDL-C) was significantly elevated (p<0.01) after the men consumed the salmon
diet for 40 days. The very low density lipoproteins (VLDL) were lowered, but the trend did not reach statistical significance
during the intervention period. The total plasma cholesterol, total low density lipoprotein (LDL) and the total high density
lipoprotein (HDL) levels were not influenced by the salmon diet. Within the HDL fraction, however, the larger HDL2 subfractions were significantly elevated (p<0.002), and the smaller, more dense HDL3 was lowered (p<0.002) by the salmon diet. These significant changes were detected by analytic ultracentrifugation and confirmed
by gradient gel electrophoresis. Analysis of the apolipoproteins (apo) AI, AII, B, and E, and Lp(a) indicated only significant
lowering of apoAI, consistent with the increased HDL2, which is higher in cholesterol but lower in the major HDL apolipoprotein, apoAI. Thus, the purported beneficial cardiovascular
effects of consumption of n−3 fatty acids by humans may, in part, be attributable to changes in the HDL distribution,i.e., the lowering of the more dense HDL3 and the elevation of the larger, less dense HDL2. 相似文献
5.
Administering 17β-estradiol (E2) to juvenile trout results in plasma hyperlipidemia and hyperlipoproteinemia associated with significant increases in the
concentrations of triglycerides (TG), free cholesterol, phospholipids, free fatty acids and proteins, both postprandial and
during starvation. TG undergo the greatest increase (9 times control level 96 h after feeding). The concentration differences
between E2-treated and control trout increase during starvation, primarily by progressive decreases in the concentrations of various
lipids in controls. E2-induced hypertriglyceridemia is mainly caused by an increase in the concentration of very low density lipoproteins (VLDL)
during both the postprandial period (6 times control level at 24 h) and during starvation (15 times control level at 96 h);
hyperlipoproteinemia lasts up to at least 7 d after the last feeding. E2 treatment does not change the concentration of high density lipoproteins, but does increase plasma concentrations of a very
high density lipoprotein, vitellogenin (VTG). In E2-treated VLDL, cholesteryl esters are depleted while proteins are enriched. During the postprandial phase, the apolipoprotein
(apo) profile of VLDL (d< 1.015 g/mL) is comparable in E2-treated and control trout. Starvation of E2-treated trout is accompanied by an enrichment in apo B240, A-I and A-II. The secretion levels of TG and VLDL-TG, as determinedin vivo, by injecting Triton WR-1339 to starving animals, are significantly higher in E2-treated trout than in controls. In trout, as in chicks, E2 administration significantly increases the concentration and hepatic secretion of plasma VLDL independent of the nutritional
status and the appearance of VTG in the plasma. This suggests the existence of similar mechanisms for the regulation of lipoprotein
metabolism by estrogens in oviparous vertebrates. 相似文献
6.
Effect of chronic glucagon administration on lipoprotein composition in normally fed,fasted and cholesterol-fed rats 总被引:2,自引:0,他引:2
Catherine Guettet Najmuddin Rostaqui Denis Mathe Bernard Lecuyer Nicole Navarro Bernard Jacotot 《Lipids》1991,26(6):451-458
Male adult Wistar rats received daily (at 9 a.m. and 5 p.m.) 10 μg of zinc-protamine glucagon by subcutaneous injection for
8 days. Plasma cholesterol levels were decreased by 36% in fed rats, 33% in cholesterol-fed rats and by 55% in fasted rats.
Lipoproteins were separated into 22 fractions by ultracentrifugation using a density gradient. Glucagon administration decreased
the cholesterol content in all lipoproteins except low density lipoprotein (LDL1) (1.006–1.040) and very low density lipoprotein (VLDL) from cholesterol-fed rats. The main decrease (−57 to −81%) was observed
in 1.050–1.100 g/mL lipoproteins (LDL2 and HDL2), which contained a large amount of apo E, while HDL3 cholesterol was not affected. Triacylglycerol levels were decreased only in chylomicrons and VLDL (−70%) of fed and cholesterol-fed
rats, while plasma and lipoprotein triacylglycerol levels were not changed in fasted rats treated with glucagon. In normally
fed rats glucagon administration increased by 42% the fractional catabolic rate of [125I]HDL2 while the absolute catabolic rate appeared to be unchanged. Glucagon seems to be a potent hypolipidemic agent affecting mainly
the apo E-rich lipoproteins. Its chronic administration limits lipoprotein accumulation which occurs upon cholesterol feeding. 相似文献
7.
Maria Luz Fernandez A. Karin Conde Laura R. Ruiz Carlos Montano John Ebner Donald J. McNamara 《Lipids》1995,30(7):619-626
To test the effects of exchanging dietary complex and simple carbohydrate for fat calories on lipoprotein metabolism, guinea
pigs were fed two different fat/carbohydrate ratios: 2.5∶58% (w/w) or 25∶29% (w/w) with either sucrose or starch as the carbohydrate
source. Animals fed high-fat had higher plasma low-density lipoprotein (LDL) and hepatic cholesterol concentrations than animals
fed low-fat diets (P<0.01). The cholesteryl ester content per particle was higher, and the number of triacylglycerol (TAG) molecules was lower
in very low density lipoprotein (VLDL) and LDL from animals fed high-fat diets. Intake of high-fat/sucrose resulted in higher
plasma LDL concentrations than intake of high-fat/starch, and animals fed low-fat/starch had the highest plasma TAG concentrations
associated with VLDL particles containing more TAG molecules, as well as a TAG-enriched LDL. The activity of plasma lecithin
cholesteryl:acyl transferase (LCAT) was highest in animals fed high-fat/sucrose, and heart lipoprotein lipase (LPL) activity
was higher in animals fed high-fat diets. Hepatic apoprotein B/E (apo B/E) receptor number (Bmax) was increased 21% with low-fat diets (P<0.01). These results suggest that the hypercholesterolemia induced by high-fat and by sucrose intake are associated with
a higher plasma LCAT activity which results in a cholesteryl ester-enriched VLDL which, by the action of LPL, might be more
readily converted to LDL through the delipidation cascade leading to downregulation of hepatic apo B/E receptors. The hypertriglyceridemia
associated with low-fat intake may result from increased production of VLDL TAG, which would explain the increased TAG content
and the higher TAG/CE ratio of VLDL from animals fed the low-fat/starch diet. 相似文献
8.
Takahashi M Saibara T Nemoto Y Ono M Akisawa N Iwasaki S Toda K Ogawa Y Wakatsuki A Inagaki S Onishi S 《Lipids》2003,38(7):687-692
The unique inborn hypertriglyceridemia seen in FLS (fatty liver Shionogi) mice was relieved by the administration of purified
apolipoprotein (apo) C-II. Lipoprotein lipase (LPL) and its cofactor, apoC-II, play a pivotal role in VLDL metabolism. Therefore,
we investigated the genetic background involved in this hypertriglyceridemia. Plasma levels of TG and total cholesterol as
well as LPL activity were measured in male FLS mice and C57/BL6J mice. Agarose gel electrophoresis and fast protein liquid
chromatography were used to analyze the lipoprotein profile. A cross experiment was done to determine the genetic background
of hypertriglyceridemia observed in FLS mice. cDNA sequences of apoC-II and apoC-III of FLS mice were determined. Preα-lipoprotein
was the predominant lipoprotein class in FLS mouse plasma. LPL activity remained in the range observed in C57/BL6J mice, and
purified apoC-II transiently relieved FLS mice from hypertriglyceridemia. Preα-lipoproteinemia was inherited in an autosomal
recessive manner. ApoC-III appeared to be a causal factor for this unique hypertriglyceridemia. Microsatellite analysis, however,
revealed that the responsible chromosome was not 7; rather, apoC-III mapped onto chromosome 9. Therefore, we suggest apoC-III
as a candidate causative factor for the hypertriglyceridemia observed in FLS mice because an excessive amount of apoC-III
attenuates LPL activity in vivo and in vitro. 相似文献
9.
Postprandial triglyceride-rich lipoproteins (TRL) levels are a predictor for coronary atherosclerosis. The aim of the study was to compare fasting high density lipoprotein (HDL) cholesterol, plasma lipoprotein lipase (LPL) activity, and postprandial TRL between elderly survivors of myocardial infarction (MI) and healthy controls. A case-control study was performed in 44 elderly patients 65-85 years of age with a previous history of MI and 43 age- and sex-matched healthy controls. Each participant underwent physical examination and was given a standard oral fat load with subsequent blood sampling over the next 8 h. Total and chylomicron triglycerides were assessed by area under the curve (AUC), incremental are under the curve (AUCi) and triglyceride response (TGR). Elderly MI patients had significantly lower postheparin LPL activity (87.4 +/- 36.9 mU/ml) (mean +/- 1 SD) than healthy controls (106.0 +/- 29.0 mU/ml) (P = 0.014). Decreased postheparin LPL activity was accompanied by significant increased and delayed clearance of postprandial TRL. Fasting HDL cholesterol was significantly lower in elderly MI patients than controls (1.45 +/- 0.32 and 1.66 +/- 0.47 mmol/l, respectively, P = 0.048). Multiple regression analysis revealed postheparin LPL activity as an independent predictor for postprandial TRL and fasting HDL cholesterol. Logistic regressions analysis revealed HDL cholesterol, triglycerides measured 2 h after the oral fat load, and postheparin LPL activity as independent predictors for MI. Our findings indicate that decreased fasting HDL cholesterol is associated with increased postprandial triglyceridemia which could be a target for life-style and therapeutic interventions in patients at risk for cardiovascular disease. 相似文献
10.
E. Gerasimova N. Perova I. Ozerova V. Polessky V. Metelskaya I. Sherbakova M. Levachev S. Kulakova Yu. Nikitin T. Astakhova 《Lipids》1991,26(4):261-265
Native Chukot Peninsula residents, in contrast to Muscovites, consume a diet rich in n−3 polyunsaturated fatty acids. This
dietary peculiarity is reflected in differences in plasma lipid and apolipoprotein contents. The Chukot residents have lower
contents of total cholesterol, triglyceride, LDL (low density lipoprotein) cholesterol and apolipoprotein B, but higher HDL
(high density lipoprotein) cholesterol levels than do Muscovites. The apolipoprotein A-I levels were identical in both groups.
A higher HDL cholesterol to apolipoprotein A-I ratio was determined in the coastline Chukot residents (0.52±0.01) than in
Muscovites (0.43±0.01; p<0.01). In contrast to Muscovites, the coastline Chukot residents also had higher n−3 and lower n−6
polyunsaturated fatty acid percentages in plasma and erythrocyte lipids, and lower phosphatidylcholine and higher sphingomyelin
or phosphatidylethanolamine levels in HDL2b and HDL3. The higher HDL cholesterol levels in the plasma of the coastline Chukot residents appears to reflect the higher cholesterol-scavenging
capacity of their HDL.
We conclude from this study that the regular consumption of dietary n−3 polyunsaturated fatty acids by the coastline Chukot
residents decreased LDL cholesterol transfer from plasma to peripheral cells, and enhanced cholesterol efflux from cellular
membranes toward HDL. 相似文献
11.
William R. Hazzard Patricia W. Wahl Claude Gagne Deborah Applebaum-Bowden G. Russell Warnick John J. Albers 《Lipids》1984,19(2):73-79
The responses of 14 hyperlipidemic subjects to 4 hypolipidemic agents were compared by measureing cholesterol and triglyceride
in whole plasma, very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL)
monthly for 2 months before and 3 months during treatment with each of 4 drugs: clofibrate, 2 g/d; colestipol, 20 g/d; para-aminosalicylic
acid-ascorbate (PAS-C), 6–8 g/d; and oxandrolone, 7.5 mg/d. Lipid responses proved to be stable by the first monthly evaluation
both off and on each drug. Mean adherence was high and similar for all agents (81–92% of the prescribed dose). Clofibrate
was associated with significant decreases in mean plasma cholesterol (−16%, p<.01), plasma triglyceride (−51%, p<.005), VLDL-cholesterol
(−61%, p<.005) and VLDL-triglyceride (−61%, P<.005), while HDL cholesterol increased (+20%, p<.01), and the LDL-cholesterol/HDL
ratio declined (−24%, p<.05). Colestipol was associated with decreases in mean plasma cholesterol (−15%, p<.01) and LDL-cholesterol
(−22%, p<.05), while VLDL-triglyceride increased (+41%, p<.05), and the LDL-cholesterol/HDL-cholesterol ratio declined (−25%,
p<.05). PAS-C was associated with decreases in VLDL-cholesterol (−30%, p<.05), and VLDL-triglyceride (−29%, p<.05), while
the LDL-cholesterol/HDL-cholesterol ratio remained unchanged. Oxandrolone was associated with increases in mean plasma cholesterol
(+7%, p<.05), LDL-cholesterol (+45%, p<.005 [+25% excluding one subject who increased 298%]), and LDL-triglyceride (+24%,
p<.01), while decreases occurred in plasma triglyceride (−31%, p<.05), VLDL-cholesterol (−26%, p<.05), VLDL-triglyceride (−42%,
p<.005), HDL-cholesterol (−45%, p<.005), and HDL-triglyceride (−43%, p<.01). The mean LDL-cholesterol/HDL-cholesterol ratio
increased by 109% (p<.005), reflecting the reciprocal changes in LDL and HDL. Thus, while both clofibrate and colestipol were
associated with significant, equivalent reductions in theoretical atherogenic risk, oxandrolone produced a net effect that
was not only adverse but 4 times that magnitude, suggesting caution in its long-term use, even for the management of hypertriglyceridemia.
William R. Hazzard was an investigator of the Howard Hughes Medical Institute during the course of this study
Claude Gagne was a research fellow of the Medical Research Council of Canada during the course of this study.
John J. Albers is an established investigator of the American Heart Association. of this study 相似文献
12.
Plasma kinetic behavior in hyperlipidemic subjects of a lipidic microemulsion that binds to low density lipoprotein receptors 总被引:2,自引:2,他引:2
Raul C. Maranhão Ivete A. Roland Odaly Toffoletto José Antonio Ramires Romélia P. Gonçalves Carlos H. Mesquita Fulvio Pileggi 《Lipids》1997,32(6):627-633
It was previously reported that a protein-free microemulsion (LDE) with structure roughly resembling that of the lipid portion
of low density lipoprotein (LDL) was presumably taken up by LDL receptors when injected into the bloodstream. In contact with
plasma, LDE acquires apolipoproteins (apo) including apo E that would be the ligand for receptor binding. Currently, apo were
associated to LDE by incubation with high density lipoprotein (HDL). LDE-apo uptake by mononuclear cells showed a saturation
kinetics, with an apparent K
m of 13.1 ng protein/mL. LDE-apo is able to displace LDL uptake by mononuclear cells with a K
i of 11.5 ng protein/mL. LDE without apo is, however, unable to displace LDL. The uptake of 14C-HDL is not dislocated by increasing amounts of LDE-apo, indicating that HDL and LDE-apo do not bind to the same receptor
sites. In human hyperlipidemias, LDE labeled with 14C-cholesteryl ester behaved kinetically as expected for native LDL. LDE plasma disappearance curve obtained from eight hypercholesterolemic
patients was markedly slower than that from 10 control normolipidemic subjects [fractional clearance rate (FCR)=0.02±0.01
and 0.12±0.04 h−1, respectively; P<0.0001]. On the other hand, in four severely hypertriglyceridemic patients, LDE FCR was not significantly different from
the controls (0.07±0.03 h−1). These results suggest that LDE can be a useful device to study lipoprotein metabolism. 相似文献
13.
This experiment was designed to evaluate the effects of dietary red wine phenolic compounds (WP) and cholesterol on lipid
oxidation and transport in rats. For 5 wk, weanling rats were fed polyunsaturated fat diets (n−6/n−3=6.4) supplemented or
not supplemented with either 3 g/kg diet of cholesterol, 5 g/kg diet of WP, or both. The concentrations of triacylglycerols
(TAG, P<0.01) and cholesterol (P<0.0002) were reduced in fasting plasma of rats fed cholesterol despite the cholesterol enrichment of very low density lipoprotein
+ low density lipoprotein (VLDL+LDL). The response was due to the much lower plasma concentration of high density lipoprotein
(HDL) (−35%, P<0.0001). In contrast, TAG and cholesteryl ester (CE) accumulated in liver (+120 and +450%, respectively, P<0.0001). However, the cholesterol content of liver microsomes was not affected. Dietary cholesterol altered the distribution
of fatty acids mainly by reducing the ratio of arachidonic acid to linoleic acid (P<0.0001) in plasma VLDL+LDL (−35%) and HDL (−42%) and in liver TAG (−42%), CE (−78%), and phospholipids (−28%). Dietary WP
had little or no effect on these variables. On the other hand, dietary cholesterol lowered the α-tocopherol concentration
in VLDL+LDL (−40%, P<0.003) and in microsomes (−60%, P<0.0001). In contrast, dietary WP increased the concentration in microsomes (+21%, P<0.0001), but had no effect on the concentration in VLDL+LDL. Cholesterol feeding decreased (P<0.006) whereas WP feeding increased (P<0.0001) the resistance of VLDL+LDL to copper-induced oxidation. The production of conjugated dienes after 25 h of oxidation
ranged between 650 (WP without cholesterol) and 2,560 (cholesterol without WP) μmol/g VLDL+LDL protein. These findings show
that dietary WP were absorbed at sufficient levels to contribute to the protection of polyunsaturated fatty acids in plasma
and membranes. They could also reduce the consumption of α-tocopherol and endogenous antioxidants. The responses suggest that,
in humans, these substances may be beneficial by reducing the deleterious effects of a dietary overload of cholesterol. 相似文献
14.
The content and structure of glycosphingolipids (GSL) in human plasma lipoproteins were studies. The quantitative distribution
of the neutral GSL(Glc-Cer, Gal-Glc-Cer, Gal-Gal-Glc-Cer, and GalNAc-Gal-Gal-Glc-Cer) and the principal ganglioside (AcNeu-Gal-Glc-Cer)
within the different lipoprotein classes was similar to that of whole plasma. The total amounts (μmol glucose/100 ml plasma)
of GSL in the plasma lipoproteins of three normal subjects were VLDL (very low density lipoproteins) (trace to 0.46), LDL
(low density lipoproteins) (1.08–1.48), HDL2 (high density lipoproteins2) (0.62–0.85), and HDL3 (high density lipoproteins3) (trace to 0.28). In subjects with Lp(a) lipoproteins, HDL2 rather than HDL3 contained most of the GSL in HDL. When the data were corrected for differences in the plasma concentrations of the lipoproteins,
the total amounts of GSL(nmol glucose/mg lipoprotein cholesterol) were VLDL(trace to 21.20), LDL(11.70–15.36), HDL2(8.50–9.10), and HDL3(3.12). No GSL were detected in lipoprotein deficient plasma. Mass spectrometry of the trimethylsilyl derivatives of the GSL
in LDL showed major fragment ions characteristic of their individual structural components. The elevated plasma levels of
the GSL(2–18 fold), in a homozygote for familial hypercholesterolemia, resided in LDL which contained an absolute increase
(per mg lipoprotein cholesterol) of GSL. Most, if not all, of the plasma GSL are associated with plasma lipoproteins and may
have an important role in their biological functions. 相似文献
15.
The net transfer of labeled α-tocopherol from donor to acceptor lipoproteins at physiological concentrations was investigated.
Labeled lipoproteins were isolated i) followingin vitro addition of [3,4-3H]all rac-α-tocopherol to plasma, or ii) from plasma obtained 12–16 h after ingestion by normal subjects of an oral dose (100 mg each)
of 2R,4′R,8′R-α-[5,7-(C2H3)2]tocopheryl acetate and 2S,4′R′,R-α-[5-C2H3]tocopheryl acetate. A constant amount (on a protein basis) of labeled lipoprotein was incubated with an increasing amount
of unlabeled acceptor lipoprotein for 2 h at 37°C. No discrimination between stereoisomers of α-tocopherol was detected. Labeled
VLDL and labeled LDL (very low and low density lipoproteins, respectively) tended to retain their labeled tocopherol. Labeled
high density lipoproteins (HDL) readily transferred the labeled tocopherol to VLDL (>60% transferred), while the transfer
to LDL was dependent upon the ratio of labeled HDL/LDL with a lower net transfer at higher ratios. This dependency of the
distribution of tocopherol upon the ratio of HDL/LDL was also observedin vivo. The tocopherol/mg HDL protein was measured in 11 subjects with varying HDL levels. As the %HDL in the plasma increased from
14 to 50%, the tocopherol/HDL protein also increased (r2=0.37,P<0.05). 相似文献
16.
High performance liquid chromatography with gel exclusion columns was used for quantitative measurement of plasma lipoproteins.
A combination of columns TKS 4000 PW and 3000 PW gave good separation of very low (VLDL), low (LDL) and high (HDL) density
lipoproteins. The area under each lipoprotein peak detected by absorbance at 280 nm was measured by digitizing and was expressed
as cm2. Purified lipoprotein standards isolated by ultracentrifugation were also chromatographed in increasing concentrations. The
area under the lipoprotein standard peak was linearly related to the amount of total protein over a wide range. The areas
of most of the measured plasma lipoproteins were within the linear range. The relationship between the area and the amount
of protein for each standard was used to quantitate the amount of protein and was expressed as mg/dl plasma. This technique
is simple and requires a small amount of plasma. The validated technique was applied to a large population of pedigreed baboons.
An average plasma lipoprotein profile of feral baboons on the chow diet was characterized by a high level of HDL (90.9±30.7
mg/dl) with a lesser amount of LDL (29.1±13.2 mg/dl). VLDL was present in much lower concentration (8.6±2.6 mg/dl). Feeding
a high cholesterol and high saturated fat (HCHF) diet raised both LDL (1.5-fold) and HDL levels (1.3-fold) without changing
VLDL levels. Progeny of sires with low response to dietary cholesterol increased their HDL protein when challenged with HCHF
diet without any change in their LDL or VLDL. Progeny of high-responding sires, however, had increases in both their HDL and
LDL levels when challenged with HCHF diet. The survey of lipoprotein profiles of the pedigreed baboon colony disclosed a number
of animals with interesting and unusual lipoprotein patterns. 相似文献
17.
The effect of estrogen on compositional changes, apolipoprotein (apo) A-I metabolism and the morphology of plasma high density lipoprotein (HDL) were investigated in chicks. The administration of 17β-estradiol (25 mg/kg body weight) to growing male chicks (8-week-old) markedly reduced the concentrations of plasma HDL components, except for triglyceride (TG). At the same time, levels of TG, total cholesterol (TC) and phospholipid (PL) in plasma were greatly elevated. The respective values for TG, TC, PL and protein in HDL were 13.9, 89.3, 154.1 and 231.7 (mg/dL) in the control, and 39.0, 35.1, 113.8 and 160.0 (mg/dL) in chicks upon estrogen treatment for one day.In vivo kinetic studies showed that the fractional catabolic rate of HDL apo A-I was significantly higher (p<0.05) in estrogen-treated chicks than in control birds, indicating an increased efficiency of HDL removal in the former. The production rate of HDL apo A-I also was significantly lower (p<0.05) in estrogen-treated chicks. Sodium dodecyl sulfate-acrylamide gel electrophoresis followed by laser scanning densitometry of HDL apolipoproteins in estrogen-treated chicks revealed a reduction of apo A-I and the occurrence of new apolipoproteins which had been absent in HDL of untreated birds. The HDL particles showed that the mean particle size of HDL became larger upon estrogen treatment. Particles with diameters between 70 and 123 Å were predominant in HDL of control chicks, while particles with diameters between 97 and 143 Å were most abundant in HDL of estrogen-treated chicks. 相似文献
18.
The metabolic fate of high density lipoprotein (HDL) sphingomyelin in plasma was studied in rats over a 24-hr period after
injection of HDL containing sphingomyelin which was14C-labeled in the stearic (18∶0) or lignoceric acid (24∶0) moiety and3H-labeled in the choline methyl groups. Decay of label in plasma followed three phases. The first two phases were similar
for both isotopes and both types of sphingomyelin (t1/2≃10 and 110 min). However, during the third phase (from 10 hr after injection),3H label disappeared more slowly than14C label from 18∶0 sphingomyelin, whereas the3H/14C ratio remained relatively constant when 24∶0 sphingomyelin was used. Intact, doubly-labeled 18∶0 sphingomyelin disappeared
from HDL rapidly (t1/2=38 min) by tissue uptake and by transfer to very low density lipoprotein (VLDL). VLDL contained up to 12% of the sphingomyelin
1 hr after injection. This is the first demonstration of a transferin vivo of sphingomyelin from HDL to VLDL. A similarly rapid transfer was also observedin vitro. Some nontritated, [14C]18∶0 or [14C]24∶0 sphingomyelin was redistributed more slowly into HDL. Doubly-labeled phosphatidylcholine appeared in VLDL and HDL within
1 hr after injection and reached 1.8 and 2.1% of the injected14C and3H in VLDL at 1 hr, and 4.8 and 6.9% in HDL at 3 hr, respectively. 相似文献
19.
The triacylglycerol (TG) analog 1,3-dioctadecenoyl-2-hexadecyl glycerol was used in the study of the transport of dietary
lipids by lipoprotein fractions of rat intestinal lymph. 1,3-Diacyl-2-alkyl glycerols (DAG) are hydrolyzed by pancreatic lipase
to form 2-alkyl glycerols and free fatty acids. These hydrolysis products are then absorbed, and DAG are resynthesized within
the intestinal mucosa. Intestinal lymph of rats was collected following intragastric administration of 1,3-dioctadecenoyl-2-hexadecyl
glycerol. The DAG to TG ratios in very low density lipoprotein (VLDL) and chylomicron fractions were determined as a measure
of the incorporation of lipid of dietary origin. The ratio of DAG to TG in the VLDL-2 (Sf 12–100) fraction ranged from0.06 to 0.56 indicating a significant amount of DAG transported relative to TG. The glyceryl
ether to TG ratio increased with mean lipoprotein volume from the VLDL-2 fraction to the chylomicron (Sf>400) fraction. The correlation between glyceryl ether to TG ratio and average volume and between the amount of DAG per ml
of original lymph and average volume within the chylomicron fraction was 0.99. Thus, the amount of dietary fat transported
was correlated with the size of the chylomicrons produced. The glyceryl ether to TG ratio was positively correlated with the
average volume of the lipoprotein fractions isolated (chylomicrons, chylomicron rich (Sf>100), VLDL-1 (Sf 100–400) and VLDL-2) (r=0.87). These results suggest that the size of the lipoproteins produced by the intestine is determined
by the amount of fat available for transport and that particles of larger diameter are formed by the addition of lipid of
dietary origin to existing VLDL.
Scientific contribution no. 702, Agricultural Experiment Station, University of Connecticut, Storrs, Connecticut 06268 相似文献
20.
Serum cholesterol precursor sterols reflect the activity of cholesterol synthesis. In this study, squalene, methyl sterol
and lathosterol contents were studied in very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density
lipoprotein (HDL) of heterozygous familial hypercholesterolemia patients without and with ileal bypass. The contents of lathosterol
and all methyl sterols (lanosterol, Δ8,24-dimethylsterol, Δ8-dimetylsterol, Δ8-methostenol and methostenol), but not of squalene were increased in all lipoproteins by ileal bypass. The increase in the
free methyl sterols was more marked than that in the esterified ones. The percentage esterification of the methyl sterols
was highest in HDL and lowest in VLDL. Lipoprotein methyl sterol contents were positively correlated with each other and with
cholesterol synthesis. The methyl sterols were slightly concentrated in LDL, and squalene strongly concentrated in VLDL. It
is concluded that long-term stimulation of cholesterol synthesis increases the methyl sterols in all lipoproteins. 相似文献