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1.
The activities of lipoprotein lipase in postheparin plasma, retroperitoneal adipose and gastrocnemius muscle tissues were
determined in the rats fed 2.8 ppm of dietary zinc for eight weeks, as compared with pair-fed and ad libitumfed rats given
30.8 ppm of zinc. The postheparin lipoprotein lipase activity, as determined by using a lipid emulsion labeled with [3H]triolein as the substrate, was significantly lower in the first group of rats, relative to that in the second and third
groups. Tissue lipoprotein lipase activities were compared using the lipid emulsion and activator serum obtained from the
zinc-deficient rats and the ad libitum-fed rats. The activator sera were devoid of very low density and low density lipoproteins,
but enriched in high density lipoproteins. Muscle lipoprotein lipase activities were significantly lower when assayed with
the activator serum from the zinc-deficient compared with the activities determined with the activator serum from the ad libitum-fed.
Similarly, muscle lipoprotein lipase activities were lower in all groups when [3H]-triolein-labeled chylomicrons from the zinc-deficient were used as the substrate, compared with the activities determined
using the chylomicrons from the ad libitum-fed. Lipoprotein lipase activities in the adipose tissues were not affected by
the different sources of the activator sera and chylomicrons. The results strongly suggest that the decrease in postheparin
lipoprotein lipase activity in zinc deficiency is not due to changes in tissue lipoprotein lipase enzyme per se, but to compositional
alterations in with regard to C apolipoproteins, modulators of lipoprotein lipase activity.
Presented in abstract form at the 71st annual meeting of the Federation of American Societies for Experimental Biology.Fed. Proc. 46:1472, 1987. 相似文献
2.
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. 相似文献
3.
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
4.
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. 相似文献
5.
Marine lipid-based liposomes increase <Emphasis Type="Italic">in vivo</Emphasis> FA bioavailability 总被引:1,自引:0,他引:1
Liposomes made from an extract of natural marine lipids and containing a high n-3 PUFA lipid ratio were envisaged as oral
route vectors for FA supplements in order to increase PUFA bioavailability. The absorption of FA in thoracic lymph duct-cannulated
rats, after intragastric feeding of dietary fats in the form of liposomes or fish oil, was compared. Lipid and FA analyses
were also performed on feces. Five mole percent α-tocopherol was added to fish oil and incorporated into the liposome membrane.
The influence of α-tocopherol on FA lymph recovery was also investigated. In vivo, FA absorption in rats was favored by liposomes (98±1%) compared to fish oil (73±6%). In the same way, the DHA proportion
in lymph was higher after liposome ingestion (78%) than after fish oil ingestion (47%). However, phospholipid (PL) concentration
in lymph was not affected by the kind of dietary fat ingested, suggesting a PL regulation due to de novo TAG synthesis. The influence of the intramolecular distribution of n-3 PUFA in dietary lipids (TAG and PL) on the intramolecular
FA distribution in TAG of chylomicrons was also investigated. The results obtained showed that the distribution of n-3 PUFA
esterified on the sn-2 of chylomicron TAG depended on the lipid source administered. All these results correlated, at least partly, with in vitro liposome behavior under conditions that mimic those of the gastrointestinal tract. As a whole, this study pointed out that
marine PL may constitute an attractive material for the development of liposomes as oral PUFA supplements. 相似文献
6.
Absorption of dietary cholesterol oxidation products and incorporation into rat lymph chylomicrons 总被引:1,自引:0,他引:1
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. 相似文献
7.
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. 相似文献
8.
The effect of zinc deficiency on the levels of n−6 and n−3 polyunsaturated fatty acids (PUFA) in lipids from tissues of rats
fed a diet containing linseed oil was investigated. Rats were fed either a control diet (25 mg Zn/kg) or a zinc-deficient
diet (0.8 mg Zn/kg) for 10 d. To avoid energy and nutrient deficiency, 11.6 g of diet per day was administered by gastric
tube. At the end of the experiment, rats fed the zinc-deficient diet had drastically reduced plasma zinc concentration and
alkaline phosphatase activity consistent with severe zinc deficiency in these rats. Zinc-deficient rats had higher levels
of n−3 PUFA, in particular eicosapentaenoic acid (EPA), and lower levels of n−6 PUFA, in particular linoleic acid, in liver
and plasma phosphatidylcholine (PC) and in erythrocyte membrane total lipids than did control rats. By contrast, the levels
of n−3 PUFA in PC from testes and heart, and in phosphatidylethanolamine (PE) from liver, testes and heart, were only slightly
different between zinc-deficient and control rats. The study suggests that desaturation of α-linolenic acid is not inhibited
by zinc deficiency, and that in zinc-deficient rats, n−3 PUFA preferentially incorporated into phospholipids at the expense
of n−6 PUFA, especially EPA into PC. The study also shows that the effect of zinc deficiency on PUFA levels is different for
PC and PE in rat tissues. 相似文献
9.
14C-Palmitate (16∶0) and3H-oleate (18∶1) were infused into unanesthetized dogs for 90 min. Lipid and isotopic analyses were then performed on the left
ventricular outer and inner walls. Average values in μmoles per gram wet weight tissue for both outer wall trigly ceride (TG)
(7.0±2.6 (S.E.)) and phospholipid (PL) (17.3±2.4) were higher then the inner wall TG (1.4±0.3) and PL (12.0±2.4). TG fatty
acid distribution was similar in the outer and inner myocardium. Thus those factors regulating incorporation of various fatty
acids may operate at comparable rates in both heart segments. The same observation and relationship was observed for PL, but
the two classes had markedly different fatty acid spectra. The transmural gradients for these classes may be related to relatively
hypoxic conditions in the inner wall. Uniform14C DPM concentrations were found in both TG and PL of the outer and inner myocardium. A similar distribution pattern was found
for3H. This may indicate that an individual species of plasma free fatty acid (FFA) undergoes uniform initial incorporation into
TG and PL despite the existence of transmural gradients and fatty acid distribution differences. The mean outer and inner
wall TG and PL3H to14C DPM concentration ratio (range of 3.9 to 4.8) was similar to a calculated plasma3H-18∶1 to14C-16∶0 specific activity ratio of 4.23. This indicates that net incorporation of fatty acids into TG and PL over 90 min was
proportional to their plasma FFA concentrations, rather than to endogenous tissue lipid concentrations. The lipid gradients
and fatty acid spectrum differences observed may thus be caused by recycling and catabolic pathways rather than to direct
control of plasma FFA entry into TG and PL.
The research presented here was performed in partial fulfillment of the requirements for the M.Sc. degree in Physiology at
Hahnemann Medical College by J.S. Steinberg.
Two abstracts related to this study were published previously (1,2) 相似文献
10.
Effects of dietary triacylglycerol structure on triacylglycerols of resultant chylomicrons from fish oil- and seal oil-fed rats 总被引:3,自引:0,他引:3
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). 相似文献
11.
Isabel S. Chen Truc Le Satchithanandam Subramanian Marie M. Cassidy Alan J. Sheppard George V. Vahouny 《Lipids》1987,22(5):318-321
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. 相似文献
12.
Helvi M. Vidgren Anne M. Louheranta Jyrki J. Ågren Ursula S. Schwab Matti I. J. Uusitupa 《Lipids》1998,33(10):955-962
Trans fatty acids may be involved in atherosclerotic vascular diseases. We investigated the incorporation of dietary trans fatty acids and oleic acid into the serum triglycerides (TG), cholesterol esters (CE), and phospholipids (PL). Fourteen healthy
female volunteers, aged 23.2±3.1 yr (mean±SD), body mass index 20.8±2.1 kg/m2 participated in this study. All subjects consumed both a trans fatty acid-enriched diet (TRANS diet) and an oleic acid-enriched diet (OLEIC diet) for 4 wk according to a randomized crossover
design. Both experimental diet periods were preceded by consumption of a baseline diet for 2 wk which supplied 37% of total
energy (E%) as fat: 18 E% from saturated fatty acids (SFA), 12 E% from monounsaturated fatty acids, and 6 E% from polyunsaturated
fatty acids. Five E% of the SFA in the baseline diet was replaced by trans fatty acids (18∶1 t and 18∶2 c,t+18∶2t,t, where c is cis and t is trans) in the TRANS diet and by oleic acid (18∶1n-9) in the OLEIC diet. After the TRANS diet, the proportions of 18∶1t and 18∶2t increased (P <0.001) in all serum lipid fractions analyzed. The increase of 18∶1 t in TG and PL (1.80±0.28 vs. 5.26±1.40; 1.07±0.34 vs. 3.39±0.76 mol% of total fatty acids, respectively) was markedly higher
than that in CE (0.44±0.07 vs. 0.92±0.26), whereas that of 18∶2t was nearly the same in all three fractions. The proportions of palmitic, stearic, arachidonic, and eicosapentaenoic acids
in TG, CE, and PL and that of oleic acid in TG and CE were decreased when compared with the baseline value. In contrast, the
proportion of palmitoleic acid in TG and PL and that of linoleic acid in PL increased on the TRANS diet. After consumption
of the OLEIC diet, the proportion of oleic acid increased in all three lipid fractions analyzed, and the percentage increase
was nearly the same in all fractions. In contrast, the proportions of 18∶1 t in TG and PL and 18∶2 t in TG and CE decreased when compared with the baseline value. In conclusion, a moderate increase in dietary trans fatty acids resulted in a marked incorporation into serum lipids and decreased the conversion of linoleic acid to its more
unsaturated long-chain metabolites. Analysis of 18∶1 t from serum TG and PL seems to reflect reliably the dietary intake of this fatty acid. 相似文献
13.
There have been a limited number of studies investigating surfactant lipid changes in lung with trace elements. The present
investigation was designed to examine the effect of moderate zinc deficiency on the lipid metabolism in rat lung. We also
evaluated whether zinc deficiency, which is a wide-spread problem, could play a role in adult respiratory distress syndrome
(ARDS). For that purpose, adult male Wistar rats were fed two diets differing in zinc concentration. The rats were divided
into two groups. One group was fed a zinc-deficient diet containing 3 mg Zn/kg, and the other group received a zincadequate
control diet with 30 mg Zn/kg according to AIN 93-M. After 2 mon of treatment, we observed that in the zinc-deficient group
(i) total lipids, phospholipids, and cholesterol increased whereas TG decreased in whole lung; (ii) phospholipid (PC) concentration
increased in lamellar bodies and alveolar macrophages and decreased in extracellular surfactant but did not change in microsomes;
(iii) protein concentration decreased in whole lung, extracellular surfactant, lamellar bodies, and macrophages; (iv) the
incorporation of [Me-14C]choline into PC (phospholipids) of lung slices increased; and (v) the activity of CTP/phosphocholine cytidylyltransferase
bound to the microsomes increased in the lung. These results suggest that the lipid concentration in the lung (especially
the phospholipids) is modified directly or indirectly by a zinc-deficient diet. In a zincdeficient diet, the lung changes
the pattern of PC for an adaptive or recovery stage. Therefore, zinc deficiency implications are important for the design
of therapies and public health interventions involving targeted zinc supplementation for high-risk groups or groups with certain
diseases, such as ARDS. 相似文献
14.
Male rats were fed 100 nM dichlorodiphenyltrichloroethane-14C in oil by gastric tube. Recovery of dichlorodiphenyltrichloroethane-14C in thoracic duct lymph was 60% in 12 hr. Lymph dichlorodiphenyltrichloroethane-14C (97%) occurred in lipoproteins of d<1.006, designated chylomicrons. Mechanical separation of chylomicron triglyceride core
(labeled with triglyceride-3H) from chylomicron membrane (labeled with phospholipid-32P) showed that 97% dichlorodiphenyltrichloroethane-14C was present in triglyceride core. To investigate possible association of plasma clearance of the two core lipids, rats were
pulse injected with chylomicrons, doubly labeled with triglyceride-3H and dichlorodiphenyltrichloroethane-14C. The decay of dichlorodiphenyltrichloroethane-14C in sequential serum samples was rapid (T1/2=2 min) and was independent of triglyceride-3H decay. In tissues removed 14 min after injection of chylomicrons, 30% administered dichlorodiphenyltrichloroethane-14C was found in liver but only 1% in adipose tissue. In hepatectomized (eviscerated) rats, the decay of serum dichlorodiphenyltrichloroethane-14C (T1/2=10 min) was also independent of and more rapid than triglyceride-3H decay. With sucrose density gradients, it was shown that chylomicron dichlorodiphenyltrichloroethane-14C transferred to higher density serum proteins in vitro and in vivo and to bovine albumin in vitro. Thus, dichlorodiphenyltrichloroethane
was transported from intestine largely in the triglyderide phase of chylomicrons; disappearance of chylomicron-dichlorodiphenyltrichloroethane
from the systemic circulation was rapid and partly independent of the presence of the liver and of triglyceride hydrolysis;
some dichlorodiphenyltrichloroethane was transported from serum chylomicrons to albumin or other plasma proteins before tissue
uptake. 相似文献
15.
Insulin-resistant muscle tissue contains low proportions of arachidonic acid (AA), and increased proportions of muscle AA
correlate with improved insulin sensitivity. Dehydroepiandrosterone (DHEA) and AA, like the thiazolidinedione drugs that decrease
insulin resistance (IR), are peroxisome proliferators. Long-chain fatty acids (FA) have been named the “one true” endogenous
ligand for activating the peroxisome proliferator-activator receptor (PPAR), and DHEA has been named a “good candidate” as
a naturally occurring indirect activator of PPAR. This study was conducted to determine DHEA’s effects on lipid profiles of
skeletal and cardiac muscle in lean and obese Zucker rats (ZR), a model of IR, type 2 diabetes mellitus, and obesity. We hypothesize
that DHEA may alter long-chain FA profiles in muscle tissue of obese rats such that they more closely resemble that of the
lean. In our experiments we employed a DHEA and a pair-fed (PF) group (n=6) for 12 lean and 12 obese ZR. For 30 d, the diet of the two DHEA groups was supplemented with 0.6% DHEA; PF groups were
given the average daily calories consumed by their corresponding treatment group. Hearts and gastrocnemius muscles were assayed
for phospholipid (PL), free FA, and triglyceride (TG) FA profiles. The proportion of PL AA was significantly greater in both
muscle types of lean compared to obese rats. Hearts from both DHEA groups had greater PL proportions of AA and less oleic
(18∶1) acid than their PF controls. Likewise, 18∶1 proportions were significantly lower in the gastrocnemius; however, AA
proportions were not significantly different. Similar phenotypic profile differences were observed in the TG fraction of both
muscle types. There were no DHEA-related TG FA profile alterations. 相似文献
16.
Reportedly’ randomly rearranging the position of fatty acids (FA) in butterfat triacylglycerol (TAG) by interesterification’
thereby lowering the proportion of saturated FA in the sn-2 position’ reduces its hypercholesterolemic and hypertriglyceridemic properties when fed to humans. The aim of this work
was to determine if these reductions in plasma cholesterol and TAG could be explained by an improved rate of clearance from
the plasma of chylomicrons composed of randomized butterfat’ using a rat model. Acute chylomicron clearance studies demonstrated
no differences in fractional clearance rates of cholesteryl esters and TAG from the plasma of rats infused with chylomicrons
produced from gastric feeding of either native (NBF) or randomized (RBF) butterfat. Although there was a 14% decrease in the
level of saturated FA occupying the sn-2 position of TAG in RBF compared with NBF’ this difference became negligible (∼5%)’ following digestion of the fat and subsequent
repackaging of TAG into chylomicrons. These observations suggest that the previously observed reduction in hypercholesterolemic
properties of randomized butterfat in rat is unlikely to be explained by improved clearance of chylomicron TAG. 相似文献
17.
The effect of zinc deficiency on the Δ6-desaturation of [1-14C] linoleic acid was studied in mammary tissue microsomes from lactating rats. The rats were maintained on zinc-adequate (20
ppm zinc) or zinc-deficient (10 ppm zinc changing to 0.5 ppm zinc during last trimester) diets throughout gestation and for
the first 3 days of lactation. Mammary tissue microsomes were incubated with [1-14C] linoleic acid and other samples of mammary tissue, mammary milk and the milk in the stomachs of the pups were analyzed
for total fatty acid composition. In mammary microsomes from zinc-deficient rats, Δ6-desaturation of linoleic acid was 3.4 times greater than in microsomes from zinc-adequate rats. This change in metabolism
of linoleic acid was reflected by comparable changes in the relative tissue and milk composition of linoleic and arachidonic
acids and in the ratios of palmitic to palmitoleic acid, stearic to oleic acid and linoleic and arachidonic acid. 相似文献
18.
The mechanism for the increase in plasma cholesterol levels in cholesterol-fed rats following chylomicron transport was investigated
in intact animals, in isolated perfused liver, and in hepatocytes in monolayer cultures. Intravenous administration of egg
phosphatidylcholine in amounts greater than those required to cause a plasma cholesterol response when given as chylomicrons
was without effect. This makes it unlikely that increased plasma cholesterol levels resulted from the recruitment of tissue
cholesterol by the plasma chylomicron phospholipids that persisted in the plasma after triacylglycerol clearance. The hepatic
origin of the increased plasma cholesterol levels was directly confirmed by two hepatic perfusion experiments. When cholesterol-fed
rats received intravenous chylomicrons prior to isolated hepatic perfusion, more cholesterol was secreted by the liver than
when the rats were injected intravenously with buffer. Perfusion of apolipoprotein E (apo E)-rich triacylglycerol emulsions
through the livers also enhanced cholesterol secretion. The increase in hepatocyte cholesterol secretion seen with cholesterol-fed
rats was also noted in monolayer cultures following incubation with apo E rich-triacylglycerol emulsions. The apolipoprotein
or the emulsion alone, or apo E-rich phosphatidylcholine liposomes, had no effect. The data confirm previous indirect observations
that the liver is the source of cholesterol that appears in plasma following transport of chylomicrons or following a lipid-rich
meal in cholesterol-fed rats. The data also re-emphasize the importance of providing apo E with triacylglycerol emulsions
to initiate secretion of lower density lipoproteins by the liver. 相似文献
19.
Fourteen healthy male volunteers were given two separate high-saturated-fat meals with and without the addition of 4 g highly
purified ethyl esters of either eicosapentaenoic acid (EPA) (95% pure, n=7) or docosahexaenoic acid (DHA) (90% pure, n=7) supplied as 1-g capsules each containing 3.4 mg vitamin F. The chylomicrons were isolated 6 h after the meals, at peak concentrations
of n−3 fatty acids (FA). Addition of n−3 FA with the meal caused a 10.4-fold increase in the concentration of n−3 FA in chylomicrons
compared to the saturated fat meal without addition of n−3 FA. After the saturated-fat meal, the concentration of thiobarbituric
acid-reactive substances (TBARS) was 327.6±34.6 nmol/mmol triacylglycerol (TAG), which increased to 1015.8±212.0 nmol/mmol
TAG (P<0.0001, n=14) after EPA and DHA were added to the meal. There was no significant correlation between the concentrations of TBARS and
vitamin E in the chylomicrons collected 6 h after the test meal. The present findings demonstrate an immediate increase in
chylomicron peroxidation ex vivo provided by intake of highly purified n−3 FA. The capsular content of vitamin E was absorbed into chylomicrons, but the amount
of vitamin E was apparently not sufficient to protect chylomicrons against lipid peroxidation ex vivo. Daily intake of 4 g n−3 FA either as EPA or DHA for 5 wk did not change the plasma concentration of TBARS. Although not
significantly different between groups, DHA supplementation decreased total glutathione in plasma (P<0.05) and EPA supplementation increased plasma concentration of vitamin E (P<0.05). The other lipid-soluble and polar antioxidants in plasma remained unchanged during 5 wk of intervention with highly
purified n−3 FA. 相似文献
20.
In previous studies, zinc-deficient rats force-fed a diet with coconut oil as the major dietary fat developed a fatty liver,
whereas zinc-deficient rats force-fed a diet with linseed oil did not. The present study was conducted to elucidate the reason
for this phenomenon. In a bifactorial experiment, rats were fed zinc-adequate or zinc-deficient diets containing either a
mixture of coconut oil (70 g/kg) and safflower oil (10 g/kg) (“coconut oil diet”) or linseed oil (80 g/kg) (“linseed oil diet”)
as a source of dietary fat, and activities of lipogenic and glycolytic enzymes in liver were determined. In order to ensure
adequate food intake, all the rats were force-fed. Zinc-deficient rats on the coconut oil diet developed a fatty liver, characterized
by elevated levels of triglycerides with saturated and monounsaturated fatty acids. These rats also had markedly elevated
activities of the lipogenic enzymes acetyl-CoA carboxylase, fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH),
6-phosphogluconate dehydrogenase (6PGDH), and citrate cleavage enzyme, whereas activities of malic enzyme and glycolytic enzymes
were not different compared with zinc-adequate rats on the coconut oil diet. In contrast, rats receiving the linseed oil diet
had similar triglyceride concentrations regardless of zinc status, and activities of lipogenic enzymes and glycolytic enzymes
were not different between the two groups. Zinc-deficient rats fed either type of dietary fat exhibited statistically significant
correlations between activities of FAS, G6PDH, 6PGDH and concentrations of saturated and monounsaturated fatty acids in liver.
The concentrations of serum lipids were elevated in zinc-deficient rats fed either type of dietary fat. These results demonstrate
that fatty liver in zinc-deficient rats on the coconut oil diet is caused by elevated activities of lipogenic enzymes, and
not by disturbed lipid secretion from liver. Dietary linseed oil prevents both the elevation of lipogenic enzyme activity
and fatty liver in zinc-deficient rats. 相似文献