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1.
The influence of the linoleic acid levels of diets containing partially hydrogenated marine, oils (HMO) rich in isomeric 16∶1,
18∶1, 20∶1 and 22∶1 fatty acids on the fatty acid profiles of lipids from rat liver, heart and adipose tissue was examined.
Five groups of rats were fed diets containing 20 wt% fat−16% HMO+4% vegetable oils. In these diets, the linoleic acid contents
varied between 1.9% and 14.5% of the dietary fatty acids, whereas the contents oftrans fatty acids were 33% in all groups. A sixth group was fed a partially hydrogenated soybean oil (HSOY) diet containing 8%
linoleic acid plus 32%trans fatty acids, mainly 18∶1, and a seventh group, 20% palm oil (PALM), with 10% linoleic acid and notrans fatty acids.
As the level of linoleic acid in the HMO diets increased from 1.9% to 8.2%, the contents of (n−6) polyunsaturated fatty acids
(PUFA) in the phospholipids increased correspondingly. At this dietary level of linoleic acid, a plateau in (n−6) PUFA was
reached that was not affected by further increase in dietary 18∶2(n−6) up to 14.5%. Compared with the HSOY- or PALM-fed rats,
the plateau value of 20∶4(n−6) were considerably lower and the contents of 18∶2(n−6) higher in liver phosphatidylcholines
(PC) and heart PC. Heart phosphatidylethanolamines (PE) on the contrary, had elevated contents of 20∶4(n−6), but decreased
22∶5(n−6) compared with the PALM group.
All groups fed HMO had similar contents oftrans fatty acids, mainly 16∶1 and 18∶1, in their phospholipids, irrespective of the dietary 18∶2 levels, and these contents were
lower than in the HSOY group.
High levels of linoleic acid consistently found in triglycerides of liver, heart and adipose tissue of rats fed HMO indicated
that feeding HMO resulted in a reduction of the conversion of linoleic acid into long chain PUFA that could not be overcome
by increasing the dietary level of linoleic acid. 相似文献
2.
The effect of very low levels of dietary long-chain n−3 fatty acids on Δ6 desaturation of linoleic acid (18∶2n−6) and α-linolenic
acid (18∶3n−3), and on Δ5 desaturation of dihomo-γ-linolenic acid (20∶3n−6), in liver microsomes and its influence on tissue
fatty acids were examined in obese and lean Zucker rats and in Wistar rats. Animals fed for 12 wk a balanced diet containing
ca. 200 mg of long-chain polyunsaturated n−3 fatty acids per 100 g of diet were compared to those fed the same amount of α-linoleic
acid. Low amounts of long-chain n−3 fatty acids greatly inhibited Δ6 desaturation of 18∶2n−6 and Δ5 desaturation of 20∶3n−6,
while Δ6 desaturation of 18∶3n−3 was not inhibited in Zucker rats and was even stimulated in Wistar rats. Inhibition of the
biosynthesis of long-chain n−6 fatty acids was reflected in a decrease in arachidonic acid (20∶4n−6) content of serum lipids
when fasting, and also in the phospholipid fatty acids of liver microsomes. On the contrary, heart and kidney phospholipids
did not develop any decrease in 20∶4n−6 during fish oil ingestion. Docosahexaenoic acid (22∶6n−3), present in the dietary
fish oil, was increased in serum lipids and in liver microsome, heart, and kidney phospholipids. 相似文献
3.
The addition of long-chain polyunsaturated fatty acids (LCP: C20, and C22) to infant formula may permit fatty acid accretion
rates similar to breast-fed infants, and may have long-term outcome benefits, such as improved visual acuity and cognitive
development. Although fish oil may provide a source of n-3 LCP, sources of n-6 LCP have been more difficult to identify. The
present study evaluates the effects of n-3 and n-6 LCP derived from single-cell oils on liver, plasma, and brain fatty acid
levels in a neonatal animal model. Newborn rat pups were suckled for 14 d by dams receiving diets containing n-3 LCP alone
or combinations of n-3 LCP and increasing doses of linoleic acid (18∶2n−6) or arachidonic acid (20∶4n−6). Dietary groups received
2% n−3 LCP and 1, 2, or 5% of either 18∶2n−6 or 20∶4n−6. The 20∶4n−6 source also contained modest levels of 18∶2n−6. At the
termination of the study, liver, plasma, and brain were obtained from the rat pups and the phospholipid fatty acid profiles
determined. The results indicate complex interactions of n−3 and n−6 fatty acids. Groups receiving dietary 20∶4n−6 incorporated
higher levels of n−6 LCP into tissues than did the groups receiving 18∶2n−6. The brain was relatively resistant to changes
in fatty acid composition compared with the liver and plasma. As expected, tissue n−3 LCP levels were reciprocally related
to n−6 levels. The present results document that single-cell LCP oils are bioavailable in a neonatal animal model. The use
of 20∶4n−6 is a more effective means of supporting n−6 status than the use of 18∶2n−6. These results may have implications
for the addition of LCP to infant formula. 相似文献
4.
Poumès-Ballihaut C Langelier B Houlier F Alessandri JM Durand G Latge C Guesnet P 《Lipids》2001,36(8):793-800
Animal and human studies have indicated that developing mammals fed only α-linolenic acid (18∶3n−3) have lower docosahexaenoic
acid (22∶6n−3) content in brain and tissue phospholipids when compared with mammals fed 18∶3n−3 plus 22∶6n−3. The aim of this
study was to test the hypothesis that low bioavailability of dietary 18∶−3 to be converted to 22∶6n−3 could partly explain
this difference in fatty acid accretion. For that purpose, we determined the partitioning of dietary 18∶3n−3 and 22∶6n−3 between
total n−3 fatty acid body accumulation, excretion, and disappearance (difference between the intake and the sum of total n−3
fatty acids accumulated and excreted). This was assessed using the quantitative method of whole-body fatty acid balance in
growing rats fed the same amount of a 5% fat diet supplying either 18∶3n−3 or 22∶6n−3 at a level of 0.45% of dietary energy
(i.e., 200 mg/100 g diet). We found that 58.9% of the total amount of 18∶3n−3 ingested disappeared, 0.4% was excreted in feces,
21.2% accumulated as 18∶3n−3 (50% in total fats and 46% in the carcass-skin compartment), and 17.2% accumulated as long-chain
derivatives (14% as 22∶6n−3 and 3.2% as 20∶5n−3+22∶5n−3). Similar results were obtained from the docosahexaenoate balance
(as % of the total amount ingested): disappearance, 64.5%; excretion, 0.5%; total accumulation, 35% with 30.1% as 22∶6n−3.
Thus, rats fed docosahexaenoate accumulated a twofold higher amount of 22∶6n−3, which was mainly deposited in the carcass-skin
compartment (68%). Similar proportions of disappearance of dietary 18∶−3 and 22∶6n−3 lead us to speculate that these two n−3
polyunsaturated fatty acids were β-oxidized in the same amount. 相似文献
5.
Guinea pigs were fed one of three diets containing 10% black currant seed oil (a source of gamma-linolenic (18∶3 n−6) and
stearidonic (18∶4 n−3) acids), walnut oil or lard for 40 days. The fatty acid composition of liver triglycerides, free fatty
acids, cholesteryl esters, phosphatidylinositol, phosphatidylserine, cardiolipin, phosphatidylcholine and phosphatidylethanolamine
were determined.
Dietary n−3 fatty acids found esterified in liver lipids had been desaturated and elongated to longer chain analogues, notably
docosapentaenoic acid (22∶5 n−3) and docosahexaenoic acid (22∶6 n−3). When the diet contained low amounts of n−6 fatty acids,
proportionately more of the n−3 fatty acids were transformed. Significantly more eicosapentaenoic acid (EPA) (20∶5 n−3) was
incorporated into triglycerides, cholesteryl esters, phosphatidylcholine and phosphatidylethanolamine of the black currant
seed oil group compared with the walnut oil group.
Feeding black currant seed oil resulted in significant increases of dihomogamma-linolenic acid (20∶3 n−6) in all liver lipid
classes examined, whereas the levels of arachidonic acid (20∶4 n−6) remained relatively stable. The ratio dihomo-gamma-linolenic
acid/arachidonic acid was significantly (2.5-fold in PI to 17-fold in cholesteryl esters) higher in all lipid classes from
the black currant seed oil fed group. 相似文献
6.
Cod (mean start weight of 26 g) were fed three diets for 15 months, each based on a dry pellet coated at a level of 9g/100
g with soybean oil, capelin oil or sardine oil. The fatty acid compositions of neutral lipids and four glycerophospholipids
of white muscle, liver, gills and heart were determined. The fatty acid composition of dietary lipids influenced the composition
of neutral lipids in all organs. Linoleic acid (18∶2n−6) from soybean oil was selectively incorporated into phosphatidylcholine
of the four tissues. Similar levels of 20∶5n−3 and 22∶6n−3 in phosphatidylcholine and phosphatidylethanolamine were found
in all organs from cod fed capelin oil and sardine oil in spite of highly differentiated feed fatty acid levels. The polyunsaturated
fatty acid (PUFA) composition of phosphatidylinositol was least influenced by dietary lipids. The preferred monoenic fatty
acid in phospholipids of cod was 18∶1n−9, independent of dietary intake, whereas the longer chain monoenoic acids seemed to
be preferentially catabolized. The results suggest that 20∶4n−6 as well as 20∶5n−3 and 22∶6n−3 fatty acids are essential for
cod. 相似文献
7.
Y. -S. Huang P. E. Wainwright P. R. Redden D. E. Mills B. Bulman-Fleming D. F. Horrobin 《Lipids》1992,27(2):104-110
This report examines the distribution of n−3 and n−6 fatty acids in heart, kidney and liver phosphatidylcholine and phosphatidylethanolamine
of suckling mice from dams fed a fat-supplemented diet with variable n−3/n−6 ratios. After conception and throughout the pregnancy
and lactation period, dams were fed a fat-free liquid diet supplemented with 20% by energy of oil mixtures (fish oil concentrate,
rich in 20∶5n−3 and 22∶6n−3, and safflower oil concentrate, rich in 18∶2n−6). The diets contained similar amounts of combined
n−3 and n−6 fatty acids but variable ratios of n−3 to n−6 fatty acids (0,025, 0.5, 1, 2, and 4). In 12-day-old suckling mice,
as the n−3nn−6 ratio in the maternal diet increased (up to approx. 0.5), the tissue levels of 20∶5n−3, 22∶5n−3 and 22∶6n−3
increased, whereas those of 18∶2n−6 and 20∶4n−6 decreased. The responses were similar in both phospholipid subclasses, but
varied between different tissues. Generally, the n−3/n−6 ratios were significantly greater in pup tissues than in milk fat,
indicating preferential incorporation of n−3 over n−6 fatty acids into phospholipids during growth. However, the incorporation
of n−3 fatty acids in pups was significantly suppressed whereas that of n−6 fatty acids was increased when 18∶2n−6 was replaced
by its δ6-desaturation product, 18∶3n−6 (concentrated from evening primrose oil), as the source on n−6 fatty acid. This result
suggests that δ6 desaturase activity in neonate tissues is low, and consequently, the metabolism of 18∶2n−6 to longer chain
n−6 fatty acids is reduced. The preformed long-chain n−3 fatty acids, which bypass δ6-desaturation, were thus, preferentially
incorporated into tissue phospholipids. 相似文献
8.
The importance of n−6 and n−3 polyunsaturated fatty acids (PUFA) in neonatal development, particularly with respect to the
developing brain and retina, is well known. This review combines recent information from basic science and clinical studies
to highlight recent advances in knowledge on PUFA metabolism and areas where research is still needed on infant n−6 and n−3
fatty acid requirements. Animal, cell culture, and infant studies are consistent in demonstrating that synthesis of 22∶6n−3
involves C24 PUFA and that the amounts of 18∶2n−6 and 18∶3n−3 influence PUFA metabolism. Studies to show that addition of
n−6 fatty acids beyond Δ6-desaturase alters n−6 fatty acid metabolism with no marked increase in tissue 20∶4n−6 illustrate
the limitations of analyses of tissue fatty acid compositions as an approach to study the effects of diet on fatty acid metabolism.
New information to show highly selective pathways for n−6 and n−3 fatty acid uptake in brain, and efficient path-ways for
conservation of 22∶6n−3 in retina emphasizes the differences in PUFA metabolism among different tissues and the unique features
which allow the brain and retina to accumulate and maintain high concentrations of n−3 fatty acids. Further elucidation of
the Δ6-desaturases involved in 24∶5n−6 and 22∶6n−3 synthesis; the regulation of fatty acid movement between the endoplasmic
reticulum and peroxisomes; partitioning to acylation, desaturation and oxidation; and the effects of dietary and hormonal
factors on these pathways is needed for greater understanding of neonatal PUFA metabolism. 相似文献
9.
P. E. Wainwright Y. S. Huang D. E. Mills G. R. Ward R. P. Ward D. McCutcheon 《Lipids》1989,24(12):989-997
This study assesses the combined effects on brain and behavioral development of ethanol administration and supplementation
of the maternal diet with long chain n−3 polyunsaturated fatty acids. From day 7 to 17 of gestation, pregnant mice were fed
equivalent daily amounts of isocaloric liquid diets; 20% of the energy was provided by either ethanol or maltose-dextrin,
and a further 20% by either safflower oil (rich in linoleic acid, 18∶2n−6), or a combination of safflower oil with a fish
oil concentrate (rich in eicosapentaenoic acid, 20∶5n−3, and docosahexaenoic acid, 22∶6n−3). On day 18 the liquid diets were
replaced by lab chow; a fifth group was maintained on lab chow throughout the experiment. Measures on the pups included brain
weight and the fatty acid composition of the brain phospholipids on days 22 and 32 post-conception (birth=day 19), as well
as behavioral development. Maternal weight gain during gestation was decreased by ethanol relative to maltose-dextrin, and
increased by fish relative to safflower oil. On day 32, the brain weight of ethanoltreated animals fed fish oil was greater
than their safflower oil controls, whereas the reverse was true in the two maltose-dextrin groups; a similar trend was apparent
on day 22. The brain phospholipid content of the longer chain fatty acids (20∶4n−6, 22∶4n−6, 22∶5n−6, 20∶5n−3, 22∶5n−3, 22∶6n−3)
on day 22 reflected that of the prenatal diet, with the proportion of n−3 compounds being higher and that of n−6 floer in
the fish oil than safflower oil groups. Prenatal dietary effects were absent by day 32, with the exception of lower 22∶5n−6
in fish oil groups. Dietary supplementation with n−3 fatty acids increased the ratio of 20∶3n−6 to 20∶4n−6, which is consistent
with a blockade of the activity of Δ-5 desaturase. On day 22 the incorporation of dietary long chain n−3 fatty acids into
the brain phosphatidylcholine fraction was enhanced in the ethanol-treated animals; by day 32 the animals treated prenatally
with ethanol also showed increased levels of long chain n−6 compounds. Behavioral development was retarded by ethanol, but
there was no effect of the dietary oils. These results support the hypothesis that effects of ethanol on the developing brain
may be modified by the availability of an exogenous supply of long chain fatty acids. 相似文献
10.
Four sources of long-chain polyunsaturated fatty acids (LCP) differing in their chemical structure (triglycerides or phospholipids)
and in their origin (tuna triglycerides, fungal triglycerides, egg phospholipids, and pig brain phospholipids) were analyzed
to determine the distribution of the component fatty acids within the molecule. Lipase and phospholipase A2 hydrolysis was performed to obtain 2-monoacylglycerols and lysophospholipids, respectively, which allowed us to determine
the distribution of fatty acids between the sn-2 and sn-1,3 positions of triglycerides or between the sn-1 and sn-2 position of phospholipids. Fatty acids in the LCP sources analyzed were not randomly distributed. In tuna triglycerides,
half of the total amount of 22∶6n−3 was located at the sn-2 position (49.52%). In fungal triglycerides, 16∶0 and 18∶0 were esterified to the sn-1,3 (92.22% and 91.91%, respectively) 18∶1 and 18∶2 to the sn-2 position (59.77% and 62.62%, respectively), and 45% of 20∶3n−6 and only 21.64% of 20∶4n−6 were found at the sn-2 position. In the lipid sources containing phospholipids, LCP were mainly esterified to the phosphatidylethanolamine fraction.
In egg phospholipids, most of 20∶4n−6 (5.50%, sn-2 vs. 0.91%, sn-1) and 22∶6n−3 (2.89 vs. 0.28%) were located at the sn-2 position. In pig brain phospholipids, 22∶6n−3 was also esterified to the sn-2 (13.20 vs. 0.27%), whereas 20∶4n−6 was distributed between the two positions (12.35 vs. 5.86%). These results show a different
fatty acid composition and distribution of dietary LCP sources, which may affect the absorption, distribution, and tissue
uptake of LCP, and should be taken into account when supplementing infant formulas. 相似文献
11.
The effect of dietary docosahexaenoic acid (22∶6n−3, DHA) on the metabolism of oleic, linoleic, and linolenic acids was investigated
in male subjects (n=6) confined to a metabolic unit and fed diets containing 6.5 or <0.1 g/d of DHA for 90 d. At the end of the diet period,
the subjects were fed a mixture of deuterated triglycerides containing 18∶1n−9[d6], 18∶2n−6[d2], and 18∶3n−3[d4]. Blood samples
were drawn at 0, 2, 4, 6, 8, 12, 24, 48, and 72 h. Methyl esters of plasma total lipids, triglycerides, phospholipids, and
cholesterol esters were analyzed by gas chromatography-mass spectrometry. Chylomicron triglyceride results show that the deuterated
fatty acids were equally well absorbed and diet did not influence absorption. Compared to the low-DHA diet (LO-DHA), clearance
of the labeled fatty acids from chylomicron triglycerides was modestly higher for subjects fed the high DHA diet (HI-DHA).
DHA supplementation significantly reduced the concentrations of most n-6[d2] and n-3[d4] long-chain fatty acid (LCFA) metabolites
in plasma lipids. Accumulation of 20∶5n−3[d4] and 22∶6n−3[d4] was depressed by 76 and 88%, respectively. Accumulations of
20∶3n−6[d2] and 20∶4n−6[d2] were both decreased by 72%. No effect of diet was observed on acyltransferase selectivity or on
uptake and clearance of 18∶1n−9[d6], 18∶2n−6[d2], and 18∶3n−3[d4]. The results indicate that accumulation of n−3 LCFA metabolites
synthesized from 18∶3n−3 in typical U.S. diets would be reduced from about 120 to 30 mg/d by supplementation with 6.5 g/d
of DHA. Accumulation of n−6 LCFA metabolites synthesized from 18∶2n−6 in U.S. diets is estimated to be reduced from about
800 to 180 mg/d. This decrease is two to three times the amount of n−6 LCFA in a typical U.S. diet. These results support
the hypothesis that health benefits associated with DHA supplementation are the combined result of reduced accretion of n−6
LCFA metabolites and an increase in n−3 LCFA levels in tissue lipids. 相似文献
12.
The emperor penguin (Aptenodytes forsteri) is an Antarctic seabird feeding mainly on fish and therefore has a high dietary intake of n-3 polyunsaturated fatty acids.
The yolk is accumulated in the developing oocyte while the females are fasting, and a large proportion of the fatty acid components
of the yolk lipids are derived by mobilization from the female's adipose tissue. The fatty acid composition of the total lipid
of the yolk was characterized by high levels of n-3 polyunsaturated fatty acids. However, it differed in several respects
from that of the maternal adipose tissue. For example, the proportions of 14∶0, 16∶1n−7, 20∶1n−9, 22∶1n−9, 20∶5n−3, and 22∶6n−3
were significantly greater in adipose tissue than in yolk. Thus adipose tissue lipids contained 7.6±0.3% and 8.0±0.3% (wt%
of total fatty acids; mean ±SE; n=5) of 20∶5n−3 and 22∶6n−3, respectively, whereas the yolk total lipid contained 1.6±0.1 and 5.5±0.3% of these respective
fatty acids. The proportions of 16∶0, 18∶0, 18∶1n−9, 18∶2n−6, and 20∶4n−6 were significantly lower in the adipose tissue than
in the yolk lipids. The proportions of triacylglycerol, phospholipid, free cholesterol, and cholesteryl ester in the yolk
lipid were, respectively, 67.0±0.2, 25.4±0.3, 5.3±0.2, and 1.8±0.2% (wt% of total yolk lipid). The proportions of 20∶4n−6,
20∶5n−3, 22∶5n−3, and 22∶6n−3 were, respectively, 5.7±0.3, 2.8±0.2, 1.4±0.1, and 11.7±0.5% in phospholipid and 0.4±0.0, 1.2±0.1,
0.8±0.1 and 3.6±0.3% in triacylglycerol. About 95% of the total vitamin E in the yolks was in the form of α-tocopherol with
γ-tocopherol forming the remainder. Two species of carotenoids, one identified as lutein, were present. 相似文献
13.
Docosahexaenoic acid (22∶6n−3) can be synthesized in the liver and/or brain from α-linolenic acid (18∶3n−3) and is required
in large amounts in structural membranes of developing brain and retina. The adequacy and efficacy of formulas containing
18∶3n−3 and/or fish oil in providing 22∶6n−3 for deposition was investigated in piglets fed formula from birth to 15 days.
The test formulas contained high (HL) or low (LL) 18∶3n−3 (3.9 or 0.7% of the total formula fatty acids, respectively), or
low 18∶3n−3 plus fish oil (LL+FO) to provide C20 and C22 n−3 polyunsaturated fatty acids (0.8% of total fatty acids). Fatty acid analyses of synaptic plasma membrane and retina ethanolamine
phospholipids (EPL), which are especially enriched in 22∶6n−3, were compared to those of 15-day-old piglets fed sow milk (SM).
Feeding LL resulted in lower 22∶6n−3 in synaptic plasma membrane. Fatty acid levels in HL and LL+FO piglets were equivalent
to SM, with the exception of lower 22∶5n−3 in the synaptic plasma membrane of LL+FO and in the retina of HL and LL+FO-fed
piglets. Levels of 22∶4n−6 were also lower in the retina of the LL+FO group. The results suggest formula 18∶3n−3 is at least
24% as effective as C20 and C22 n−3 fatty acids as a source of membrane 22∶6n−3. This study shows dietary 18∶3n−3, as the only n−3 fatty acid, can support
deposition of comparable percentage of 22∶6n−3 to natural milk. Fish oil also supported tissue levels of 22∶6n−3 similar to
natural milk; however, lower 22∶4n−6 may indicate possible inhibitory effects on n−6 metabolism.
Recipient of the 1967 Science and Engineering Scholarship, Natural Sciences & Engineering Research Council of Canada. 相似文献
14.
Modulation by fatty acids of the cytotoxic effect of recombinant tumor necrosis factor alpha (TNF) toward WEHI 164 mouse fibrosarcoma
cells has been examined. Preincubating the highly TNF-sensitive WEHI clone 13 cells for 44 hr with 50 μmol/L of 20∶5n−3, 22∶6n−3,
18∶3n−6, 20∶3n−6 or 20∶4n−6 reduced cell survival 22 hr after challenge with TNF (40 ng/L) by 65%, 72%, 60%, 98% and 85%,
respectively. In comparison, 18∶3n−3, 18∶2n−6 and 18∶1n−9 had only negligible effects on TNF-induced toxicity. Different extent
of fatty acid incorporation into cell total phospholipids or triglycerides could not explain the observed effects on TNF cytotoxicity,
and the enhanced cytotoxicity could therefore not be explained merely by an increased unsaturation of the cell membranes.
In addition to the fatty acid supplied, preincubation with 18∶2n−6, 18∶3n−6 or 18∶3n−3 also enriched the cells with 20∶2n−6,
20∶3n−6 and 20∶3n−3, respectively, most likely due to chain elongation. The results suggest that the WEHI cells have a low
Δ6 desaturase activity, and that n−6 and n−3 acids must have at least 3 or 4 double bonds, respectively, to enhance TNF cytotoxicity
in WEHI cells. Dexamethasone partly inhibited TNF-induced cytotoxicity, while cyclooxygenase, thromboxane synthetase or lipoxygenase
inhibitors had no or negligible effects. The antioxidant butylated hydroxyanisole (BHA) completely inhibited TNF-induced cytotoxicity,
while the structurally and functionally similar antioxidant butylated hydroxy-toluene had no such effect, indicating that
BHA does not block TNF cytotoxicity through its antioxidant effect. The results suggest that TNF cytotoxicity involves, directly
or indirectly, metabolism of long-chain polyun-saturated fatty acids, and we speculate that fatty acid metabolites are involved. 相似文献
15.
This study examined the effects of n−3 and n−6 polyunsaturated fatty acid alimentation on murine peritoneal macrophage phospholipids.
Mice were fed complete diets supplemented with either corn oil predominantly containing 18∶2n−6, borage oil containing 18∶2n−6
and 18∶3n−6, fish/corn oil mixture containing 18∶2n−6, 20∶5n−3 and 22∶6n−3, or fish/borage oil mixture containing 18∶2n−6,
18∶3n−6, 20∶5n−3 and 22∶6n−3. After two weeks, the fatty acid levels of glycerophosphoserines (GPS), glycerophosphoinositols
(GPI), sphingomyelin (SPH), and of the glycerophosphocholine (GPC) and glycerophosphoethanolamine (GPE) phospholipid subclasses
were determined. We found that mouse peritoneal macrophage GPC contain primarily 1-0-alkyl-2-acyl (range for the dietary groups, 24.6–30.5 mol %) and 1,2-diacyl (63.2–67.2 mol %), and that GPE contains 1-O-alk-1-enyl-2-acyl (40.9–47.4 mol. %) and 1,2-diacyl (44.2–51.2 mol %) subclasses. In general, fish oil feeding increased
macrophage 20∶5n−3, 22∶5n−3 and 22∶6n−3 levels while simultaneously reducing 20∶4n−6 in GPS, GPI, GPE and GPC subclasses except
for 1-O-alk-1′-enyl-2-acyl GPC. Administration of 18∶3n−6 rich diets (borage and fish/borage mixture) resulted in the accumulation
of 20∶3n−6 (2-carbon elongation product of 18∶3n−6) in most phospholipids. In general, the novel combination of dietary 18∶3n−6
and n−3 PUFA produced the highest 20∶3n−6/20∶4n−6 phospholipid fatty acid ratios. This study demonstrates that marked differences
in the responses of macrophage phospholipid classes and subclasses exist following dietary manipulation. The reduction of
20∶4n−6, while simultaneously increasing 30∶3n−6 and n−3 PUFA levels, may be important in relation to the putative beneficial
effects of 20∶3n−6 and fish oil on macrophage eicosanoid and platelet activating factor (PAF) biosynthesis. 相似文献
16.
When rats were fed 5% corn oil, the heart phospholipids contained large amounts of 22-carbon (n−6) acids. When half of the
corn oil was replaced with fish oil, the reduced level of arachidonate and 22-carbon (n−6) acids in phospholipids was accompanied
by increases in the levels of 22-carbon (n−3) acids while only small amounts of 20∶5(n−3) were acylated. Heart myocytes readily
took up and acylated [1-14C]-labeled 20∶4(n−6), 20∶5(n−3) and 22∶6(n−3) into phospholipids. The uptake and acylation of 20∶4(n−6) was greater than for
20∶5(n−3) but the intracellular labeling profiles were similar. Uptake and acylation of 22∶6(n−3) was somewhat lower. In addition
the intracellular labeling profile differed in that more 22∶6(n−3) was incorporated into the ethanolamine-containing phospholipids
than when 20∶4(n−6) or 20∶5(n−3) were the substrates. Neither 20∶4(n−6) nor 20∶5(n−3) was chain elongated. When [3-14C]-labeled 22∶4(n−6) and 22∶5(n−3) were the substrates, it was not possible to detect radioactive 22∶5(n−6) or 22∶6(n−3).
Both [3-14]-labeled substrates were acylated into phospholipids and retroconverted with the subsequent esterification of radioactive
20∶4(n−6) and 20∶5(n−3) into triglycerides and phospholipids. These studies show that cardiomyocytes lack the ability to make
22-carbon acids from 20-carbon precursors but they retroconvert 22-carbon acids to 20-carbon acids. The high levels of 22-carbon
polyunsaturated acids in total heart lipids thus cannot be attributed to the synthetic capacities of cardiomyocytes. 相似文献
17.
L. Ulmann J. P. Blond C. Maniongui J. P. Poisson G. Durand J. Bézard G. Pascal 《Lipids》1991,26(2):127-133
The combined effects of age and dietary n−6 and n−3 fatty acids were studied in 3-, 6- and 9-month-old rats. At each age,
two groups were fed diets containing 5% (w/w) of vegetable oils rich in either 18∶3n−6 (borage group) or 18∶3n−6 plus 18∶4n−3
(black currant group), for a period increasing with age. A control group was fed the essential fatty acids 18∶2n−6 and 18∶3n−3
only. For each group, Δ6, Δ5 and δ9 desaturase activities were measured in liver microsomes, and fatty acid composition was
determined in microsomal phospholipids. Desaturase activity varied as a function of age and dietary lipids. Δ6 Desaturation
of 18∶3n−3 was more sensitive to these factors while Δ6 desaturation of 18∶2n−6 and Δ9 desaturation were more dependent on
season than the other two. Desaturase activity was influenced more by the black currant than by the borage diet, especially
at 6 and 9 months of age. A large proportion of arachidonic acid was maintained in the microsomes independent of the diet.
Changes in the fatty acid composition did not strictly reflect the differences in desaturase activities. The effects of the
two factors (age and diet) on the activities of the desaturases are complex, suggesting that the enzymes are susceptible to
other factors as well. 相似文献
18.
The effects of dietary n−3 and n−6 polyunsaturated fatty acids on the fatty acid composition of phospholipid, Ca++· Mg++ ATPase and Ca++ transport activities of mouse sarcoplasmic reticulum were investigated. Mice were fed a 2 weight percent fat diet containing
either 0.5 weight percent ethyl esters of 18∶3n−3, 20∶5n−3 or 22∶6n−3 as a source of n−3 polyusaturated fatty acid or 0.5
weight percent safflower oil as a cource of n−6 polyunsaturated fatty acid for 10 days. Olive oil (2 weight percent) was used
as a control diet. Although feeding n−6 polyunsaturated fatty acid induced very little modifications of the phospholipid sarcoplasmic
reticulum fatty acid composition, feeding n−3 polyunsaturated fatty acid altered it markedly. Inclusion of 18∶−3, 20∶5n−3
or 22∶6n−3 in the diet caused an accumulation of 22∶6n−3, which replaced 20∶4n−6 and 18∶2n−6 in phospholipid sarcoplasmic
reticulum. The saturated fatty acids were significantly increased with a concurrent reduction of 18∶1n−9. These changes in
the fatty acid composition resulted in a decrease in the values of the n−6/n−3 polyunsaturated fatty acid ratio and a decrease
in the ratio of 20 carbon to 22 carbon fatty acids esterified in the phospholipid sarcoplasmic reticulum. This was associated
with a decrease in Ca++ uptake by n−3 polyunsaturated fatty acid enriched sarcoplasmic reticulum vesicles as compared with n−6 fatty acid and control
diet sarcoplasmic reticulum vesicles. However, neither the affinity for Ca++ nor the maximal velocity of ATP hydrolysis activity of Ca++·MG++ ATPase were altered by the different diets. The data suggest that the incorporation of 22∶6n−3 and/or the decrease of 20∶4n−6
plus 18∶2n−6 in the phospholipid sarcoplasmic reticulum may affect the membrane lipid bilayer structure and make it more permeable
to Ca++. 相似文献
19.
The present study was designed to investigate the metabolism of the n−3 olyunsaturated fatty acids (PUFA) in adipose tissue
and its dependence upon dietary factors. Changes in the positional distribution of the fatty acids in triacylglycerols from
retroperitoneal adipose tissue were studied as a function of time on rats fed for 4 wk a diet enriched with fish oil. The
stereospecific analysis of triacylglycerols was based on random formation ofrac-1,2-diacylglycerols by Grignard degradation. This was followed by synthesis ofrac-phosphatidic acids and treatment with phospholipase A2. In the triacylglycerols of the fish oil diet, 57% of the total n−3 fatty acids were in position 3,i.e., two-thirds of 22∶5n−3 and 22∶5n−3 were esterified insn-3 position, whereas 22∶6n−3 was equally distributed in positions 2 and 3. After 4 wk of feeding fish oil, the fatty acid
composition of adipose tissue triacylglycerols reached a steady state. Half of the n−3 fatty acids were found in position
3, namely 75% of 22∶5n−3, 50% of 20∶5n−3 and 18∶4n−3 and 45% of 22∶6n−3, the latter being equally distributed in positions
2 and 3. This pattern of distribution resembled that found in triacylglycerols of the fish oil diet, except for a higher proportion
of 20∶5n−3 in adipose tissue in position 1 at the expense of position 3. Throughout the 4-wk period of fish oil feeding, the
distribution pattern of minor n−3 fatty acids (18∶4n−3 and 22∶5n−3) in adipose tissue triacylglycerols remained unchanged.
On the other hand, at the onset of fish oil feeding, 20∶5n−3 and 22∶6n−3 became concentrated in position 3, but thereafter
20∶5n−3 was progressively incorporated into position 1 and 22∶6n−3 into position 2. We thus conclude that n−3 fatty acids
are differentially esterified in triacylglycerols of white adipose tissue. Despite the complex sequence of hydrolysis and
acylation steps involved, the positional distribution of n−3 fatty acids was found to be similar in both the fish oil diet
and the stored fat, in contrast to what was observed for nonessential fatty acids. 相似文献
20.
Duplicate groups of Atlantic salmon (Salmo salar) post smolts were given diets in which the lipid component was either fish oil or a mixture of corn oil and lard. This difference
in the dietary lipid did not significantly affect growth over a period of sixteen weeks.
Proportions of docosahexaenoic acid [22∶6(n−3)] and total (n−3) fatty acids in the polar lipids of liver and white muscle
were unaffected by this difference in dietary lipid component over the time period used. Fish given the diet containing corn
oil and lard had significantly higher levels of 20∶2(n−6), 20∶3(n−6) and 20∶4(n−6) in the polar lipids of these tissues than
were present in the tissues of the fish given diets containing fish oil. There results suggest that linoleic acid [18∶2(n−6)]
undergoes elongation and desaturation to arachidonic acid [20∶4(n−6)] in post-smolt Atlantic salmon. 相似文献