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1.
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
2.
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
3.
The purpose of this study was to examine the influence of long-term feeding of dietary fat rich in either n−3 or n−6 fatty
acids on the availability of arachidonic acid (20∶4n−6) in major phospholipids of gastric mucosa in rats. Three groups of
male Wistar rats were fed either a standard diet, a cod liver oil-enriched diet (10% by weight), or a corn oil-enriched diet
(10% by weight) for 8 mon. Dietary cod liver oil significantly reduced the level of 20∶4n−6 in phosphatidylcholine (PC) and
in phosphatidylethanolamine (PE) of gastric mucosa. The loss of 20∶4n−6 was compensated for by eicosapentaenoic acid (20∶5n−3)
in PC, whereas the decrease in 20∶4n−6 in PE corresponded to the increase in three n−3 fatty acids: 20∶5n−3, docosapentaenoic
acid (22∶5n−3), and docosahexaenoic acid (22∶6n−3). The level of 20∶5n−3 was higher than the level of 22∶6n−3 both in PC and
PE of mucosa in rats fed cod liver oil. Diets supplemented with corn oil increased the level of 18∶2n−6 but decreased the
monoene fatty acids 16∶1 and 18∶1n−7 in PC but not in PE of gastric mucosa. The 20∶4n−6 levels of both PC and PE were markedly
reduced by dietary cod liver oil, to about one-third of control levels. Similar changes were also observed in the stomach
wall. Gastric erosions were observed in all rats exposed to restriction stress, but this form of stress induced twice the
number of erosions in rats fed fish oil compared to control rats or rats fed corn oil. We conclude that a diet rich in fish
oil altered the balance between n−6 and n−3 fatty acids in major gastric mucosal phospholipids, markedly reduced the availability
of 20∶4n−6, and increased the incidence of gastric erosions induced by restriction or emotional stress. 相似文献
4.
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
5.
Atlantic salmon post-smolts were fed diets rich in linoleic acid (sunflower oil, SO), α-linolenic acid (linseed oil, LO) or
long-chain polyunsaturated fatty acids (fish oil, FO) for a period of 12 wk. In the liver phospholipids of fish fed SO, the
levels of 18∶2n−6, 20∶2n−6, 20∶3n−6 and 20∶4n−6 were significantly elevated compared to both other treatment. In choline phospholipids
(CPL), ethanolamine phospholipids (EPL) and phosphatidylserine (PS) the levels of 22∶4n−6 and 22∶5n−6 were significantly elevated
in fish fed SO. In liver phospholipids from fish fed LO, 18∶2n−6, 20∶2n−6 and 20∶3n−6 were significantly elevated but 20∶4n−6,
22∶4n−6 and 22∶5n−6 were similar or significantly decreased compared to fish fed FO. Liver phospholipids from fish fed LO
had increased 18∶3n−3 and 20∶4n−3 compared to both other treatments while EPL and phosphatidylinositol (PI) also had increased
20∶5n−3. In fish fed LO, 22∶6n−3 was significantly reduced in CPL, PS and PI compared to fish fed FO. Broadly similar changes
occurred in gill phospholipids. Production of 12-lipoxygenase metabolites in isolated gill cells stimulated with the Ca2+-ionophore A23187 were significantly reduced in fish fed either SO or LO compared to those fed FO. However, the ratio 12-hydroxy-5,8,10,14-eicosatetraenoic
acid (12-HETE)/12-hydroxy-5,8,10,14,17-eicosapentaenoic acid (12-HEPE) was significantly elevated in stimulated gill cells
from SO-fed fish. Although mean values of thromboxane B2 (TXB2) and prostaglandin E2 (PGE2) were increased in fish fed SO, they were not significantly different from those of the other two treatments. 相似文献
6.
Joanna K. Chan Bruce E. McDonald Jon M. Gerrard Vivian M. Bruce Bonnie J. Weaver Bruce J. Holub 《Lipids》1993,28(9):811-817
The effect of dietary α-linolenic acid (18∶3n−3) and its ratio to linoleic acid (18∶2n−6) on platelet and plasma phospholipid
(PL) fatty acid patterns and prostanoid production were studied in normolipidemic men. The study consisted of two 42-d phases.
Each was divided into a 6-d pre-experimental period, during which a mixed fat diet was fed, and two 18-d experimental periods,
during which a mixture of sunflower and olive oil [low 18∶3n−3 content, high 18∶2/18∶3 ratio (LO-HI diet)], soybean oil (intermediate
18∶3n−3 content, intermediate 18∶2/18∶3 ratio), canola oil (intermediate 18∶3n−3 content, low 18∶2/18∶3 ratio) and a mixture
of sunflower, olive and flax oil [high 18∶3n−3 content, low 18∶2/18∶3 ratio (HI-LO diet)] provided 77% of the fat (26% of
the energy) in the diet. The 18∶3n−3 content and the 18∶2/18∶3 ratio of the experimental diets were: 0.8%, 27.4; 6.5%, 6.9;
6.6%, 3.0; and 13.4%, 2.7, respectively. There were appreciable differences in the fatty acid composition of platelet and
plasma PLs. Nevertheless, 18∶1n−9, 18∶2n−6 and 18∶3n−3 levels in PL reflected the fatty acid composition of the diets, although
very little 18∶3n−3 was incorporated into PL. Both the level of 18∶3n−3 in the diet and the 18∶2/18∶3 ratio were important
in influencing the levels of longer chain n−3 fatty acid, especially 20∶5n−3, in platelet and plasma PL. Production of 6-keto-PGF1α was significantly (P<0.05) higher following the HI-LO diet than the LO-HI diet although dietary fat source had no effect on bleeding time or thromboxane
B2 production. The present study showed that both the level of 18∶3n−3 in the diet and its ratio to 18∶2n−6 were important in
influencing long-chain n−3 fatty acid levels in platelet and plasma PL and that prostanoid production coincided with the diet-induced
differences in PL fatty acid patterns. 相似文献
7.
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
8.
Because alterations in the dietary content of fatty acids are an important method for modulating macrophage eicosanoid production,
we have quantitated the levels of n−6 and n−3 polyunsaturated fatty acids in peritoneal macrophage individual phospholipids
from mice fed diets (3 wk) with either safflower oil (SAF), predominantly containing 18∶2n−6, borage (BOR) containing 18∶2n−6
and 18∶3n−6, fish (MFO) containing 20∶5n−3 and 22∶6n−3, and borage/fish mixture (MIX) containing 18∶2n−6, 18∶3n−6, 20∶5n−3
and 22∶6n−3. Dietary n−3 fattya cids were readily incorporated into macrophage phosphatidylcholine (PC), phosphatidylethanolamine
(PE), phosphatidylserine (PS) and phosphatidylinositol (PI). The increase in n−3 fatty acid levels was accompanied by a decrease
in the absolute levels of 18∶2n−6, 20∶4n−6 and 22∶4n−6 in PC, PE and PS. Interestingly, PI 20∶4n−6 levels were not significantly
lowered (P>0.05) in MIX and MFO macrophages relative to SAF and BOR. These data demonstrate the unique ability of this phospholipid
to selectively maintain its 20∶4n−6 levels. In BOR and MIX animals, 20∶3n−6 levels were significantly increased (P<0.05) in
all phospholipids relative to SAF and MFO. The combination of borage and fish oils (MIX diet) produced the highest 20∶3n−6/20∶4n−6
ratio in all phospholipids. These data show that the macrophage eicosanoid precursor levels of 20∶3n−6, 20∶4n−6 and n−3 acids
can be selectively manipulated through the use of specific dietary regimens. This is noteworthy because an increase in phospholipid
levels of 20∶3n−6 and 20∶5n−3, while concomitantly reducing 20∶4n−6, may have therapeutic potential in treating inflammatory
disorders. 相似文献
9.
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
10.
The extent to which exogenous 18∶3(n−3) and 18∶3(n−6) were desaturated and elongated and the degree to which they and their
derivatives altered the unsaturation index of cell glycerolipids were compared using clone 4 MDCK cells grown in lipid- and
serum-free medium. Despite differences in the degree of unsaturation of the individual polyunsaturated fatty acids produced
from 18∶3(n−3) or 18∶3(n−6), the unsaturation index of phospholipids increased similarly from 0.7 in control cells grown in
serum- and lipid-free medium to ca. 1.6 in those supplemented with fatty acid. The added fatty acids had little effect on
cell growth. The conversion of 18∶3(n−6) to 20∶3(n−6) and 20∶4(n−6) was more rapid than that of 18∶3(n−3) to 20∶4(n−3) and
20∶5(n−3). No significant quantities of 20∶3(n−3) or 18∶4(n−3) were noted. When both 18∶3 isomers were supplied simultaneously,
marked differences in the amounts of some species of n−3 and n−6 polyunsaturated fatty acids were observed. The presence of
18∶3(n−6) and/or its derivatives suppressed levels of 20∶4(n−3) and 20∶5(n−3), perhaps through inhibition of the Δ6 and Δ5
desaturases responsible for their synthesis from 18∶3(n−3). Similarly 18∶3(n−3), and/or its longer more unsaturated derivatives,
diminished the formation of 20∶4(n−6) from 18∶3(n−6). No marked effect on the products derived from elongation alone were
observed. 相似文献
11.
Roberto J. de Antueno Richard C. Cantrill Yung-Sheng Huang Michele Elliot David F. Horrobin 《Lipids》1993,28(4):285-290
This study was undertaken to investigate the total plasma fatty acid composition and the relationship between plasma triacylglycerol
(TG) levels and liver Δ9 desaturase activity in mice fed n−3 and/or n−6 fatty acid or hydrogenated coconut oil (HCO) (maximum
25 mg/g) supplemented diets. Generally, plasma TG levels and Δ9 desaturase activity were inversely correlated with the ratio
of the sum of long chain n−3 fatty acids to 18∶2n−6 and to the ratio of the sum of long chain n−3 fatty acids to 18∶n−3, but
they were positively correlated with the ratio of products and substrates (18∶1/18∶0) of the enzyme in plasma total lipids.
The n−3 fatty acid (mainly 20∶5n−3) enriched diet, when compared to the HCO diet at 21 d, caused a significant reduction in
plasma TG levels but not in Δ9 desaturase activity. However, a marked reduction in plasma TG content (50–60%) and Δ9 desaturase
activity (55–70%) was observed when both 20∶5n−3 and 18∶3n−6 were supplemented in the diet. The plasma TG levels and Δ9 desaturase
activity rose again when the animals were fed the HCO diet or chow. The results suggest that low dose supplementation of a
mixture of n−3 (mainly 20∶5n−3) and n−6 (18∶3n−6) fatty acids modified both plasma TG content and liver Δ9 desaturase activity,
in parallel. 相似文献
12.
The effects of hypothyroidism and of daily treatment for up to 21 days with thyroxin (T4, 0.5 μg/100 g body weight) on the
fatty acid composition of total lipid, phosphatidylethanolamine, and phosphatidylcholine of rat liver mitochondria were studied.
The fatty acid compositions of hypothyroid and euthyroid (control) rats of similar age were compared. The n−6 and n−3 polyunsaturated
fatty acids (PUFA) were affected differently by the hypothyroid state. The levels of linoleic (18∶2n−6), γ-linolenic (18∶3n−6)
and dihomo-γ-linolenic acids (20∶3n−6) were higher in hypothyroid rats than in controls, while the level of arachidonic acid
(20∶4n−6) was lower, which suggests an impairment of the elongase and desaturase activities. The n−3 polyunsaturated fatty
acids, eicosapentaenoic (EPA, 20∶5n−3) and docosapentaenoic (22∶5n−3) acids, were higher in hypothyroid rats, whereas the
linolenic acid (18∶3n−3) content remained constant. The level of docosahexaenoic acid (DHA, 22∶6n−3) was dramatically decreased
in hypothyroid rats, while the levels of C22 n−6 fatty acids were unchanged. The differences were probably due to the competition between n−3 and n−6 PUFA for desaturases,
elongases and acyltransferases. When hypothyroid rats were treated with thyroxin, the changes induced by hypothyroidism in
the proportions of n−6 fatty acids were rapidly reversed, while the changes in the n−3 fatty acids were only partially reversed.
After 21 days of thyroxin treatments, the DHA content was only half as high in hypothyroid rats than in euthyroid rats. These
results suggest that the conversion of 18∶2n−6 to 20∶4n−6 is suppressed in the hypothyroid state which favors the transformation
of 18∶3n−3 to 20∶5n−3. The marked decrease in DHA content indicates an impairment of the enzymes involved in the DHA metabolism,
possibly the n−3 Δ4 desaturase or the acyltransferases. The increased levels of EPA and 22∶5n−3 is consistent with the inhibition
of the n−3 pathway at the Δ4 desaturase step. Observed modifications in the fatty acid composition may significantly alter
eicosanoid synthesis and membrane functions in hypothyroidism. 相似文献
13.
The metabolism of α-linolenic acid from canola oil was studied in eight normolipidemic men. The 42-day study was divided into
three periods: a 6-day pre-experimental and two 18-day experimental. Approximately 75% of the dietary fat (28% of total energy)
was provided by a mixture of fats during the pre-experimental period and either canola oil (CO) or sunflower oil (SO) during
the experimental periods. The CO and SO diets were fed in a cross-over design. The ratios of linoleic to linolenic acid were
2.6∶1 and 73.9∶1 in the CO and SO diets, respectively. Dietary fat source had an effect on plasma phospholipid fatty acids:
18∶1n−9, 18∶3n−3 and 20∶5n−3 were higher (p<0.05), and 18∶2n−6 was lower in the phosphatidylcholine fraction; 18∶1n−9 was
higher and 20∶4n−6 lower in the phosphatidyl-ethanolamine fraction; and 18∶1n−9 and 20∶5n−3 were higher and 20∶4n−6 and 22∶6n−3
were lower in the alkenylacyl-ethanolamine phospholipid fraction on the CO diet as compared to the SO diet. Consumption of
the canola oil diet resulted in higher n−3 fatty acid levels and lower n−6 fatty acid levels in plasma phospholipids than
consumption of the sunflower oil diet. 相似文献
14.
The effect of fish oil high in docosahexaenoic acid (22∶6n−3) and low in eicosapentaenoic acid (20∶5n−3) in formula on blood
lipids and growth of full-term infants was studied. Infants were fed formula with about 15% oleic acid (18∶1), 32% linoleic
acid (18∶2n−6), 4.9% linolenic acid (18∶3n−3) and 0, 0.10 or 0.22% 22∶6n−3, or 35% 18∶1, 20% 18∶2n−6, 2.1% 18∶3n−3 and 0,
0.11 or 0.24% 22∶6n−3 from 3 d to 16 wk of age (n=16, 18, 17, 21, 17, 16, respectively). The formulae had <0.1% 20∶5n−3 and no arachidonic acid (20∶4n−6). Breast-fed infants
(n=26) were also studied. Plasma phospholipid and red blood cell (RBC) phosphatidylcholine (PC) and phosphatidylethanolamine
(PE) fatty acids were determined at 3 d and 4, 8, and 16 wk of age. These longitudinal analyses showed differences in blood
lipid 22∶6n−3 between breast-fed and formula-fed infants depending on the feeding duration. At 16 wk, infants fed formula
with 0.10, 0.11% 22∶6n−3, or 0.22% 22∶6n−3 had similar 22∶6n−3 levels in the plasma phospholipid and RBC PC and PE compared
with breast-fed infants and higher 22∶6n−3 than infants fed formula without 22∶6n−3. Formula with 0.24% 22∶6n−3, however,
resulted in higher plasma phospholipid 22∶6n−3 than in breast-fed infants at 16, but not 4 or 8 wk of age. Plasma and RBC
phospholipid 20∶4n−6 was lower in formula-fed than breast-fed infants, but no differences in growth were found. Higher blood
lipid C20 and C22 n−6 and n−3 fatty acids in infants fed formula with 20% 18∶2n−6 and 2.4% 18∶3n−3 compared with 32% 18∶2n−6 and 4.9% 18∶3n−3
show the increase in blood lipid 22∶6n−3 in response to dietary 22∶6n−3 depending on other fatty acids in the formula. 相似文献
15.
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
16.
The fatty acid compositions of lipids from two species of Crinoidea and two species of Ophiuroidea have been investigated
with open-tubular gas chromatography. About 5–10% of tetracosahexaenoic acid was found in total fatty acids from all the samples,
and the structure was determined as all-cis-6,9,12,15,18,21-tetracosahexaenoic acid [24∶6(n−3)] by13C-NMR of the methyl esters and mass spectrometric analyses of the methyl esters, the pyrrolidides and the ozonolysis products.
The 24∶6(n−3) was concentrated in the polar lipids rather than neutral lipids. The n−3 hexaenoic structure suggested chain
elongation of 22∶6(n−3) as the source.
The 5-olefinic acids (5−18∶1, 5−20∶1, 5,11- and 5,13−20∶2) were low in Crinoidea (0.2–1.3%) but were present in higher levels
(2.5–5.2%) in Ophiuroidea. Polyunsaturated acids found other than 24∶6(n−3) were 20∶4(n−6), 20∶5(n−3) and 22∶6(n−3) as major
components and 16∶3(n−3), 18∶2(n−6), 18∶3(n−6), 18∶3(n−3), 18∶4(n−3), 20∶2(n−9), 20∶2(n−6), 20∶3(n−6), 20∶3(n−3), 21∶5(n−3)
and 22∶5(n−3) as minor components in all the samples. 相似文献
17.
Starting three weeks before mating, 12 groups of female rats were fed different amounts of linoleic acid (18∶2n−6). Their
male pups were killed when 21-days-old. Varying the dietary 18∶2n−6 content between 150 and 6200 mg/100 g food intake had
the following results. Linoleic acid levels remained very low in brain, myelin, synaptosomes, and retina. In contrast, 18∶2n−6
levels increased in sciatic nerve. In heart, linoleic acid levels were high, but were not related to dietary linoleic acid
intake. Levels of 18∶2n−6 were significantly increased in liver, lung, kidney, and testicle and were even higher in muscle
and adipose tissue. On the other hand, in heart a constant amount of 18∶2n−6 was found at a low level of dietary 18∶2n−6.
Constant levels of arachidonic acid (20∶4n−6) were reached at 150 mg/100 g diet in all nerve structures, and at 300 mg/100g
diet in testicle and muscle, at 800 mg/100 g diet in kidney, and at 1200 mg/100 g diet in liver, lung, and heart. Constant
adrenic acid (22∶4n−6) levels were obtained at 150, 900, and 1200 mg/100 g diet in myelin, sciatic nerve, and brain, respectively.
Minimal levels were difficult to determine. In all fractions examined accumulation of docosapentaenoic acid (22∶5n−6) was
the most direct and specific consequence of increasing amounts of dietary 18∶2n−6. Tissue eicosapentaenoic acid (20∶5n−3)
and 22∶5n−3 levels were relatively independent of dietary 18∶2n−6 intake, except in lung, liver, and kidney. In several organs
(muscle, lung, kidney, liver, heart) as well as in myelin, very low levels of dietary linoleic acid led to an increase in
20∶5n−3. Dietary requirements for 18∶2n−6 varied from 150 to 1200 mg/100 g food intake, depending on the organ and the nature
of the tissue fatty acid. Therefore, the minimum dietary requirement is estimated to be about 1200 mg/100 g (i.e., the level
that ensures stable and constant amounts of arachidonic acid). 相似文献
18.
14C1-Linolenic acid was incorporated into lipids of hearts, livers, and carcasses of male rats. We studied the influence of diet
composition on extent and distribution of radioactivity. A CHOW diet, a purified, essential fatty acid (EFA)-deficient diet,
a purified control diet, and EFA-deficient diets with four fatty acid supplements were used. Supplements of 18∶2n−6, 20∶4n−6,
18∶3n−3, and 22∶6n−3 were given as single doses. Radioactivities in liver phosphatidyl ethanolamines (PE), phosphatidyl cholines,
and neutral lipids were measured. The distribution of radioactivity among the fatty acids in liver phospholipids was determined.
Rats on CHOW diet incorporated far less radioactivity than any other group into lipids of hearts and livers. Most of the activity
in livers was recovered as 20∶5n−3 and 22∶6n−3 in all rats. In EFA-deficient rats, the radioactivity in 22∶6n−3 of liver PE
was still increasing 36 hr after14C1-linolenic acid had been administered. The n−6 supplements (18∶2n−6 and 20∶4n−6) seemed to reduce the conversion of 20∶4n−3
to 20∶5n−3 (desaturation), whereas the n−3 supplements (18∶3n−3 and 22∶6n−3) reduced the conversion of 20∶5n−3 to 22∶5n−3
(elongation). Formation of 22∶6n−3 may be controlled by 22∶6n−3 itself at the elongation of 20∶5n−3 to 22∶5n−3. 相似文献
19.
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
20.
J. T. Venkatraman R. K. Tiwari B. Cinader J. Flory T. Wierzbicki M. T. Clandinin 《Lipids》1991,26(3):198-202
Inbred congenic mice of strains MRL/Mp-lpr/lpr (lpr/lpr) and MRL/Mp-+/+ (+/+) were fed nutritionally adequate semipurified
diets containing 20% (w/w) fat and differing in linoleic acid content. Levels of linoleic acid (18∶2n−6) and arachidonic acid
(20∶4n−6) in phospholipids of splenocytes, liver mitochondria and liver nuclear envelopes were determined. Membranes of lpr/lpr
mice exhibited significantly lower levels of 18∶2n−6 and 20∶4n−6 in phospholipids compared with the +/+ strain. The high linoleic
acid diet increased incorporation of 18∶2n−6 and 20∶4n−6 in most phospholipid fractions of these membranes. These observations
indicate that genotype as well as dietary 18∶2n−6 content significantly influenced incorporation of 18∶2n−6 and 20∶4n−6 into
membrane phospholipids. The results also suggest that membrane compositional abnormalities found in the lpr/lpr mice, which
develop lymphoma and age faster than +/+ mice, are not restricted to the immune system but also extend to other organs. Differences
observed in phospholipid fatty acid composition in splenocytes and liver subcellular membranes for mice fed diets differing
in linoleic acid content suggest that the early expression of the lpr gene resulting in progression of autoimmunity may be
delayed through dietary manipulation. 相似文献