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1.
ROC-1 cells are a hybrid of C−6 rat glioma and rat oligodendroglia cells. Biochemically these cells resemble the oligodendroglia
parent, but their lipid composition is unknown. The phospholipid composition in mole % was: cardiolipin, 1.0; phosphatidylglycerol,
1.2; ethanolamine glycerophospholipids, 27.6; phosphatidylinositol, 5.8; lysophosphatidylethanolamine, 0.8; phosphatidylserine,
5.6; choline glycerophospholipids, 43.7; sphingomyelin, 13.7; phosphatidylinositol-4-monophosphate, 0.8; and lysophosphatidylcholine,
0.6. The choline and ethanolamine plasmalogens made up 7.2 and 18.4% of the total phospholipids, respectively. The phospholipid
composition reflects that of both parental cells. The cells had moderate to high levels of 20∶3n−9 indicating n−6 series fatty
acid deficiency. The phosphatidylinositol had very high 20∶3n−9 levels with a 20∶3n−9/20∶4n−6 ratio of 2.1 compared to 0.44
and 0.58 for ethanolamine glycerophospholipids (EtnGpl) and choline glycerophospholipids (ChoGpl) respectively. The saturated/polyenoic
fatty acid ratios were 0.40 for EtnGpl, 3.38 for ChoGpl and 1.48 for phosphatidylinositol. 相似文献
2.
Docosahexaenoic acid (DHA, 22∶6n−3) is one of the major polyunsaturated fatty acids esterified predominantly in aminophospholipids
such as ethanolamine glycerophospholipid (EtnGpl) and serine glycerophospholipid (SerGpl) in the brain. Synaptosomes prepared
from rats fed an n−3 fatty acid-deficient safflower oil (Saf) diet had significantly decreased 22∶6n−3 content with a compensatory
increased 22∶5n−6 content when compared with rats fed an n−3 fatty acid-sufficient perilla oil (Per) diet. When the Saf group
was shifted to a diet supplemented with safflower oil plus 22∶6n−3 (Saf+DHA) after weaning, 22∶6n−3 content was found to be
restored to the level of the Per group. The uptake of [3H]ethanolamine and its conversion to [3H]EtnGpl did not differ significantly among the three dietary groups, whereas the formation of [3H]lysoEtnGpl from [3H]ethanolamine was significantly lower in the Saf group than in the other groups. The uptake of [3H]serine, its incorporation into [3H]SerGpl, and the conversion into [3H]EtnGpl by decarboxylation of [3H]SerGpl did not differ among the three dietary groups. The observed decrease in lysoEtnGpl formation associated with a reduction
of 22∶6n−3 content in rat brain synaptosomes by n−3 fatty acid deprivation may provide a clue to reveal biochemical bases
for the dietary fatty acids-behavior link. 相似文献
3.
Docosahexaenoic acid (DHA, 22∶6n−3) is an n−3 polyunsaturated fatty acid which attenuates the development of hypertension
in spontaneously hypertensive rats (SHR). The effects of DHA on delta-9-desaturase activity in hepatic microsomes and fatty
acid composition were examined in young SHR. Two groups of SHR were fed either a DHA-enriched diet or a control diet for 6
wk. Desaturase activity and fatty acid composition were determined in hepatic microsomes following the dietary treatments.
Delta-9-desaturase activity was decreased by 53% in DHA-fed SHR and was accompanied by an increase in 16∶0 and a reduction
in 16∶1n−7 content in hepatic microsomes. The DHA diet also increased the levels of eicosapentaenoic acid (20∶5n−3) and DHA.
The n−6 fatty acid content was also affected in DHA-fed SHR as reflected by a decrease in gamma-linolenic acid (18∶3n−6),
arachidonic acid (20∶5n−6), adrenic acid (22∶4n−6), and docosapentaenoic acid (22∶5n−6). A higher proportion of dihomo-gamma-linolenic
acid (20∶3n−6) and a lower proportion of 20∶4n−6 is indicative of impaired delta-5-desaturase activity. The alterations in
fatty acid composition and metabolism may contribute to the antihypertensive effect of DHA previously reported. 相似文献
4.
Rats were fed for two generations a purified, linolenic acid-deficient diet in which the only source of lipid was purified
methyl linoleate. This diet contained about 38 mg linolenic acid/kg diet. Control rats were given the same diet supplemented
with methyl linolenate (2,500 mg/kg diet). Male and female rats ranged in age from weanling pups to adults. Lipids were extracted
from liver, brain, kidney, spleen, heart, muscle, gastrointestinal tract, lung, ovary, testis, adrenal, plasma, erythrocytes,
retina, and adipose tissue. Fatty acids of major phospholipid classes (choline phosphoglycerides, ethanolamine phosphoglycerides,
and mixed serine phosphoglycerides plus inositol phosphoglycerides) or of total lipid extracts were measured by gas liquid
chromatography. Growth rates and organ weights were similar in control and linolenic acid-deficient rats. The major effect
of the deficiency was to lower the proportions of n−3 fatty acids, especially 22∶6 n−3, in all the organs analyzed. Docosahexaenoic
acid (22∶6 n−3) was mainly replaced by 22∶5 n−6 in deficient rats. The greatest changes in composition were found in brain,
heart, muscle, retina, and liver. 相似文献
5.
Although fatty acid-binding proteins (FABP) differentially affect fatty acid uptake, nothing is known regarding their role(s)
in determining cellular phospholipid levels and phospholipid fatty acid composition. The effects of liver (L)- and intestinal
(I)-FABP expression on these parameters were determined using stably transfected L-cells. Expression of L- and I-FABP increased
cellular total phospholipid mass (nmol/mg protein) 1.7- and 1.3-fold relative to controls, respectively. L-FABP expression
increased the masses of choline glycerophospholipids (ChoGpl) 1.5-fold, phosphatidylserine (PtdSer) 5.6-fold, ethanolamine
glycerophospholipids 1.4-fold, sphingomyelin 1.7-fold, and phosphatidylinositol 2.6-fold. In contrast, I-FABP expression only
increased the masses of ChoGpl and PtdSer, 1.2- and 3.1-fold, respectively. Surprisingly, both L- and I-FABP expression increased
ethanolamine plasmalogen mass 1.6- and 1.1-fold, respectively, while choline plasmalogen mass was increased 2.3- and 1.7-fold,
respectively. The increase in phospholipid levels resulted in dramatic 48 and 33% decreases in the cholesterol-to-phospholipid
ratio in L- and I-FABP expressing cells, respectively. L-FABP expression generally increased polyunsaturated fatty acids,
primarily by increasing 20∶4n−6 and 22∶6n−3, while decreasing 18∶1n−9 and 16∶1n−7. I-FABP expression generally increased only
20∶4n−6 proportions. Hence, expression of both I- and L-FABP differentially affected phospholipid mass, class composition,
and acyl chain composition. Although both proteins enhanced phospholipid synthesis, the effect of L-FABP was much greater,
consistent with previous work suggesting that these two FABP differentially affect lipid metabolism. 相似文献
6.
The effect of dietary restriction of n−3 fatty acids during development on brain phospholipid fatty acid composition and exploratory
behavior has been studied in male Sprague Dawley rats. Female rats were fed semipurified diets containing either 5.5% safflower
oil or 6% soybean oil for 6 wk prior to mating and throughout gestation and lactation. Control rats were maintained on laboratory
chow. The male pups were weaned to the diets of the dams except for one group which was switched from safflower to soybean
oil at weaning. Behavioral studies and brain phospholipid analyses were conducted at 16–18 wk of age. Rats fed safflower oil
showed significantly lower levels of 22∶6n−3 in phospholipids of synaptic membranes and myelin than rats fed soybean oil or
chow. The decrease in 22∶6n−3 was compensated for by an increase in 22∶5n−6, the total content of polyunsaturated fatty acids
remaining approximately constant. The brain phospholipid fatty acid composition of rats switched from safflower to soybean
oil at weaning was similar to that of rats fed soybean oil throughout the experiment. There was no difference in spontaneous
locomotor activity among the different dietary groups. However, rats raised on safflower oil displayed a significantly lower
exploratory activity (horizontal movements and rearings) in a novel environment than rats fed soybean oil or chow. In contrast
to the brain phospholipid fatty acid composition, there was no recovery of exploratory behavior in rats raised on safflower
oil and switched to soybean oil at weaning suggesting a specific requirement of n−3 fatty acids during development. 相似文献
7.
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
8.
Watkins SM Lin TY Davis RM Ching JR DePeters EJ Halpern GM Walzem RL German JB 《Lipids》2001,36(3):247-254
Diet and fatty acid metabolism interact in yet unknown ways to modulate membrane fatty acid composition and certain cellular
functions. For example, dietary precursors or metabolic products of n-3 fatty acid metabolism differ in their ability to modify
specific membrane components. In the present study, the effect of dietary 22∶6n−3 or its metabolic precursor, 18∶3n−3, on
the selective accumulation of 22∶6n−3 by heart was investigated. The mass and fatty acid compositions of individual phospholipids
(PL) in heart and liver were quantified in mice fed either 22∶6n−3 (from crocodile oil) or 18∶3n−3 (from soybean oil) for
13 wk. This study was conducted to determine if the selective accumulation of 22∶6n−3 in heart was due to the incorporation
of 22∶6n−3 into cardiolipin (CL), a PL most prevalent in heart and known to accumulate 22∶6n−3. Although heart was significantly
enriched with 22∶6n−3 relative to liver, the accumulation of 22∶6n−3 by CL in heart could not quantitatively account for this
difference. CL from heart did accumulate 22∶6n−3, but only in mice fed preformed 22∶6n−3. Diets rich in non-22∶6n−3 fatty
acids result in a fatty acid composition of phosphatidylcholine (PC) in heart that is unusually enriched with 22∶6n−3. In
this study, the mass of PC in heart was positively correlated with the enrichment of 22∶6n−3 into PC. The increased mass of
PC was coincident with a decrease in the mass of phosphatidylethanolamine, suggesting that 22∶6n−3 induced PC synthesis by
increasing phosphatidylethanolamine-N-methyltransferase activity in the heart. 相似文献
9.
The combined effects of age and of diet deficient in n−3 fatty acids on Δ6 desaturation of linoleic acid and on lipid fatty
acid composition were studied in the liver of the rat at 2, 6, 12, 18 and 24 mon of age. The profiles of Δ6 desaturase activity
and fatty acid composition were studied in the deficient rats refed, at these different ages either with 18∶3n−3 (mixture
of peanut and rapeseed oils) or with 20∶5n−3+22∶6n−3 (fish oil) diets for 2, 4, 8 or 12 wk. Results showed that the liver
Δ6 desaturation activity in the control rats remained high at 2 and 6 mon, decreased by 30% from 6 to 12 mon, and then remained
stable from 12 to 24 mon. In the deficient rats, this activity remained high during the entire period studied. Thus, the profile
of liver Δ6 desaturase activity after puberty was not related to age only; it also depended on the polyunsaturated fatty acid
(PUFA) n−6 and n−3 balance in the diet. In the controls, in parallel with the Δ6 desaturase activity, PUFA metabolism could
be divided into three periods: a “young” period, and “old age” period, separated by a period of transition between 6 and 12
mon. Recovery from PUFA n−3 deficiency occurred at all ages but in a different manner depending on whether the rats were “young”
or “old”. Recovery was faster if long-chain n−3 PUFA rather than α-linolenic acid were supplied in the diet. 相似文献
10.
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
11.
The influence of age and cholesterol on polyunsaturated fatty acids (PUFa) levels was studied in young and old male Sprague-Dawley
rats. Animals were fed a fat-free diet supplemented with 10% (by wt) safflower oil with or without 1% cholesterol for 8 wk.
As a result of cholesterol feeding, proportions of linoleic acid (18∶2n−6) and dihomo-γ-linolenic acid (30∶3n−6) were increased
and and that of arachidonic acid (20∶4n−6) was decreased in the liver and platelet phospholipids in 64-wk-old rats, suggesting
inhibitory effects of cholesterol on 20∶4n−6 synthesis from 18∶2n−6. The prominent age-dependent effect on the levels of PUFA
was a retention of C−22 n−3 PUFA, accompanied by decreased C−22 n−6 PUFA and increased 20∶3n−6 in the liver and platelet phospholipids.
Ratio of 20∶3n−6/20∶4n−6 increased in 64-wk-old rats regardless of dietary cholesterol, suggesting depressed Δ5-desaturase
with age. In aorta phospholipids, 20∶3n−6 content and 20∶3n−6/20∶4n−6 ratio increased with cholesterol supplementation, but
not with age. These results suggest that changes of PUFA composition of platelet phospholipids with age are closely linked
with changes in liver phospholipids. The 20∶4n−6 content in both platelet and aorta phospholipids is kept constant, despite
other n−6 and n−3 PUFA being affected by age. 相似文献
12.
The fatty acid composition of serum total lipids, of phospholipids of various organs (liver, heart, kidney), and of nervous
structures (brain, retina, sciatic nerve, myelin, synaptosomes) have been compared in lean (Fa/−) and genetically obese (fa/fa)
Zucker female rats. Both received a standard commercial diet including 37% of 18∶2n−6 and 5% of n−3 polyunsaturated fatty
acids (PUFA), 1.7% of which were in the form of 20∶5n−3 and 22∶6n−3. In comparison with lean rats, the results for the obese
rats pointed out (i) no difference in the fatty acid composition of nervous structures: (ii) a decrease of 18∶2n−6 (from −8%
to −35%) and of 20∶4n−6 (from −9% to −49%) in serum, liver and in kidney; this was compensated for by an increase in 20∶3n−6
(from +30% to +320%) and in total n−3 PUFA (from +68% to +76%); (iii) a decrease of 20∶4n−6 (−18%) and of 22∶6n−3 (−24%) in
heart compensated for by an increase in 18∶2n−6 (+39%) and in 20∶3n−6 (+233%); and (iv) constant levels of total PUFA (n−6
and n−3) in the various fractions studied, except in serum where this level decreased (−23%). Finally, except for the nervous
structures, tissue phospholipids of obese rats included a lower proportion of 20∶4n−6 and a higher proportion of 20∶3n−6.
This resulted in a significant reduction in the 20∶4n−6/20∶3n−6 ratio; by contrast, the 20∶3n−6/18∶2n−6 ratio increased. The
results suggest that in Zucker rats, the obese character (fa/fa) affects the desaturation-elongation process of 18∶2n−6 to
20∶4n−6 by specifically decreasing Δ5-desaturase activity. 相似文献
13.
(n−3) and (n−6) polyunsaturated fatty acids in the phosphoglycerides of salt-secreting epithelia from two marine fish species 总被引:3,自引:0,他引:3
Fatty acid analyses were carried out on phosphoglycerides isolated from microsomal fractions of the rectal gland of the dogfish,Scyliorthinus canicula, and gills of the cod,Gadus morhua. Ratios of (n−3)/(n−6) polyunsaturated fatty acids were ca. 10 for phosphatidylcholine, (PC), phosphatidylethanolamine (PE)
and phosphatidylserine (PS) from cod gills, reflecting high concentrations of 20∶5 (n−3) and 22∶6(n−3). The ratio for phosphatidylinositol
(PI) from cod gills was 1.3, reflecting high concentrations of 20∶4(n−6) as well as (n−3) polyunsaturates. PC, PE and PS from
rectal glands all had much lower (n−3)/(n−6) ratios than in cod gills, reflecting higher concentrations of 20∶4(n−6), but
the lowest ratio was again present in PI. The latter phospholipid had high concentrations of 18∶0 in both tissues. The relative
constancy of the fatty acid composition of PI in the two salt-secreting tissues and its similarity to mammalian phospholipids
is considered to reflect its specialized role in biomembranes. 相似文献
14.
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
15.
A fat-deficient diet was initiated in mice before birth and at different ages during development and maturation. The induction
of an essential fatty acid deficiency in brain was most effective when the deficient diet was initiated prenatally. With increasing
time on the deficient diet, there was an increase in 20∶3(n−9) and a decrease in 20∶4(n−6) in the phosphoglycerides of subcellular
brain fractions. The highest ratio of 20∶3(n−9) to 20∶4(n−6) observed was 1.5 for both diacyl and alkenylacyl glycerophosphorylethanolamines
in the synaptosome-rich fraction from mice on the deficient diet from before birth to 7 months of age. The acyl groups of
brain ethanolamine plasmalogens are quite susceptible to alteration by the fat-deficient diet. Elongated products of 20∶3(n−9),
tentatively identified as 22∶3(n−9) and 22∶5(n−9), also were present in brain during essential fatty acid deficiency. These
fatty acids were preferentially linked to the alkenylacyl glycerophosphorylethanolamines. It further was observed that, even
when the deficient diet was initiated after maturation, similar changes in fatty acid composition occurred in both myelin
and synaptosomerich fractions, but at a slower rate. For mice on the deficient diet from 12–18 months of age, the highest
ratio of 20∶3(n−9) to 20∶4(n−6) was 0.6 for the alkenylacyl glycerophosphorylethanolamines from the myelin. 相似文献
16.
Three groups of male mice were fed a normal diet or a semisynthetic diet containing either 10% hydrogenated coconut oil (CO
group) or 10% menhaden oil (MO group) for two wk. The synthetic diet altered the fatty acid composition of lung microsomal
lipids. Mice ingesting menhaden oil contained greater amounts of eicosapentaenoic acid (20∶5 n−3), docosapentaenoic acid (22∶5
n−3) and docosahexaenoic acids (22∶6 n−3) and decreased amounts of n−6 fatty acids such as arachidonic and adrenic. Synthesis
of prostaglandin E2 and prostaglandin F2α from exogenous arachidonic acid was significantly depressed in n−3 fatty acid-enriched lung microsomes. These studies indicated
that dietary fish oil not only alters the fatty acid composition of lung microsomes but also lowers the capacity of lungs
to synthesize prostaglandins from arachidonic acid. 相似文献
17.
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
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.
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
20.
P. Hoffmann H. -U. Block J. Beitz Ch. Taube W. Forster P. Wortha P. Singer E. Naumann H. Heine 《Lipids》1986,21(12):733-737
Following the suckling period, four groups of male four-week-old spontaneously hypertensive rats (SHR) were fed semisynthetic
diets with 14% (by weight) of either sunflower seed oil [46% 18∶2(n−6); linoleic acid (LA)-rich], linseed oil [62.5% 18∶3(n−3)+12.9%
18∶2(n−6); α-linolenic acid (LNA)-rich], evening primrose oil [9.2% 18∶3(n−6)+71% 18∶2(n−6); γ-linolenic acid (LNA)-rich]
or hydrogenated palm kernel fat [1.5% 18∶2(n−6); polyunsaturated fatty acid (PUFA)-deficient], respectively, up to an age
of 18 wk. All diets enriched with PUFA provoked an attenuation of hypertension development. The effect was lowest in the LA-rich
group and highest in the γ-LNA-rich group. Differences in fatty acid composition of renal phospholipids between groups reflect
the fatty acids present in the respective dietary fats. Renomedullary production of PGF2α was significantly reduced in α-LNA-rich and slightly diminished in γ-LNA-rich fed rats. Aortic formation of 6-keto-PGF1α and TXB2 was increased in animals fed the γ-LNA-rich diet. Thus, the attenuation of hypertension development cannot be explained only
by changes in prostanoid formation. Other mechanisms possibly involved should be pursued. 相似文献