共查询到20条相似文献,搜索用时 31 毫秒
1.
Jeannie Leonardi Elise Termine Florence Morand Raymond Lafont Henri Portugal Huguette Lafont Gilles Nalbone 《Lipids》1987,22(7):517-522
Rats were fed lard-enriched (17%) or corn oil-enriched (17%) diets and were compared with rats fed a low fat (4.5%) diet.
Cardiac protein, DNA, phospholipid (PL) and fatty acid (FA) compositions were analyzed. Neutral phospholipase A, lysophospholipase
and creatine kinase activities in the membrane and cytosolic compartments were also investigated.
No significant modification of cardiac protein, DNA nor PL was observed among the three groups. Some alterations appeared
in the FA composition. A lard-enriched diet induced a significant increase of 22∶5n−3 and 22∶6n−3 in heart phosphatidylcholine
(PC) and phosphatidylethanolamine (PE), whereas a linoleic acid-rich diet induced a specific increase of 22∶4n−6 and 22∶5n−6
in these two major PL.
Compared to rats fed the low fat diet, membrane-associated phospholipase A activity, measured by endogenous hydrolysis of
membrane PC and PE, showed a significant increase (+45%) for both PL in rats fed corn oil. However, the activity of membrane-associated
phospholipases, measured with exogenous [1-14C]dioleoyl PC, was not different among the three groups of rats. Cytoplasmic activity was decreased in rats fed corn oil,
and lysophospholipase and creatine phosphate kinase activities were not significantly affected by diet.
FA modification of the long chain n−6 FA induced by corn oil may be responsible for the observed increase in phospholipase
activity. Physiological implications are suggested in terms of membrane degradation and prostaglandin production.
Presented in part at the International Symposium on Lipid Metabolism in the Normoxic and Ischemic Heart, Rotterdam, The Netherlands,
September 1986. 相似文献
2.
The sciatic nerve of rats fed sunflower oil (6 mg 18∶3n−3/100 g of diet) presented dramatic alterations in the long chain
polyunsaturated fatty acids in comparison with those fed soy oil (130 mg 18∶3n−3/100 g of diet). In both 15-day-old and 60-day-old
animals fed sunflower oil, 22∶6n−3 (cervonic acid) was fourfold less, 22∶5n−6 was 10-fold greater; adrenic acid (22∶4n−6)
was slightly greater and arachidonic acid (20∶4n−6) was close to that in rats fed soy oil. The percentage distribution of
total polyunsaturated fatty acids as well as the individual saturated and monounsaturated fatty acids were the same in both
groups.
When the sunflower oil-fed animals were switched to a soy oil-containing diet for either 15 or 60 days, the percentage distribution
of 22∶6n−3 increased slowly to reach the control value 2.5 months later. Conversely 22∶5n−6 decreased slowly. The decay of
22∶5n−6 was more rapid than the increase of 22∶6n−3. 相似文献
3.
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
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.
(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
6.
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
7.
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
8.
Menhaden oil (MO), whose polyunsaturated fatty acids consist mainly of (n−3) fatty acids, was fed to spontaneously hypertensive
rats to determine the effect of (n−3) fatty acid on the in vitro production of prostaglandins produced from arachidonic acid
(20∶4[n−6]). Capacity to form PGE2 and PGF2α was impaired in homogenates of kidney medullae and cortices from rats fed the MO diet compared to rats fed the control diet.
The lower amounts of diene prostaglandins produced corresponded to the decrease in the amount of 20∶4 (n−6) in the tissue.
Possibly changes produced in tissue lipids by dietary fatty acids affect prostaglandin production by reducing the availability
of substrate in tissue lipids. 相似文献
9.
Male Fischer rats were fed the AIN76A diet containing varying n−6/n−3 FA ratios using sunflower oil (SFO), soybean oil (SOY),
and SFO supplemented with EPA-50 and GLA-80 (GLA) as fat sources. Hepatocyte nodules, induced using diethylnitrosamine followed
by 2-acetylaminofluorene/partial hepatoctomy promotion, were harvested, with surrounding and respective dietary control tissues,
3 mon after partial hepatectomy. The altered growth pattern of hepatocyte nodules in rats fed SFO is associated with a distinct
lipid pattern entailing an increased concentration of PE, resulting in increased levels of 20∶4n−6. In addition, there is
an accumulation of 18∶1n−9 and 18∶2n−6 and a decrease in the end products of the n−3 metabolic pathway in PC, suggesting a
dysfunctional Δ-6-desaturase enzyme. The hepatocyte nodules of the SFO-fed rats exhibited a significantly reduced lipid peroxidation
level that was associated with an increaser in the glutathione (GSH) concentration. The low n−6/n−3 FA ratio diets significantly
decreased 20∶4n−6 in PC and PE phospholipid fractions with a concomitant increase in 20∶5n−3, 22∶5n−3, and 22∶6n−3. The resultant
changes in the 20∶4/20∶5 FA ratio and the 20∶3n−6 FA level in the case of the GLA diet suggest a reduction of prostaglandin
synthesis of the 2-series. The GLA diet also counteracted the increased level of 20∶4n−6 in PE by equalizing the nodule/surrounding
ratio. The low n−6/n−3 ratio diets significantly increased lipid peroxidation levels in hepatocyte nodules, mimicking the
level in the surrounding and control tissue while GSH was decreased. An increase in n−3 FA levels and oxidative status resulted
in a reduction in the number of glutathione-S-transferase positive foci in the liver of the GLA-fed rats. Modulation of cancer
development with low n−6/n−3 ratio diets containing specific dietary FA could be a promising tool in cancer intervention in
the liver. 相似文献
10.
Klaus Eder 《Lipids》1999,34(7):717-725
This study was carried out to investigate the effects of a dietary oxidized oil on lipid metabolism in rats, particularly
the desaturation of fatty acids. Two groups of rats were fed initially for a period of 35 d diets containing 10% of either
fresh oil or thermally treated oil (150°C, 6d). The dietary fats used were markedly different for lipid peroxidation products
(peroxide value: 94.5 vs. 3.1 meq O2/kg; thiobarbituric acid-reactive substances: 230 vs. 7 μmol/kg) but were equalized for their fatty acid composition by using
different mixtures of lard and safflower oil and for tocopherol concentrations by individual supplementation with dl-α-tocopherol acetate. In the second period which lasted 16 d, the same diets were supplemented with 10% linseed oil to study
the effect of the oxidized oil on the desaturation of α-linolenic acid. During the whole period, all the rats were fed identical
quantities of diet by a restrictive feeding system in order to avoid a reduced food intake in the rats fed the oxidized oil.
Body weight gains and food conversion rates were only slightly lower in the rats fed the oxidized oil compared to the rats
fed the fresh oil. Hence, the effects of lipid peroxidation products could be studied without a distortion by a marked reduced
food intake and growth. To assess the rate of fatty acid desaturation, the fatty acid composition of liver and heart total
lipids and phospholipids was determined and ratios between product and precursor of individual desaturation reactions were
calculated. Rats fed the oxidized oil had reduced ratios of 20∶4n−6/18∶2n−6, 20∶5n−3/18∶3n−3, 20∶4n−6/20∶3n−6, and 22∶6n−3/22∶5n−3
in liver phospholipids and reduced ratios of 20∶4n−6/18∶2n−6, 22∶5n−3/18∶3n−3, and 22∶6n−3/18∶3n−3 in heart phospholipids.
Those results suggest a reduced rate of desaturation of linoleic acid and α-linolenic acid by microsomal Δ4-, Δ5-, and Δ6-desaturases.
Furthermore, liver total lipids of rats fed the oxidized oil exhibited a reduced ratio between total monounsaturated fatty
acids and total saturated fatty acids, suggesting a reduced Δ9-desaturation. Besides those effects, the study observed a slightly
increased liver weight, markedly reduced tocopherol concentrations in liver and plasma, reduced lipid concentrations in plasma,
and an increased ratio between phospholipids and cholesterol in the liver. Thus, the study demonstrates that feeding an oxidized
oil causes several alterations of lipid and fatty acid metabolism which might be of great physiologic relevance. 相似文献
11.
The fatty acid composition of diacyl- and alkylacylglycerophosphocholine (PC), phosphatidylinositol (PI), phosphatidylserine
(PS), alkenylacyl-glycerophosphoethanolamine (aPE), and diacyl- and alkylacyl-glycerophosphoethanolamine (dPE) was assessed
in isolated splenocytes from C3H/Hen mice fed one of four purified isocaloric diets for six weeks. Diets contained 20% by
weight of either a high-linoleate sunflower oil (Hi 18∶2), a high-oleate sunflower oil (Hi 18∶1), a mixture of 17% menhaden
fish oil and 3% high-linoleate sunflower oil (Hi n−3), or a mixture of 17% coconut oil and 3% high-linoleate sunflower oil
(Hi SFA). Spleen weight and immune cell yield were significantly higher (P<0.05) in mice fed the Hi 18∶1 or the Hi n−3 diets
compared with those fed the Hi 18∶2 and Hi SFA diets. Distinctive patterns of fatty acids were observed for each phospholipid
in response to dietary fatty acids. Dietary fat significantly affected (P<0.05) total polyunsaturated fatty acids (PUFA) in
PC and dPE, total saturated fatty acids (SFA) in PC, total monounsaturated fatty acids (MUFA), and n−3 PUFA in all phospholipid
classes examined. In mice fed the Hi n−3 diet, n−3 PUFA were significantly elevated, whereas n−6 PUFA decreased in all of
the phospholipids. In these mice, eicosapentaenoic acid (EPA) was the predominant n−3 PUFA in PC and PI, whereas docosahexaenoic
acid (DHA) was the major n−3 PUFA in aPE and PS. Interestingly, the ratios of n−3/n−6 PUFA in the phospholipids from these
mice were 3.2, 2.4, 1.8, 0.8 and 0.8 for aPE, PS, dPE, PC and PI, respectively. These data suggest a preferential incorporation
of n−3 PUFA into aPE, PS and dPE over PC and PI. 相似文献
12.
Renée Grataroli Jeannie Léonardi Monique Charbonnier Raymond Lafont Huguette Lafont Gilles Nalbone 《Lipids》1988,23(7):666-670
Three groups of male rats were fed either a corn oilenriched diet (17%, w/w), a salmon oil-enriched diet (12.5%) supplemented
with corn oil (4.5%) or a low-fat diet (4.4%) for eight wk to investigate the possible relationships between dietary fatty
acids and lipid composition, and prostaglandin E2 level and phospholipase A2 activity in the rat gastric mucosa.
High-fat diets induced no important variation in total protein, phospholipid and cholesterol contents of gastric mucosa.
Compared with a low-fat diet, corn oil produced a higher n−6/n−3 ratio in mucosal lipids, whereas this ratio was markedly
lowered by a fish oil diet.
In comparison with the low-fat diet, the production of prostaglandin E2(PGE2) in gastric mucosa of rats fed salmon oil was significantly, decreased by a factor of 2.8. In the corn oil group, PGE2 production tended to decrease, but not significantly.
In comparison with the low-fat diet, both specific and total gastric mucosal phospholipase A2 activities were increased (+18 and 23%, respectively) in the salmon oil group; they were unchanged in the corn oil group.
It is suggested that the decrease of gastric PGE2 in rats fed fish oil is not provoked by a decrease in phospholipase A2 activity but may be the result of the substitution of arachidonic acid by n−3 PUFA or activation of PGE2 catabolism. 相似文献
13.
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
14.
Female pigs were fed from three wk of age and up to two years a diet containing partially hydrogenated fish oil (PHFO, 28%trans monoenoic fatty acids), partially hydrogenated soybean oils (PHSBO, 36%trans fatty acids) or lard. No consistent differences were found between PHFO and PHSBO with regard to incorporation oftrans fatty acids in organ lipids, buttrans incorporations were highly organ-specific. Notrans fatty acids were detected in brain phosphatidylethanolamine (PE). The incorporation of monoenoictrans isomers, as a percentage of totalcis + trans, in other organs was highest in subcutaneous adipose tissue and liver mitochondria PE, followed by blood lipids with the
lowest level in heart PE. The percentage oftrans isomers compared with that of dietary lipids was consistently lower for 20∶1, compared with 18∶1 in organs from PHFO-fed
pigs. The only effect of dietarytrans fatty acids on the fatty acid pattern of brain PE was an increased level of 22∶5n−6. Heart PE and total serum lipids of pigs
fed the hydrogenated fats contained higher levels of 18∶2n−6, and these lipids of the PHFO-fed group also contained slightly
elevated amounts of 20∶3n−6, 18∶3n−3 and 20∶5n−3. Liver mitochondria PE of the PHFO group also contained higher levels of
20∶3n−6 and 22∶5n−6. Dietarytrans fatty acids caused a consistent decrease of saturated fatty acids compensated by increased levels of monoenes. Thus, it may
be concluded that dietary long-chaintrans fatty acids in PHFO behaved similarly metabolically to 18∶1-trans in PHSBO in pigs, without noticeable influence on brain PE composition and with moderate to slight effects on the fatty acid
profile of the other organs. 相似文献
15.
P. E. Wainwright Y. S. Huang B. Bulman-Fleming D. Dalby D. E. Mills P. Redden D. McCutcheon 《Lipids》1992,27(2):98-103
This study examines the effects of the ratio of n−3/n−6 fatty acids (FA) on brain development in mice when longchain n−3 FA
are supplied in the diet. From conception until 12 days after birth, B6D2F1 mice were fed liquid diets, each providing 10% of energy from olive oil, and a further 10% from different combinations of
free FA concentrates derived from safflower oil (18∶2n−6), and fish oil (20∶5n−3 and 22∶6n−3). The range of dietary n−3/n−6
ratios was 0,025, 0.5, 1.0, 2.0, and 4.0, with an n−6 content of greater than 1.5% of energy in all diets, and similar levels
of total polyunsaturated fatty acids (PUFA). In an additional group of ratio 0.5, 18∶2n−6 was partially replaced by its δ6
desaturation product, 18∶3n−6. Biochemical analyses were conducted on 12-day-old pup brains, as well as on samples of maternal
milk. No obvious effects on overall pup growth and development were observed, apart from a smaller litter size at ratio 1.
Co-variance analysis indicated that increasing the n−3/n−6 ratio was associated with slightly smaller brains, relative to
body weight. We found that 18∶2n−6 and 20∶5n−3 were the predominant n−6 and n−3 FA in the milk; in the brain these were 20∶4n−6
and 22∶6n−3, respectively. Increasing dietary n−3/n−6 ratios generally resulted in an increase in n−3 FA, with a corresponding
decrease in n−6 FA. The n−3/n−6 ratio of the milk lipids showed a strong linear relationship with the diet, but in the brain
the rate of increase tended to decrease beyond 0.5 (phosphatidylcholine, PC) and 0.25 (phosphatidylethanolamine, PE), such
that there was a significant quadratic contribution to the relationship. The partial replacement of dietary 18∶2n−6 with 18∶3n−6
raised levels of 20∶4n−6 in milk, brain PC, and brain PE. These results indicate that the n−3/n−6 ratio of the phospholipids
in the developing mouse brain responds maximally to maternal dietary long-chain n−3/n−6 ratios of between 0.25 and 0.5. 相似文献
16.
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
17.
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
18.
Fish oil-enriched diets increase n−3 FA in tissue phospholipids; however, a similar effect by plant-derived n−3 FA is poorly
defined. To address this question, we determined mass changes in phospholipid FA, individual phospholipid classes, and cholesterol
in the liver, heart, and brain of rats fed diets enriched in flax oil (rich in 18∶3n−3), fish oil (rich in 22∶6n−3 and 20∶5n−3),
or safflower oil (rich in 18∶2n−6) for 8 wk. In the heart and liver phospholipids, 22∶6n−3 levels increased only in the fish
oil group, although rats fed flax oil accumulated 20∶5n−3 and 22∶5n−3. However, in the brain, the flax and fish oil diets
increased the phospholipid 22∶6n−3 mass. In all tissues, these diets decreased the 20∶4n−6 mass, although the effect was more
marked in the fish oil than in the flax oil group. Although these data do not provide direct evidence for 18∶3n−3 elongation
and desaturation by the brain, they demonstrate that 18∶3n−3-enriched diets reduced tissue 20∶4n−6 levels and increased cellular
n−3 levels in a tissuedependent manner. We hypothesize, based on the lack of increased 22∶6n−3 but increased 18∶3n−3 in the
liver and heart, that the flax oil diet increased circulating 18∶3n−3, thereby presenting tissue with this EFA for further
elongation and desaturation. 相似文献
19.
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
20.
The effect of zinc deficiency on the levels of n−6 and n−3 polyunsaturated fatty acids (PUFA) in lipids from tissues of rats
fed a diet containing linseed oil was investigated. Rats were fed either a control diet (25 mg Zn/kg) or a zinc-deficient
diet (0.8 mg Zn/kg) for 10 d. To avoid energy and nutrient deficiency, 11.6 g of diet per day was administered by gastric
tube. At the end of the experiment, rats fed the zinc-deficient diet had drastically reduced plasma zinc concentration and
alkaline phosphatase activity consistent with severe zinc deficiency in these rats. Zinc-deficient rats had higher levels
of n−3 PUFA, in particular eicosapentaenoic acid (EPA), and lower levels of n−6 PUFA, in particular linoleic acid, in liver
and plasma phosphatidylcholine (PC) and in erythrocyte membrane total lipids than did control rats. By contrast, the levels
of n−3 PUFA in PC from testes and heart, and in phosphatidylethanolamine (PE) from liver, testes and heart, were only slightly
different between zinc-deficient and control rats. The study suggests that desaturation of α-linolenic acid is not inhibited
by zinc deficiency, and that in zinc-deficient rats, n−3 PUFA preferentially incorporated into phospholipids at the expense
of n−6 PUFA, especially EPA into PC. The study also shows that the effect of zinc deficiency on PUFA levels is different for
PC and PE in rat tissues. 相似文献