共查询到20条相似文献,搜索用时 15 毫秒
1.
We evaluated the utilization of α-linolenic acid (18∶3n−3) in growing rats consuming a diet deficient in n−6 PUFA. After 90
d, whole-body 18∶3n−3 accumulation was 55% lower, total n−3 PUFA accumulation was 21% lower, and 18∶3n−3 disappearance was
14% higher in n−6 PUFA-deficient rats. Part of the reduction of whole-body 18∶3n−3 in n−6 PUFA-deficient rats was due to the
25% increase in net conversion of 18∶3n−3 to long-chain n−3 PUFA. Despite adequate 18∶3n−3 intake, n−6 PUFA deficiency decreased
the accumulation of 18∶3n−3 and total n−3 PUFA. 相似文献
2.
Flaxseed, echium, and canola oils contain α-linolenic acid (18∶3n−3, ALA) in a range of concentrations. To examine their effect
on elevating cardiac levels of long-chain n−3 FA, diets based on these n−3-containing vegetable oils were fed to rats for
4 wk. Sunflower oil, which contains little ALA, was a comparator. Despite canola oil having the lowest ALA content of the
three n−3-containing vegetable oils, it was the most potent for elevating DHA (22∶6n−3) levels in rat hearts and plasma. However,
the relative potencies of the dietary oils for elevation of EPA (20∶5n−3) in heart and plasma followed the same rank order
as their ALA content, i.e., flaxseed>echium>canola>sunflower oil. This paradox may be explained by lower ALA intake leading
to decreased competition for Δ6 desaturase activity between ALA and the 24∶5n−3 FA precursor to DHA formation. 相似文献
3.
Effect of dietary n−6 and n−3 polyunsaturated fatty acids on peroxidizability of lipoproteins in steers 总被引:3,自引:0,他引:3
The susceptibility of major plasma lipoproteins to lipoperoxidation was studied in relation to the FA composition of their
neutral and polar lipids in steers given PUFA-rich diets. Two trials used, respectively, 18 (“sunflower” experiment, S) or
24 (“linseed” experiment, L) crossbred Salers x Charolais steers. Each involved three dietary treatments over a 70-d period:
a control diet (CS or CL diets) consisting of hay and concentrate, or the same diet supplemented with oilseeds (4% diet dry
matter) fed either as seeds (SS or LS diets) or continuously infused into the duodenum (ISO or ILO diets). Compared with control
diets, ISO and ILO treatments tended to decrease the resistance time of LDL and HDL classes to peroxidation, mainly owing
to the enrichment of their polar and neutral lipids with PUFA. With diets SS and LS, sensitivity of major lipoprotein classes
(LDL, light and heavy HDL) was not affected because ruminal hydrogenation of dietary PUFA decreased their incorporation into
lipoparticles. ISO and ILO treatments induced a more important production of conjugated dienes and hydroperoxides generated
by peroxidation in the three lipoprotein classes due to the higher amounts of PUFA esterified in lipids of the core and the
hydrophilic envelope of particles. The production of malondialdehyde (MDA) increased in steers fed linseed supplements, indicating
that MDA production did not occur with linoleic acid provided by sunflower oil supplements. Thus, plasma peroxidation of PUFA
generates toxic products in steers fed diets supplemented with PUFA and can be deleterious for the health of the animal during
long-term treatment. 相似文献
4.
The intake of individual n−6 and n−3 PUFA has been estimated in 4,884 adult subjects (2,099 men and 2,785 women), volunteers
from the French SU.VI.MAX intervention trial. The food intakes of each subject were recorded in at least ten 24-h record questionnaires
completed over a period of 2.5 yr, allowing the estimation of the daily intake of energy; total fat; and linoleic, α-linolenic,
arachidonic, eicosapentaenoic (EPA), n−3 docosapentaenoic (DPA), and docosahexaenoic (DHA) acids. The mean total fat intake
corresponded to 94.1 g/d (36.3% of total energy intake) in men and 73.4 g/d (38.1% of energy) in women. The intake of linoleic
acid was 10.6 g/d in men and 8.1 g/d in women, representing 4.2% of energy intake; that of α-linolenic acid was 0.94 g/d in
men and 0.74 g/d in women, representing 0.37% of energy intake, with a mean linoleic/α-linolenic acid ratio of 11.3. The mean
intakes of long-chain PUFA were: arachidonic acid, 204 mg/d in men and 152 mg/d in women; EPA, 150 mg/d in men and 118 mg/d
in women; DPA, 75 mg/d in men and 56 mg/d in women; DHA, 273 mg/d in men and 226 mg/d in women; long-chain n−3 PUFA, 497 mg/d
in men and 400 mg/d in women. Ninety-five percent of the sample consumed less than 0.5% of energy as α-linolenic acid, which
is well below the current French recommendation for adults (0.8% of energy). In contrast, the mean intakes of long-chain n−6
and n−3 PUFA appear fairly high and fit the current French recommendations (total long-chain PUFA: 500 mg/d in men and 400
mg/d in women; DHA: 120 mg/d in men and 100 mg/d in women). The intakes of α-linolenic acid, and to a lesser extent of linoleic
acid, were highly correlated with that of lipids. Whereas the main source of linoleic acid was vegetable oils, all food types
contributed to α-linolenic acid intake, the main ones being animal products (meat, poultry, and dairy products). The main
source of EPA and DHA (and of total long-chain n−3 PUFA) was fish and seafood, but the major source of DPA was meat, poultry,
and eggs. Fish and seafood consumption showed very large interindividual variations, the low consumers being at risk of insufficient
n−3 PUFA intake. 相似文献
5.
Oxidation, esterification, desaturation, and elongation of [1-14C]18∶2n−6 and [1-14C]18∶3n−3 were studied using hepatocytes from Atlantic salmon (Salmo salar I.) maintained on diets deficient in n−3 and n−6 polyunsaturated fatty acids (PUFA) or supplemented with n−3 PUFA. For both
dietary groups, radioactivity from 18∶3n−3 was incoporated into lipid fractions two to three times faster than from 18∶2n−6,
and essential fatty acids (FFA) deficiency doubled the incorporation. Oxidation to CO2 was very low and was independent of substrate or diet, whereas oxidation to acid-soluble products was stimulated by EFA deficiency.
Products from 18∶2n−6 were mainly 18∶3n−6, 20∶3n−6, and 20∶4n−6, with minor amounts of 20∶2n−6 and 22∶5n−6. Products from
18∶3n−3 were mainly 18∶4n−3, 20∶5n−3, and 22∶6n−3, with small amounts of 20∶3n−3. The percentage of 22∶6n−3 in the polar lipid
fraction of EFA-deficient hepatocytes was fourfold higher than in n−3 PUFA-supplemented cells. This correlated well with our
other results obtained after abdominal injection of [1-14C]18∶3n−3 and [1-14C]18∶2n−6. In hepatocytes incubated with [4,5-3H]-22∶6n−3, 20∶5n−3 was the main product. This retrocon-version was increased by EFA deficiency, as was peroxisomal β-oxidation
activity. This study shows that 18∶2n−6 and 18∶3n−3 can be elongated and desaturated in Atlantic salmon liver, and that this
conversion and the activity of retroconversion of very long chain PUFA is markedly enhanced by FFA deficiency. 相似文献
6.
Induction of apoptosis and apoptotic mediators in balb/C splenic lymphocytes by dietary n−3 and n−6 fatty acids 总被引:5,自引:0,他引:5
The present study was designed to investigate the effect of diatery n−6 and n−3 polyunsaturated fatty acids (PUFA) on anti-CD3
and anti-Fas antibody-induced apoptosis and its mediators in mouse spleen cells. Nutritionally adequate semipurified diets
containing either 5% w/w corn oil (n−6 PUFA) or fish oil (n−3 PUFA) were fed to weanling female Balb/C mice, and 24 wk later
mice were sacrificed. In n−3 PUFA-fed mice, serum and splenocyte lipid peroxides were increased by 20 and 28.3% respectively,
compared to n−6 PUFA-fed mice. Further, serum vitamin F levels were decreased by 50% in the n−3 PUFA-fed group, whereas higher
anti0Fas- and anti-CD3-induced apoptosis (65 and 66%) and necrosis (17 and 25%), compared to the n−6 PUFA-fed group, were
found when measured with Annexin V and propidium iodide staining, respectively. In addition, decreased Bcl-2 and increased
Fas-ligand (Fas-L) also were observed in the n−3 PUFA-fed group compared to the n−6 PUFA-fed group. No difference in the ratio
of splenocyte subsets nor their Fas expression was observed between the n−3 PUFA-fed and n−6 PUFA-fed groups, whereas decreased
proliferation of splenocytes was found in n−3 PUFA-fed mice compared to n−6 PUFA-fed mice. In conclusion, our results indicate
that dietary n−3 PUFA induces higher apoptosis by increasing the generation of lipid peroxides and elevating Fas-L expression
along with decreasing Bcl-2 expression. A reduced proliferative response of immune cells also was observed in n−3 PUFA-fed
mice. 相似文献
7.
We have previously shown that the docosahexaenoate (22∶6n−3) status in membrane phospholipids influences the biosynthesis
and accumulation of phosphatidylserine (PS) in brain microsomes and C6 glioma cells. In the present study, we investigated
whether the observed effect of membrane docosahexaenoic acid status on PS accumulation is universal or occurs specifically
in neuronal tissues. We observed that rat brain cortex, brain mitochondria, and olfactory bulb, where 22∶6n−3 is highly concentrated,
contain significantly higher levels of PS in comparison to liver and adrenal, where 22∶6n−3 is a rather minor component. Phospholipid
molecular species analysis revealed that in brain cortex, mitochondria, and olfactory bulb 18∶0,22∶6n−3 was the most abundant
species representing 45–65% of total PS. In nonneuronal tissues such as liver and adrenal, 18∶0,20∶4n−6 was the major PS species.
Dietary depletion of n−3 fatty acids during prenatal and postnatal developmental periods decreased the brain 22∶6n−3 content
by more than 80%, with a concomitant increase in 22∶5n−6 in all tissues. Under these conditions, an approximately 30–35% reduction
in total PS in rat brain cortex, brain mitochondria, and olfactory bulb was observed, while PS levels in liver and adrenal
were unchanged. The observed reduction of PS content in neuronal membranes appears to be due to a dramatic reduction of 18∶0,22∶6n−3-PS
without complete replacement by 18∶0,22∶5n−6-PS. These results establish that variations in membrane 22∶6n−3 fatty acid composition
have a profound influence on PS accumulation in neuronal tissues where 22∶6n−3 is abundant. These data have implications in
neuronal signaling events where PS is believed to play an important role. 相似文献
8.
Du ZY Demizieux L Degrace P Gresti J Moindrot B Liu YJ Tian LX Cao JM Clouet P 《Lipids》2004,39(9):849-855
Fish easily accumulate n−3 PUFA of exogenous origin, but the underlying mechanisms are not well established in the whole animal.
This study was undertaken to investigate whether this feature was physiologically associated with mitochondrial and peroxisomal
capacities that differentially affect FA oxidation. For this purpose, peroxisomal FA oxidation was increased by treating rainbow
trout with fenofibrate, which strongly stimulates the peroxisome proliferator-activated receptor-α in rodents. Diets containing
EPA and DHA, with or without fenofibrate added, were administered to male trout for 12 d. After treatment, neither liver hypertrophy
nor accumulation of fat was apparent within the liver and muscle cells. However, fenofibrate treatment decreased the contents
of EPA and DHA in the liver, white muscle, and intraperitoneal fat tissue, which represented (per whole body) at least 280
mg less than in controls. Carnitine-dependent palmitate oxidation rates, expressed per gram of liver, were slightly increased
by fenofibrate when measured from tissue homogenates and were unchanged when calculated from isolated mitochondria, relative
to control fish. The treatment altered neither carnitine palmitoyltransferase I activity rates, expressed per gram of liver,
nor the sensitivity of the enzyme to malonyl-CoA inhibition, but did increase the malonyl-CoA content (+45%). Meanwhile, fenofibrate
increased (by about 30%) the peroxisome-related activities, i.e, catalase, carnitine-independent palmitate oxidation, acyl-CoA
oxidase, and the peroxisomal FA-oxidizing system, relative to the control group. The data strongly suggest that the induction
of peroxisomal activities, some of which being able to oxidize very long chain FA, was responsible for the lower contents
of EPA and DHA in the body lipids of fenofibrate-treated trout. 相似文献
9.
Linoleic (18∶2n−6) and α-linolenic acids (18∶3n−3) have many important physiological functions including immunomodulation.
We tested how immunization influences the metabolism of 18∶2n−6 and 18∶3n−3 in the neck muscle of pigs. At 35 d old, pigs
received either an intramuscular neck injection containing hen egg white lysozyme (HEWL), killed Mycobacterium tuberculosis, and Freund’s complete adjuvant (immunized) or PBS (control). At 49 d old, immunized pigs received a booster injection of
HFWI and Freund’s incomplete adjuvant, and the control pigs received PBS into the neck. At 56 d old, all pigs received an
intradermal injection of Mycobacterium bovis into the hind leg to induce a delayed-type hypersensitivity (DTH) reaction. At 57 d old, immunized pigs had a twofold increase
in serum haptoglobin, a 10-fold increase in antibodies to HEWL, and the skinfold at the DTH reaction site was 10 times thicker
than the controls. Both 18∶2n−6 and 18∶3n−3 (% composition) were approximately 25% lower in muscle IG, 40% lower in FFA, 50%
lower in phospholipids, but not different in cholesteryl esters of the neck muscle of immunized pigs. The antigens in this
model induce an increased response in the innate (haptoglobin), humoral (antibodies), and cellular (DTH) immune systems as
well as a preferential decrease of 18∶2n−6 and 18∶3n−3 in the inflamed neck muscle. It appears that 18∶2n−6 and 18∶3n−3 are
preferentially metabolized (possibly β-oxidized) in response to antigens. 相似文献
10.
Fatty acids,the immune response,and autoimmunity: A question of n−6 essentiality and the balance between n−6 and n−3 总被引:8,自引:0,他引:8
Harbige LS 《Lipids》2003,38(4):323-341
The essentiality of n−6 polyunsaturated fatty acids (PUFA) is described in relation to a thymus/thymocyte accretion of arachidonic
acid (20∶4n−6, AA) in early development, and the high requirement of lymphoid and other cells of the immune system for AA
and linoleic acid (18∶2n−6, LA) for membrane phospholipids. Low n−6 PUFA intakes enhance whereas high intakes decrease certain
immune functions. Evidence from in vitro and in vivo studies for a role of AA metabolites in immune cell development and functions shows that they can limit or regulate cellular
immune reactions and can induce deviation toward a T helper (Th)2-like immune response. In contrast to the effects of the
oxidative metabolites of AA, the longer-chain n−6 PUFA produced by γ-linolenic acid (18∶3n−6, GLA) feeding decreases the Th2
cytokine and immunoglobulin (Ig)G1 antibody response. The n−6 PUFA, GLA, dihomo-γ-linolenic acid (20∶3n−6, DHLA) and AA, and
certain oxidative metabolites of AA can also induce T-regulatory cell activity, e.g., transforming growth factor (IGF)-β-producing
T cells; GLA feeding studies also demonstrate reduced proinflammatory interleukin (IL)-1 and tumor necrosis factor (TNF)-α
production. Low intakes of long-chain n−3 fatty acids (fish oils) enhance certain immune functions, whereas high intakes are
inhibitory on a wide range of functions, e.g., antigen presentation, adhesion molecule expression, Th1 and th2 responses,
proinflammatory cytokine and eicosanoid production, and they induce lymphocyte apoptosis. Vitamin E has a demonstrable critical
role in long-chain n−3 PUFA interactions with immune functions, often reversing the effects of fish oil. The effect of dietary
fatty acids on animal autoimmune disease models depends on both the autoimmune model and the amount and type of fatty acids
fed. Diets low in fat, essential fatty acid deficient (EFAD), or high in long-chain n−3 PUFA from fish oils increase survival
and reduce disease severity in spontaneous autoantibody-mediated disease, whereas high-fat LA-rich diets increase disease
severity. In experimentally induced T cell-mediated autoimmune disease, EFAD diets or diets supplemented with long-chain n−3
PUFA augment disease, whereas n−6 PUFA prevent or reduce the severity. In contrast, in both T cell- and antibody-mediated
autoimmune disease, the desaturated/elongated metabolites of LA are protective. PUFA of both the n−6 and n−3 families are
clinically useful in human autoimmune-inflammatory disorders, but the precise mechanisms by which these fatty acids exert
their clinical effects are not well understood. Finally, the view that all n−6 PUFA are proinflammatory requires revision,
in part, and their essential regulatory and developmental role in the immune system warrants appreciation. 相似文献
11.
The purpose of this double-blind study was to investigate the influence of exercise on the FA profile of the nonesterified
FA (NEFA) and phospholipid fractions in plasma of sedentary women supplemented with n−3 FA vs. women supplemented with oil
containing no n−3 FA. Twenty sedentary, premenopausal women were randomly assigned to receive 12 capsules daily of either
fish oil (3.5 g FPA and 2.4 g DHA per day, each as the ethyl ester) or evening primrose oil capsules (no detectable EPA or
DHA). Each subject consumed the capsules for one menstrual cycle. At the end of the supplementation period, the sedentary
subjects underwent an acute exercise trial [55% maximal oxygen consumption (VO2 max), 45 min] on a cycle ergometer. Two subjects in the fish oil group were removed from all calculations owing to noncompliance
for reasons not related to side effects. There were no changes in the phospholipid composition of either group of women after
exercise. In both control and fish oil-supplemented women, NEFA levels in general rose after exercise. There were no changes
in the percentage of any given individual NEFA in either supplementation group. However, absolute levels of certain individual
NEFA (16∶0, 18∶0, 18∶1, and 18∶3n−3) increased with exercise. Women supplemented with fish oil had increased levels of n−3
NEFA [EPA, DHA, and docosapentaenoic acid (DPA)] prior to exercise. Exercise did not, however, increase the absolute levels
of n−3 NEFA in the blood. 相似文献
12.
The effect of N-ethyl-maleimide (NEM) on Δ5-and Δ6-desaturase activities and the incorporation of substrates and products into different
microsomal lipid classes and phospholipid (PL) subclasses were studied in human fetal liver microsomes, obtained after legally
approved therapeutic abortion. Desaturase activities were measured by a radiochemical method using reversed-phase high-performance
liquid chromatography (HPLC). After nonphospholipid (NPL) and PL separation on silica cartridges, the radioactivity in different
lipids of the NPL group was assessed by two-dimensional thin-layer chromatography, and their fatty acid (FA) composition by
gas-liquid chromatography. The PL subclasses were separated, and the distribution of radioactivity between products and substrates
was determined in PL subclasses. NEM inhibited the Δ5- and Δ6-desaturase activities in the n−6 series of FA but not the Δ6-desaturase
activity in the n−3 series, which suggests the existence of two distinct Δ6-desaturases, one for the n−6 series and another
for the n−3 series. Whether NEM was present or absent, most of the radioactivity was recovered in the free FA form (about
80%). The desaturation products, obtained in the presence or absence of NEM, were preferentially incorporated into PL, suggesting
a channeling of the newly synthesized FA toward microsomal PL. The comparison of the distribution of substrates and products
incorporated into the different PL classes showed that most of the labeled FA were incorporated into phosphatidylcholine and
to a lesser degree into phosphatidylethanolamine. 相似文献
13.
Sufficient availability of both n-3 and n-6 long-chain polyunsaturated fatty acids (LCPUFA) is required for optimal structural
and functional development in infancy. The question has been raised as to whether infant formulae would benefit from enrichment
with 20 and 22 carbon fatty acids. To address this issue, we determined the effect of fish oil and phospholipid (LCPUFA) sources
on the fatty acid composition of brain cortical areas and nonneural tissues of newborn piglets fed artificially for 2 wk.
They were fed sow milk, a control formula, or the formula enriched with n-3 fatty acids from a low-20:5n-3 fish oil added
at a high or a low concentration, or the formula enriched with n-3 and n-6 fatty acids from either egg yolk- or pig brain-phospholipids.
Both the fish oil- and the phospholipid-enriched formula produced significantly higher plasma phospholipid 22:6n-3 concentrations
than did the control formula. The 22:6n-3 levels in the brain, hepatic, and intestinal phospholipids were significantly correlated
with plasma values, whereas cardiac 22:6n-3 content appeared to follow a saturable dose-response. Feeding sow milk resulted
in a much higher 20:4n-6 content in nonneural tissues than did feeding formula. Supplementation with egg phospholipid increased
the 20:4n-6 content in the heart, red blood cells, plasma, and intestine in comparison to the control formula, while pig brain
phospholipids exerted this effect in the heart only. The addition of 4.5% fish oil in the formula was associated with a decline
in 20:4n-6 in the cortex, cerebellum, heart, liver, and plasma phospholipids, whereas using this source at 1.5% limited the
decline to the cerebellum, liver, and plasma. Whatever the dietary treatment, the phosphatidylethanolamine 20:4n-6 level was
10–20% higher in the brain temporal lobe than in the parietal, frontal, and occipital lobes in the temporal lobe by administering
the formula enriched with egg or brain phospholipids.
In conclusion, feeding egg phospholipids to neonatal pigs increased both the 22:6n-3 content in the brain and the 20:4n-6
content in the temporal lobe cortex. This source also increased the 22:6n-3 levels in nonneural tissues with only minor alterations
of 20:4n-6. These data support the notion that infant formulae should be supplemented with both 22:6n-3 and 20:4n-6 rather
than with 22:6n-3 alone. 相似文献
14.
n−3 PUFA are well known for their anti-inflammatory effects. However, there has been only limited study on the kinetics of
incorporation and depletion of n−3 PUFA in immune cells. In the present study we investigated the incorporation and depletion
of n−3 PUFA in erythrocytes and leukocytes in mice during a 6-wk feeding period. Over the first 3-wk period (the incorporation
period) the mice were fed a special diet with a high n−3/n−6 PUFA ratio. In the following 3-wk period (the depletion period)
the mice were fed a standard chow diet. A linear incease of the concentration of EPA and DHA in erythrocyte membranes was
observed during the incorporation period, whereas a stagnation was observed after the second week for leukocytes. The level
of EPA did not fall to the background level after the depletion period, and the level of DHA was kept almost constant during
the depletion period in the erythrocyte membranes. In leukocytes the concentration of both EPA and DHA decreased during the
depletion period, but did not reach the background level after the 3-wk depletion. In conclusion, the kinetics of EPA and
DHA in the different cells are different. The rate of incorporation is faster than that of depletion for n−3 PUFA. More n−3
PUFA can be incorporated into leukocytes in comparison with erythrocytes. The ratio of n−3/n−6 PUFA is more important than
the amount of n−3 FA in changing the FA compositions of membrane lipids. 相似文献
15.
Cleland LG Proudman SM Hall C Stamp LK McWilliams L Wylie N Neumann M Gibson RA James MJ 《Lipids》2003,38(4):419-424
Dietary fish oil supplements have been shown to have benefits in rheumatoid arthritis (RA), other inflammatory diseases, and
in cardiovascular disease. As with any medical advice, variability will exist with regard to adherence and consequent biochemical
or pharmacophysiologic effects. The aim was to explore the utility of plasma phospholipid EPA as a measure of n−3 PUFA intake
and response to standardized therapeutic advice given in an outpatient or office practice setting, to increase dietary n−3
PUFA, including a fish oil supplement. Patients with early RA were given verbal and written advice to alter their dietary
n−3 PUFA intake, including ingestion of 20 mL of bottled fish oil on juice daily. The advice included instructions to increase
n−3 PUFA and to avoid foods rich in n−6 PUFA. Every 3 mon, blood samples were obtained for analysis of plasma phospholipid
FA. Plasma phospholipid EPA was used as the primary index of n−3 PUFA intake. A diverse response was seen, with about one-third
of patients achieving a substantial elevation of plasma phospholipid EPA over the 12-mon study period. A third had little
change, with the remainder achieving intermediate levels. Data obtained longitudinally from individual patients indicated
that substantial elevations of EPA (>5% total plasma phospholipid FA) could be maintained for more than 3 yr. Plasma phospholipid
EPA is a convenient measure of adherence to advice to take a dietary n−3 PUFA-rich fish oil supplement. This measure may prove
a useful adjunct to intention to treat analyses in determining the effect of dietary fish oil supplements on long-term outcomes
in arthritis and other chronic inflammatory diseases. It may also provide a guide to the effectiveness of therapeutic and
preventive messages designed to increase n−3 PUFA intake. 相似文献
16.
Effect of 18∶1n−9, 20∶5n−3, and 22∶6n−3 on lipid accumulation and secretion by atlantic salmon hepatocytes 总被引:1,自引:0,他引:1
We have studied the effects of dietary FA on the accumulation and secretion of [3H]glycerolipids by salmon hepatocytes in culture. Atlantic salmon were fed diets supplemented with either 100% soybean oil
(SO) or 100% fish oil (FO), and grew from an initial weight of 113±5 g to a final weight of 338 ±19 g. Hepatocytes were isolated
from both dietary groups and incubated with [3H]glycerol in an FA-free medium; a medium supplemented with 0.75 mM of one of three FA—18∶1n−9, 20∶5n−3, or 22∶6n−3—or a medium
supplemented with 0.75 mM of the sulfur-substituted FA analog tetradecylthioacetic acid (TTA), which cannot undergo β-oxidation.
Incubations were allowed to proceed for 1,2,6, or 24 h. The rate of the secretion of radioactive glycerolipids with no FA
added was 36% lower from hepatocytes isolated from fish fed the FO diet than it was from hepatocytes isolated from fish fed
the SO diet. Hepatocytes incubated with 18∶1n−9 secreted more [3H]TAG than when incubated with no FA, whereas hepatocytes incubated with 20∶5n−3 or TTA secreted less labeled TAG than when
incubated with no FA. This observation was independent of the feeding group. Hepatocytes incubated with 22∶6n−3 secreted the
highest amounts of total [3H]glycerolipids compared with the other treatments, owing to increased secretion of phospholipids and mono- and diacylglycerols
(MDG). In contrast, the same amounts of [3H]TAG were secreted from these cells as from cells incubated in an FA-free medium. The lipid-lowering effect of FO is thus
independent of 22∶6n−3, showing that 20∶5n−3 is the FA that is responsible for the lipid-lowering effect. The ratio of TAG
to MDG in lipids secreted from hepatocytes to which 20∶5n−3 or TTA had been added was lower than that in lipids secreted from
hepatocytes incubated with 18∶1n−9 or 22∶6n−3, suggesting that the last step in TAG synthesis was inhibited. Morphometric
measurements revealed that hepatocytes incubated with 20∶5n−3 accumulated significantly more cellular lipid than cells treated
with 18∶1n−9, 22∶6n−3, TTA, or no treatment. The area occupied by mitochondria was also greater in these cells. The present
study shows that dietary FO reduces TAG secretion from salmon hepatocytes and that 20∶5n−3 mediates this effect. 相似文献
17.
A single-cell oil from a Mortierella alpina mutant (TGM17 oil) contains n−9 PUFA: 14.3 wt% 6,9-octadecadienoic acid (18∶2n−9; n−9 LnA) and 17.1 wt% Mead acid (20∶3n−9;
MA). Lipase screening indicated that Pseudomonas aeruginosa lipase acted strongly on n−9 LnA and weakly on MA, and Candida rugosa lipase acted weakly on the two PUFA. Hence, fractionation and enrichment of the two FA were conducted with the lipases. The
first step was selective hydrolysis of IGM17 oil with P. aeruginosa lipase. The hydrolysis fractionated the oil into FFA containing 20.4 wt% n−9 LnA and 6.3 wt% MA, and acylglycerols containing
10.7 wt% n−9 LnA and 23.7 wt% MA. The FFA fraction was used for preparation of n−9 LnA-rich FFA. After removal of saturated
FA, the FFA were esterified with lauryl alcohol (LauOH) using C. rugosa lipase. Two selective esterifications increased the n−9 LnA content to 54.0 wt% with 38.2% recovery of the initial content
of TGM17 oil. The acylglycerol fraction obtained in the hydrolysis with P. aeruginosa lipase was used for preparation of MA-rich FFA. The acylglycerol fraction was hydrolyzed under alkaline conditions, and saturated
FA were eliminated by urea adduct fractionation. Two selective esterifications of the FFA with LauOH increased the MA content
to 60.2 wt% with 53.5% recovery. Thus, the two-step enzymatic process was effective for fractionation and enrichment of n−9
LnA and MA. 相似文献
18.
The reciprocal replacement of DHA by docosapentaenoic acid (DPAn−6) was studied in rats that consumed an n−3 FA-deficient
or n−3 FA-adequate diet. Dams were fed the two experimental diets from weaning and throughout pregnancy and lactation. Their
pups were then fed the respective diets after weaning. Cortex FA analysis was performed at various times (0, 5, 10, 20, 50,
and 91 d) after birth to determine whether DPAn−6 completely replaced DHA in the n−3-deficient group. Cortical DHA levels
were significantly lower (average 86%) in the n−3-deficient rats. DPAn−6 increased significantly in the n−3-deficient rats
starting with a 6.5-fold increase at day 0 up to a 54-fold increase at day 91 compared with the n−3-adequate group. However,
this significant increase did not completely replace the loss of DHA at postnatal days 5, 10, and 20 in which there was still
an 11.5, 10.3, and 8.0% deficit in the sum of DHA and DPAn−6, respectively, in the n−3-deficient group. Once docosatetraenoic
(DTA) and arachidonic acids (AA) were included in the sum (DHA+DPAn−6+DTA+AA), the levels between the two groups were similar,
These results suggest that not only DPAn−6 but also other n−6 FA, including DTA and AA, replace DHA in n−3-deficient rats.
The lack of total 22-carbon (22C) FA in the brain during the rapid membrane biogenesis that occurs during early development
could be a factor in the nervous ystem functional deficits associated with n−3 FA deficiency. 相似文献
19.
The objective of this study was to test the hypothesis that increasing maternal dietary 18∶3n−3 by decreasing the 18∶2n−6/18∶3n−3
ratio will increase the 18∶3n−3 and 22∶6n−3 content of the whole body, liver, skin (epidermis, dermis, and subcutaneous tissue),
epididymal fat pads, and muscles (arms and legs) of 2-wk-old rat pups. Sprague-Dawley dams at parturition were fed semipurified
diets containing either a low (18∶2n−6 to 18∶3n−3 ratio of 24.7∶1) or a high (18∶2n−6 to 18∶3n−3 ratio of 1.0∶1) 18∶3n−3 fatty
acid content. During the first 2 wk of life, rat pups received only their dams' milk. Fatty acid composition of the pups'
stomach contents (dams' milk), whole body, brain, liver, skin, epididymal fat pads, and muscles was determined. The stomach
fatty acid composition of 18∶3n−3 reflected the dams' diet. The content of 18∶3n−3 in whole body, brain, liver, skin, epididymal
fat pads, and muscles was significantly (P<0.05) greater in rat pups fed the high compared with the low 18∶3n−3 fatty acid diet. The 22∶6n−3 content of the whole body,
brain, skin, epididymal fat pads, and muscles was not quantitatively different in rat pups fed either the low or high 18∶3n−3
fatty acid diet. The 20∶5n−3 and 22∶5n−3 content of the whole body, skin, and epididymal fat pads was significantly increased
in rat pups fed the high compared with the low 18∶3n−3 fatty acid diet. High content of 18∶3n−3 was found in the skin of rat
pups fed either a low or high 18∶3n−3 fatty acid diet. These findings demonstrate that high maternal dietary 18∶3n−3 significantly
increases the 18∶3n−3 but not the 22∶6n−3 content of the whole body, brain, skin, epididymal fat pads, and muscles with approximately
39 and 41% of the whole body 18∶3n−3 content being deposited in the skin of suckling rat pups fed either the low or high 18∶3n−3
diet, respectively. 相似文献
20.
Thorlaksdottir AY Skuladottir GV Petursdottir AL Tryggvadottir L Ogmundsdottir HM Eyfjord JE Jonsson JJ Hardardottir I 《Lipids》2006,41(2):119-125
PUFA are susceptible to oxidation. However, the chain-reaction of lipid peroxidation can be interrupted by antioxidants. Whether
an increased concentration of PUFA in the body leads to decreased antioxidant capacity and/or increased consumption of antioxidants
is not known. To elucidate the relationship between plasma total antioxidant capacity (TAC), the concentration of antioxidant
vitamins, and the proportion of PUFA in red blood cells (RBC), plasma TAC was measured by a Trolox equivalent antioxidant
capacity assay in blood samples from 99 Icelandic women. Concentrations of tocopherols and carotenoids in the plasma were
determined by HPLC, and the FA composition of RBC total lipids was analyzed by GC. Plasma TAC and the plasma concentration
of α-tocopherol correlated positively with the proportion of total n−3 PUFA, 20∶5n−3, and 22∶6n−3 in RBC, whereas the plasma
lycopene concentration correlated negatively with the proportion of total n−3 PUFA and 20∶5n−3. On the other hand, plasma
TAC correlated negatively with the proportion of n−6 PUFA in RBC. Plasma TAC also correlated positively with the plasma concentration
of α-tocopherol, alcohol consumption, and age. Both the plasma concentration of α-tocopherol and age correlated positively
with the proportion of n−3 PUFA in RBC; however, n−3 PUFA contributed independently to the correlation with plasma TAC. Because
the proportion of n−3 PUFA in RBC reflects the consumption of n−3 PUFA, these results suggest that dietary n−3 PUFA do not
have adverse effects on plasma TAC or the plasma concentration of most antioxidant vitamins. 相似文献