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1.
Three hundred (experiment I) and 350 (experiment II) weanling, 3-week-old male Sprague-Dawley rats weighing between 40–50
g were randomly assigned two per cage and 50 per dietary treatment to study the effect of dietary fatty acid balance on myocardial
lesions. The following oils were tested: Experiment I.Brassica napus var. Tower rapeseed oil [Tower RSO, 1974 cultivar and 1975 cultivar, each containing 0.3% erucic (22∶1) acid];B. napus var. Zephyr RSO containing 0.9% 22∶1; corn oil; olive oil; and soybean oil. Experiment II.B. napus var. Tower RSO (1974 cultivar), olive oil, soybean oil, and the following oils to which was added the indicated level of
free 22∶1; Tower +0.5% 22∶1; Tower +5.6% 22∶1; olive oil +4.4% 22∶1; soybean oil +5.7% 22∶1. In each case the oils were incorporated
in a semisynthetic diet at a level of 20% by weight. Heart and heart lipid weights of rats fed the different oils did not
differ statistically from each other. Fatty acid analyses of heart lipids revealed that the fatty acid composition of the
cardiac lipids reflected that of the diet fed. In experiment I, there was a definite but significantly lower incidence (P<0.01)
and severity (P<0.01) of heart lesions in rats fed control oils (corn, olive, soybean) than in rats fed rapeseed oils. Also,
in experiment II, a definite but lower incidence and severity of heart lesions occurred in rats fed control oils (soybean,
olive) compared to rats fed Tower RSO or this oil with added free 22∶1. Adding 22∶1 to an oil naturally high in 18∶3 (soybean)
did not alter the incidence of heart lesions, whereas adding 22∶1 to an oil naturally high in 18∶1 (olive) increased significantly
(P<0.01) both the incidence and severity of heart lesions. Thus, it appears that the background incidence of heart lesions
that are found in the rat in any case, and which are increased by rapeseed oil feeding, is caused by the imbalanced fatty
acid composition of the oil for the growing rat, i.e. high monoenes (18∶1, 20∶1, and 22∶1) and high 18∶3 and is not only due
to the presence of excess 18∶3.
Contribution No. 706, Animal Research Institute. 相似文献
2.
Male adult Sprague-Dawley rats were fed diets containing 15% by weight of sunflower oil, coconut oil, rapeseed oil or combinations
of these oils for 5 or 60 days. The digestibility of erucic acid (22∶1), lauric acid (12∶0) and linoleic acid (18∶2) was measured
and found to be decreased for erucic acid at both time intervals, and for lauric acid after 60 days when coconut oil and rapeseed
oil were blended. The cardiac lipodosis was proportional to the content of erucic acid in the diet. At 60 days, the high level
of 22∶6 in the cardiac phospholipids of rats fed rapeseed oil was reduced by the addition of sunflower oil but not by coconut
oil. Thus, the blending of rapeseed oil with coconut oil apparently is less desirable than that of rapeseed oil and sunflower
oil. 相似文献
3.
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
4.
Metabolism of erucic acid in perfused rat liver: Increased chain shortening after feeding partially hydrogenated marine oil and rapeseed oil 总被引:1,自引:1,他引:1
E. N. Christiansen M. S. Thomassen R. Z. Christiansen H. Osmundsen K. R. Norum 《Lipids》1979,14(10):829-835
The metabolism of [14-14C] erucic acid was studied in perfused livers from rats fed on diets containing partially hydrogenated marine oil or rapeseed
oil for three days or three weeks. Control rats were given groundnut oil. Chain-shortening of erucic acid, mainly to 18∶1,
was found in all dietary groups. In the marine oil and rapeseed oil groups, the percentage of chain-shortened fatty acids
in very low density lipoproteins-triacylglycerols (VLDL-TG) exported from the liver increased after prolonged feeding. A similar
increase was found in liver TG only with partially hydrogenated marine oil. This oil, rich intrans fatty acids, thus seemed to be more effective in promoting chain-shortening. The fatty acid composition of the secreted and
stored TG differed both with respect to total fatty acids and radioactively labeled fatty acids, indicating that at least
2 different pools of TG exist in the liver. The lack of lipidosis in livers from rats fed dietary oils rich in 22∶1 fatty
acids is discussed in relation to these findings. In conclusion, a discussion is presented expressing the view that the reversal
of the acute lipidosis in the hearts of rats fed rapeseed oil or partially hydrogenated marine oils is, to a large extent,
derived from the increased chain-shortening capacity of erucic acid in liver. 相似文献
5.
John K. G. Kramer Edward R. Farnworth Kathleen M. Johnston Mark S. Wolynetz H. Wayne Modler Frank D. Sauer 《Lipids》1990,25(11):729-737
This study was undertaken to determine whether the neonate was more susceptible to the effects of dietary erucic acid (22∶1n−9)
than the adult. Newborn piglets were used to assess the safety of different levels of 22∶1n−9 on lipid and histological changes
in the heart. Newborn piglets showed no myocardial lipidosis as assessed by oil red 0 staining, but lipidosis appeared with
consumption of sow milk and disappeared by seven days of age. Milk replacer diets containing soybean oil, or rapeseed oil
mixtures with up to 5% 22∶1n−9 in the oil, or 1.25% in the diet, gave trace myocardial lipidosis. Rapeseed oil mixtures with
7 to 42.9% 22∶1n−9 showed definite myocardial lipidosis in newborn piglets, which correlated to dietary 22∶1n−9, showing a
maximum after one week on diet. The severity of the lipidosis was greater than observed previously with weaned pigs. There
were no significant differences among diets in cardiac lipid classes except for triacylglycerol (TAG), which increased in
piglets fed a repeseed oil with 42.9% 22∶1n−9. TAG showed the highest incorporation of 22∶1n−9, the concentration of 22∶1n−9
in TAG was similar to that present in the dietary oil. Among the cardiac phospholipids, sphingomyelin and phosphatidylserine
had the highest, and diphosphatidylglycerol (DPG) the lowest level of 22∶1n−9. The low content of 22∶1n−9 in DPG of newborn
piglets is not observed in weaned pigs and rats fed high erucic acid rapeseed oil. The relative concentration of saturated
fatty acids was lowered in all cardiac phospholipids of piglets fed rapeseed oils, possibly due to the low content of saturated
fatty acids in rapeseed oils. The results suggest that piglets fed up to 750 mg 22∶1n−9/kg body weight/day showed no adverse
nutritional or cardiac effects. 相似文献
6.
Three groups of weanling male rats were fed on a fat-free diet for 13 weeks. One group received only the fat-free diet (FF
rats), the other 2 groups received the fat-free diet and a daily supplement of 2 energy% ethyl linoleate ([n−6] rats), or
2 energy% ethyl linolenate ([n−3] rats). Urinary excretion of prostaglandin E2 (PGE2), immunoreactive arginine vasopressin (iA VP), and kallikrein were determined. PGE2 was quantitated with a radioimmunoassay having 4.9% cross-reactivity with prostaglandin E3 (PGE3). After 4 weeks on the diet, water consumption and urinary iAVP excretion increased significantly in the FF rats and the
(n−3) rats compared with the (n−6) rats. Urinary PGE2 excretion was the same for all 3 groups during the first 10 weeks; thereafter it decreased in FF rats and (n−3) rats compared
with the (n−6) rats. There was no difference in urinary PGE2 excretion between the FF rats and the (n−3) rats, even though large differences were found in the percentage of arachidonic
acid (20∶4[n−6]), icosapentaenoic acid (20∶5[n−3]), and icosatrienoic acid (20∶3[n−9]) of total kidney fatty acids as well
as of kidney phosphatidylinositol fatty acids. Fractionation of urine extracts on high performance liquid chromatography with
radioimmunoassay detection indicated that (n−3) rats excreted very little PGE3, if any. Urine output followed the same pattern, as did urinary PGE2 excretion. Urinary kallikrein was estimated at week 12 only. It was found to be significantly lower in FF rats and (n−3)
rats. Increased water consumption and increased urinary iAVP excretion seem to be early symptoms (after 4 weeks) of EFA deficiency,
whereas decreased urine output and decreased urinary PGE2 excretion occur much later (after 10 weeks). Two energy% linolenate supplementation to a fat-free diet did not change the
appearance of any of the measured EFA-deficiency symptoms except for a slightly improved growth rate. There was no evidence
of a significant urinary PGE3 excretion in spite of an extreme enrichment of kidney lipids with 20∶5(n−3). It is suggested that urinary PGE2 is derived from precursors delivered from an arachidonic acid pool, which is rather resistant to restriction in dietary linoleate.
Presented in part at the 23rd International Conference on Biochemistry of Lipids, Nyborg, Denmark, August 1981, and at the
Vth International Conference on Prostaglandins, Florence, Italy, May 1982. 相似文献
7.
The effects of dietary stearidonic acid (18∶4n−3) on inflammatory mediator release in whole blood and splenocytes was investigated
in Balb/c mice, and the effects were compared with those of two other n−3 PUFA: α-linolenic acid (18∶3n−3) and EPA (20∶5n−3).
TAG mixtures containing 10% of 18∶4n−3, 18∶3n−3, or 20∶5n−3 as the respective sole n−3 PUFA were enzymatically synthesized.
Diets containing synthesized TAG mixtures were fed to Balb/c mice for 3 wk. The release of prostaglandin E2 (PGE2) and tumor necrosis factor (TNF) were measured in whole blood and splenocytes stimulated with lipopolysaccharide. In whole
blood, the production of INF was suppressed by all dietary n−3 PUFA (18∶3n−3, 18∶4n−3, and 20∶5n−3) as compared with the control
diet, which contained TAG prepared from safflower oil. PGE2 production was not significantly changed. Differences among the n−3 PUFA (18∶3n−3), 18∶4n−3, and 20∶5n−3) were not observed.
In splenocytes, PGE2 production was suppressed by dietary n−3 PUFA, but TNF production was not. GC analysis of plasma and splenocyte FA profiles
showed an increase in the levels of 20∶4n−3, 20∶5n−3, and 22∶6n−3 in mice fed the diet containing 18∶4n−3. 相似文献
8.
J. K. G. Kramer F. D. Sauer M. S. Wolynetz E. R. Farnworth K. M. Johnston 《Lipids》1992,27(8):619-623
Male Sprague-Dawley rats were fed for one week diets containing 20% by weight fat/oil mixtures with different levels of erucic
acid (22∶1n−9) (∼2.5 or 9%) and total saturated fatty acids (∼8 or 35%). Corn oil and high erucic acid rapeseed (HEAR) oil
were fed as controls. The same hearts were evaluated histologically using oil red O staining and chemically for cardiac triacylglycerol
(TAG) and 22∶1n−9 content in cardiac TAG to compare the three methods for assessing lipid accumulation in rat hearts. Rats
fed corn oil showed trace myocardial lipidosis by staining, and a cardiac TAG content of 3.6 mg/g wet weight in the absence
of dietary 22∶1n−9. An increase in dietary 22∶1n−9 resulted in significantly increased myocardial lipidosis as assessed histologically
and by an accumulation of 22∶1n−9 in heart lipids; there was no increase in cardiac TAG except when HEAR oil was fed. An increase
in saturated fatty acids showed no changes in myocardial lipid content assessed histologically, the content of cardiac TAG
or the 22∶1n−9 content of TAG at either 2.5 or 9% dietary 22∶1n−9. The histological staining method was more significantly
correlated to 22∶1n−9 in cardiac TAG (r=0.49;P<0.001) than to total cardiac TAG (r=0.40;P<0.05). The 22∶1n−9 content was highest in cardiac TAG and free fatty acids. Among the cardiac phospholipids, the highest
incorporation was observed into phosphatidylserine, followed by sphingomyelin. With the addition of saturated fat, the fatty
acid composition showed decreased accumulation of 22∶1n−9 and increased levels of arachidonic and docosahexaenoic acids in
most cardiac phospholipids, despite decreased dietary concentrations of their precursor fatty acids, linoleic and linolenic
acids. 相似文献
9.
Atlantic salmon post-smolts were fed diets rich in linoleic acid (sunflower oil, SO), α-linolenic acid (linseed oil, LO) or
long-chain polyunsaturated fatty acids (fish oil, FO) for a period of 12 wk. In the liver phospholipids of fish fed SO, the
levels of 18∶2n−6, 20∶2n−6, 20∶3n−6 and 20∶4n−6 were significantly elevated compared to both other treatment. In choline phospholipids
(CPL), ethanolamine phospholipids (EPL) and phosphatidylserine (PS) the levels of 22∶4n−6 and 22∶5n−6 were significantly elevated
in fish fed SO. In liver phospholipids from fish fed LO, 18∶2n−6, 20∶2n−6 and 20∶3n−6 were significantly elevated but 20∶4n−6,
22∶4n−6 and 22∶5n−6 were similar or significantly decreased compared to fish fed FO. Liver phospholipids from fish fed LO
had increased 18∶3n−3 and 20∶4n−3 compared to both other treatments while EPL and phosphatidylinositol (PI) also had increased
20∶5n−3. In fish fed LO, 22∶6n−3 was significantly reduced in CPL, PS and PI compared to fish fed FO. Broadly similar changes
occurred in gill phospholipids. Production of 12-lipoxygenase metabolites in isolated gill cells stimulated with the Ca2+-ionophore A23187 were significantly reduced in fish fed either SO or LO compared to those fed FO. However, the ratio 12-hydroxy-5,8,10,14-eicosatetraenoic
acid (12-HETE)/12-hydroxy-5,8,10,14,17-eicosapentaenoic acid (12-HEPE) was significantly elevated in stimulated gill cells
from SO-fed fish. Although mean values of thromboxane B2 (TXB2) and prostaglandin E2 (PGE2) were increased in fish fed SO, they were not significantly different from those of the other two treatments. 相似文献
10.
This study evaluated the effects of conjugated linoleic acids (CLA) on tissue fatty acid composition and ex vivo prostaglandin E2 (PGE2) production in rats given diets varying in n-6 and n-3 fatty acids. Four groups of rats were given a basal semipurified diet
(AIN-93G) containing 70 g/kg of added fat for 42 d. The fat treatments were formulated to contain CLA (0 vs. 10 g/kg of diet)
and n-6 (soybean oil having an n-6/n-3 ratio of 7.3) and n-3 fatty acids (menhaden oil+safflower oil having an n-6/n-3 ratio
of 1.8) in different ratios in a 2×2 factorial design. Fatty acids in liver, serum, muscle, heart, brain, spleen, and bone
(cortical, marrow, and periosteum) were analyzed by capillary gas-liquid chromatography. The various dietary lipid treatments
did not affect growth; however, CLA improved feed efficiency. The CLA isomers were found in all rat tissues analyzed although
their concentrations varied. Dietary CLA decreased the concentrations of 16∶1n−7, 18∶1, total monounsaturates and n−6 fatty
acids, but increased the concentrations of n−3 fatty acids (22∶5n−3 and 22∶6n−3), and saturates in the tissues analyzed. Ex vivo PGE2 production in bone organ culture was decreased by n−3 fatty acids and CLA. We speculate that CLA reduced the concentration
of 18∶1 fatty acids by inhibiting liver Δ9-desaturase activity. The fact that CLA lowered ex vivo PGE2 production in bone organ culture suggests that these conjugated fatty acids have the potential to influence bone formation
and resorption. 相似文献
11.
Male Wistar rats were fed rapeseed oil containing high or low levels or erucic acid for 20 weeks, and changes in the fatty
acid composition of cardiac mitochondrial phospholipids were studied. Treatment with rapeseed oil containing 46.2% erucic
acid showed incorporation of 22∶1 (5.6%) into isolated cardiolipin from heart mitochondria. After high or low (3.7%) erucic
rapeseed oil feeding, linoleic acid was slightly incorporated into cardiolipin. Moreover, both of these rapeseed oils induced
a significant increase of linoleate-arachidonate ratio in phosphatidylethanolamine and phosphatidylcholine. This ratio was
also significantly increased in fatty acids esterified to the β-position of these phospholipids. On the basis of such results,
we have to consider the role of linolenic acid which is present at a high level in the different rapeseed oils used, as a
possible inhibitor of heart microsomal enzymes involved in linoleate arachidonate conversion. Such alterations might account
for mitochondrial fragility and myocardial lesions obtained in long term rapeseed oil feeding experiments.
ERA-CNRS no 070497 相似文献
12.
Effects of dietary vegetable oil on atlantic salmon hepatocyte fatty acid desaturation and liver fatty acid compositions 总被引:5,自引:0,他引:5
Fatty acyl desaturase activities, involved in the conversion of the C18 EFA 18∶2n−6 and 18∶3n−3 to the highly unsaturated fatty acids (HUFA) 20∶4n−6, 20∶5n−3, and 22∶6n−3, are known to be under
nutritional regulation. Specifically, the activity of the desaturation/elongation pathway is depressed when animals, including
fish, are fed fish oils rich in n−3 HUFA compared to animals fed, vegetable oils rich in C18 FFA. The primary aims of the present study were (i) to establish the relative importance of product inhibition (n−3 HUFA)
vs. increased substrate concentration (C18 EFA) and (ii) to determine whether 18∶2n−6 and 18∶3n−3 differ in their effects on the hepatic fatty acyl desaturation/elongation
pathway in Atlantic salmon (Salmo salar). Smolts were fed 10 experimental diets containing blends of two vegetable oils, linseed (IO), and rapeseed oil (RO), and
fish oil (FO) in a triangular mixture design for 50 wk. Fish were sampled after 32 and 50 wk, lipid and FA composition of
liver determined, fatty acyl desaturation/elongation activity estimated in hepatocytes using [1-14C]18∶3n−3 as substrate, and the data subjected to regression analyses. Dietary 18∶2n−6 was positively correlated, and n−3
HUFA negatively correlated, with lipid content of liver. Dietary 20∶5n−3 and 22∶6n−3 were positively correlated with liver
FA with a slope greater than unity suggesting relative retention and deposition of these HUFA. In contrast, dietary 18∶2n−6
and 18∶3n−3 were positively correlated with liver FA with a slope of less than unity suggesting metabolism via β-oxidation and/or desaturation/elongation. Consistent with this, fatty acyl desaturation/elongation in hepatocytes was significantly
increased by feeding diets containing vegetable oils. Dietary 20∶5n−3 and 22∶6n−3 levels were negatively correlated with hepatocyte
fatty acyl desaturation. At 32 wk, 18∶2n−6 but not 18∶3n−3 was positively correlated with hepatocyte fatty acyl desaturation,
wheres the reverse was true at 50 wk. The data indicate that both feedback inhibition through increased n−3 HUFA and decreased
C18 fatty acyl substrate concentration are probably important in determining the level of hepatocyte fatty acyl desaturation
and that 18∶2n−6 and 18∶3n−3 may differ in their effects on this pathway. 相似文献
13.
Partially hydrogenated marine oils containing 18∶1-, 20∶1- and 22∶1-isomers and partially hydrogenated peanut oil containing
18∶1-isomers were fed as 24–28 wt % of the diet with or without supplement of linoleic acid. Reference groups were fed peanut,
soybean, or rapeseed oils with low or high erucic acid content. Dietary monoene isomers reduced the conversion of linoleic
acid into arachidonic acid and the deposition of the latter in liver and heart phosphatidylcholine. This effect was more pronounced
for the partially hydrogenated marine oils than for the partially hydrogenated peanut oil. The content oftrans fatty acids in liver phospholipids was similar in groups fed partially hydrogenated fats. The distribution of various phospholipids
in heart and liver was unaffected by the dietary fat. The decrease in deposition of arachidonic acid in rats fed partially
hydrogenated marine oils was shown in vitro to be a consequence of lower Δ6-desaturase activity rather than an increase in
the peroxisomal β-oxidation of arachidonic acid. The lower amounts of arachidonic acid deposited may be a result of competition
in the Δ6-desaturation not only from the C22-and C20-monoenoic fatty acids originally present in the partially hydrogenated
marine oil, but also from C18- and C16-monoenes produced by peroxisomal β-oxidation of the long-chain fatty acids.
Part of this work was presented at the ISF-AOCS Congress, New York City, 1980. 相似文献
14.
Canola oil is not approved for use in infant formula largely because of concerns over possible accumulation of triglyceride
in heart as a result of the small amounts of erucic acid (22∶1n−9) in the oil. Therefore, the concentration and composition
of heart triglyceride were determined in piglets fed from birth for 10 (n=4–6) or 18 (n=6) d with formula containing about 50% energy fat as 100% canola oil (0.5% 22∶1n−9) or 100% soybean oil, or 26% canola oil
or soy oil (blend) with palm, high-oleic sunflower and coconut oil, providing amounts of 16∶0 and 18∶1 closer to milk, or
a mix of soy, high-oleic sunflower and flaxseed oils with C16 and C18 fatty acids similar to canola oil but without 22∶1. Biochemical analysis found no differences in heart triglyceride concentrations
among the groups at 10 or 18 d. Assessment of heart triglycerides using Oil Red O staining in select treatments confirmed
no differences between 10-d-old piglets fed formula with 100% canola oil (n=4), 100% soy oil (n=4), or the soy oil blend (n=2). Levels of 22∶1n−9 in heart triglyceride and phospholipid, however, were higher (P<0.01) in piglets fed 100% canola oil or the canola oil blend, with higher levels found in triglycerides compared with phospholipids.
The modest accumulation of 22∶1n−9 associated with feeding canola oil was not associated with biochemical evidence of heart
triglyceride accumulation at 10 and 18 d. 相似文献
15.
In this study we determined in rats the complete 24-h lymphatic fatty acid profile after administration of either rapeseed
oil (RO) or rapeseed oil interesterified with 10∶0 (RO/C10) with special emphasis on the transition from absorptive to postabsorptive phase. Rats were subjected to cannulation of the
main mesenteric lymph duct and the next day oils were administered through a gastric feeding tube. Lymph was collected in
1-h fractions for the following 24 h. The time for maximum lymphatic transport of fatty acids was at 4 h with fast changes
in fatty acid composition from the fatty acids of endogenous origin to those of the administered oils. Seven to eight hours
after administration the transport was significantly lower than maximum, indicating the change from absorptive to postabsorptive
phase. At 24 h after administration of either oil the transport of total fatty acids, palmitic acid (16∶0), and linoleic acid
(18∶2n−6) together with oleic acid (18∶1n−9) after RO had not returned to the transport at baseline. In contrast, the transport
of decanoic acid (10∶0) and α-linolenic acid (18∶3n−3) returned to baseline values between 12 and 15 h. This indicated that
the absorption of purely exogenous fatty acids (illustrated by 10∶0 and 18∶3n−3) was complete at 15 h and that the fatty acids
transported between 15 and 24 h were derived mostly from endogenous stores. 相似文献
16.
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
17.
The effect of dietary n−3 fatty acids on prostaglandin E2 (PGE2) and leukotriene C4 (LTC4) levels in rat salivary glands and gingiva was examined in two separate nutritional studies. In the first set of experiments,
two groups of male weanling Sprague-Dawley rats were fed semipurified diets containing 10% corn oil (control group) or 10%
menhaden oil (experimental group). Rats were killed after 8 wk on the diets; the fatty acid composition of total phospholipids
and the concentrations of PGE2 and its precursor, arachidonic acid, were measured in gingiva and submandibular salivary glands (SMSG). Dietary n−3 fatty
acids were incorporated into the tissue phospholipids. Arachidonic acid levels were reduced by 56% in gingiva and SMSG of
rats fed menhaden oil compared with the control rats fed the diet containing corn oil. The concentrations of PGE2 in SMSG and gingiva of rats fed the diet containing menhaden oil were reduced by 74% and 83%, respectively. In a subsequent
nutritional study, we tested whether the diet-induced reduction in tissue arachidonic acid levels would also result in a corresponding
decrease in LTC4 production. Three groups of rats were fed diets containing 5% corn oil (group 1), 4% ethyl ester concentrate of n−3 fatty
acids plus 1% corn oil (group 2), or 5% ethyl ester concentrate of n−3 fatty acids (group 3). After 6 wk of feeding, gingiva
and SMSG were analyzed for arachidonic acid content andin vitro production of LTC4. Arachidonic acid content of total phospholipids was about 60% lower in gingiva and 69% lower in SMSG of rats fed the ethyl
ester concentrate of n−3 fatty acids (groups 2 and 3) than those of the control group fed the corn oil diet (group 1). Upon
incubation with calcium ionophore, gingiva and SMSG from rats fed the n−3 fatty acids rich diet produced significantly less
TLC4 than those from rats of the control group. Because PGE2 and LTC4 are believed to be important biochemical mediators of periodontal disease, one may speculate that a diet-induced reduction
in their levels may have a beneficial effect upon the course of the disease. The function of salivary glands may also be altered
because of the role of these eicosanoids in salivary secretions.
Presented in part for the Hatton Award Competition at the American Association for Dental Research Meeting, San Francisco,
California, March 15–19, 1989, and at the International Association for Dental Research Meeting, Acapulco, Mexico, April 17–21,
1991. 相似文献
18.
We have reported that dietary fish oil (FO) leads to the incorporation of long-chain n−3 PUFA into the gut tissue of small
animal models, affecting contractility, particularly of rat ileum. This study examined the FO dose response for the incorporation
of n−3 PUFA into ileal tissue and how this correlated with in vitro contractility. Groups of ten to twelve 13-wk-old Wistar-Kyoto rats were fed 0, 1, 2.5, and 5% FO-supplemented diets balanced
with sunflower seed oil for 4 wk, after which ileal total phospholipid FA were determined and in vitro contractility assessed. For the total phospholipid fraction, increasing the dietary FO levels led to a significant increase
first evident at 1% FO, with a stepwise, nonsaturating six-fold increase in n−3 PUFA as EPA (20∶5n−3), DPA (docosapentaenoic
acid, 22∶5n−3), and DHA, but mainly as DHA (22∶6n−3), replacing the n−6 PUFA linoleic acid (18∶2n−6) and arachidonic acid
(20∶4n−6) over the dosage range. There was no difference in KCl-induced depolarization-driven contractility. However, a significant
increase in receptor-dependent maximal contractility occurred at 1% FO for carbachol and at 2.5% FO for prostaglandin E2, with a concomitant increase in sensitivity for prostaglandin E2 at 2.5 and 5% FO. These results demonstrate that significant increases in ileal membrane n−3 PUFA occurred at relatively
low doses of dietary FO, with differential receptor-dependent increases in contractility observed for muscarinic and prostanoid
agonists. 相似文献
19.
Male Sprague-Dawley rats, 3 weeks of age, were fed semisynthetic diets containing test oils at 20% by weight for 3 days, 1
week, and 16 weeks. The test oils contained up to 22.3% erucic acid. Growth retardation was evident in rats fed rapeseed oil
high in erucic acid, and soybean oil and Tower rapeseed oil diets containing about 5% erucic acid. Cardiac triglyceride accumulation
was found in rats fed diets containing about 5% erucic acid but not in rats fed Tower rapeseed oil which contains 0.2% of
this acid. The cardiac free fatty acid levels were low, 50–100 μg/g of wet heart tissue, and were not affected by feeding
diets containing about 5% erucic acid. Feeding a diet containing a high erucic acid rapeseed oil did result in higher free
fatty acid levels but only at 3 days and 1 week; the level at 16 weeks was similar to the other oils. The fatty acid analysis
of cardiac triglycerides and free fatty acids showed high percentages of erucic acid at 3 days and 1 week; at 16 weeks these
levels had declined significantly. The results indicate that the accumulated erucic and eicosenoic acids, at 3 days and 1
week, accounted for the increase in cardiac free fatty acids when rats were fed the high erucic acid rapeseed oil. There appears
to be no evidence that the early cardiac triglyceride or free fatty acid accumulation is related to the formation of the long
term myocardial lesions.
Contribution No. 739 Animal Research Institute. 相似文献
20.
No mortality was observed in 6 week old male Sprague-Dawley rats subjected to cold at 4 C for 3 weeks and fed either a control
diet (Chow) or a semisynthetic diet containing 20% by wt rapeseed oil high in erucic acid (23.6%). All rats fed the Chow diet
and 17 of 20 rats fed the rapeseed oil-containing diet survived 4 weeks in the same environment. Three rats on the latter
diet died of self-mutilation. Marked myocardial lipidosis as well as a large accumulation of 20∶1 and 22∶1 was observed in
the hearts of rats fed the rapeseed oil-containing diet. Five of 20 rats on the Chow diet and 2 of 20 rats on the rapeseed
oil-containing diet had focal necrotic areas in the myocardium. 相似文献