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1.
For eight weeks young male rats were fed diets rich in 18∶2 (stock diet, or 10% corn oil, CO) or those devoid of 18∶2 (fat
free, FF, or 10% hydrogenated coconut oil, HCNO). The CO and HCNO diets were fed in the absence or presence of eicosa-5,8,11,14-tetraynoic
acid (TYA). When 18∶2 was excluded, an increase in the level of 16∶1, 18∶1 and 20∶3 and a decrease in 18∶2 was observed in
the fatty acids of red cells. On feeding TYA, an increase in 18∶2 and in the case of the HCNO+TYA diet, a decrease of 12∶0
and 14∶0 was also observed. In all cases the levels of 20∶4 in erythrocyte fatty acids were similar. Saturated fatty acids
were predominant in phosphatidyl choline (PC), lysophosphatidylcholine, (LPC) and sphingomyelin whereas unsaturated acids
were predominant in phosphatidyl ethanolamine (PE), (PS), and phosphatidyl inositol (PI). Acids containing three or more double
bonds comprised about 90% of the total acids in PI. In all the phospholipids, the characteristic changes in the composition
of fatty acids were observed due to the exclusion of 18∶2 from the diet. However, changes due to the feeding of TYA were found
only in PC and LPC. In rats fed the 18∶2-rich diet, about 60% of the red cells were discocytes. In those fed the 18∶2-free
diet, the level of discocytes decreased to about 23%, and the levels of echinocytes II and III increased. The exclusion of
18∶2 for even a few days decreased the proportion of discocytes. The loss of discoid shape was reversed in a few days by feeding
an 18∶2-rich diet. Fatty acid analysis of erythrocytes of rats of the various dietary manipulations showed that the change
in the proportion of discocytes followed the change in the level of 18∶2. 相似文献
2.
Randall Wood 《Lipids》1982,17(11):763-770
Groups of rats were fed a fat-free diet supplemented with 0.5% safflower oil (control) or the control diet containing 0.5%
of 5,8,11,14-eicosatetraynoic acid (TYA). Blood was collected weekly and plasma lipids analyzed. After 4 weeks, the animals
were killed and the liver lipids were analyzed in detail. The acetylenic fatty acid perturbed plasma neutral lipid and phospholipid
class concentrations and reduced growth rates. Liver triglyceride concentrations were reduced dramatically in the TYA fed
animals, suggesting interference with complex lipid synthesis. Plasma and liver triglycerides were shifted to higher molecular
weight species suggesting that TYA affected fatty acid metabolism. The phospholipids showed an accumulation of 18∶2 and a
fall in 20∶4 percentages indicating an inhibition in the conversion of linoleate to arachidonate. All major lipid classes
exhibited an increase in 18∶1 levels. Analysis of the octadecenoate positional isomers indicated the proportion of oleate
increased substantually in all lipid classes whereas vaccenate proportions had fallen dramatically. All of the data collectively
suggest that TYA inhibits the elongation of unsaturated fatty acids. A group of rats bearing hepatoma 7288CTC were also fed
the TYA diet. Host liver lipids were affected by TYA similar to normal TYA fed animals, but the effects on hepatoma lipids
were marginal. 相似文献
3.
The objective of this study was to test the effect of a novel fatty acid mixture, enriched with myristoleic and palmitoleic
acids, on plasma lipoprotein cholesterol concentrations. Weanling pigs were assigned to one of six groups and each group received
a diet differing in fatty acid composition. Diets were fed for 35 days and contained 10 g added cornstarch/100 g (to provide
baseline data) or 10 g added fatty acids/100 g. For those diets containing added fatty acids, extracted lipids contained 36%
myristoleic plus palmitoleic acid combined (14∶1/16∶1 diet), 52% palmitic acid (16∶0 diet), 51% stearic acid (18∶0 diet),
47% oleic acid (18∶1 diet), or 38% linoleic acid (18∶2 diet). Witht the exception of the cornstarch diet, all diets contained
approximately 30% myristic acid. There were no significant differences in weight gain across treatment groups (P=0.22). All diets caused a significant increase in triglycerides and in total, low density lipoprotein, high density lipoprotein,
and very low density lipoprotein cholesterol. The increase in total plasma cholesterol from pretreatment values was greatest
in pigs fed the 14∶1/16∶1 and 18∶1 diets. However, the increase in low density lipoprotein cholesterol from the pretreatment
concentration was greatest in the 14∶1/16∶1-fed pigs. Increases in very low density lipoprotein cholesterol above pretreatment
concentrations were lowest in 16∶0-fed pigs and greatest in 18∶1-fed pigs. Dietary fatty acids elicited changes in plasma
fatty acids which generally were reflective of the diets, although the 18∶0 diet did not alter plasma fatty acid concentrations
and the 16∶0 diet increased plasma 16∶0 only at the end of the study. These results demonstrated that the combination of myristoleic
plus palmitoleic acids increased plasma cholesterol in young pigs, suggesting that fatty acid chain length, rather than degree
of unsaturation, is primarily responsible for the effects of fatty acids on circulating lipoprotein cholesterol concentrations. 相似文献
4.
Sheila M. Innis Roger Dyer Louis Wadsworth Paul Quinlan Deborah Diersen-Schade 《Lipids》1993,28(7):645-650
Platelet lipid composition is important to normal platelet morphology and function, and is influenced by dietary fatty acids
and cholesterol. The fatty acid composition and cholesterol content of infant formulas differs from those of human milk, but
the possible effects on platelet lipids in young infants is not known. This was studied in piglets fed from birth to 18 d
of age with one of eight formulas differing in saturated fatty acid chain length, or content of 18∶1, 20∶5n−3 plus 22∶6n−3,
or cholesterol. A reference group of piglets fed sow milk was also studied. Sow milk has a fatty acid composition and cholesterol
content similar to that of human milk. Piglets fed formulas high in 18∶1 (34.9–40.8% wt fatty acids) and low in 16.0 (≤6.5%
wt fatty acids) had lower platelet counts and greater platelet size than piglets fed sow milk (40.4% 18∶1, 30.7% 16∶0). Piglets
fed formulas high in 16∶0 (27–29.6%) and 18∶1 (40–40.6%), or low in both 16∶0 (5.9–6.1%) and 18∶1 (10.8–11.2%), had similar
platelet counts and size to piglets fed sow milk. Platelet phospholipid % 20∶4n−6 was lower in all the groups of piglets fed
formula than in the group fed sow milk. Addition of fish oil with 20∶5n−3 plus 22∶6n−3 to the formula further decreased platelet
phospholipid 20∶4n−6. Addition of cholesterol to the formula increased the platelet phospholipid % 20∶4n−6 and platelet volume. 相似文献
5.
Young male rats were fed ad libitum for 8 weeks a low iron fat-free (FF-Fe) diet or a fat-free diet supplemented with iron
(FF+Fe). The relative levels of 16∶1 to 16∶0 and 18∶1 to 18∶0 in the total fatty acids of liver and other tissues (plasma,
erythrocytes and intestinal mucosa) were considerably decreased because of a lack of dietary iron. In rats fed the FF-Fe diet,
the levels of essential fatty acids (18∶2ω6+20∶4ω6) in tissues were 2-to 3-fold greater than in the corresponding tissues
of rats fed the FF+Fe diet. Eicosatrienoic acid (20∶3ω9) levels in tissue lipids from rats fed the FF+Fe diet were high (8–16%),
whereas they were low (2–5%) in the case of animals fed the FF-Fe diet. The proportion of 20∶4 in total fatty acids of tissues
was 2-to 3-fold greater in rats fed the FF-Fe diet than when they were fed the FF+Fe diet. Therefore, the relative levels
of 20∶3ω9/20∶4ω6 varied from 1-2.9 in tissue lipids of rats fed the FF+Fe diet, while it varied only from 0.2–0.3 in animals
fed the FF-Fe diet. These results suggest that a lack of dietary iron may reduce the synthesis of 16∶1, 18∶1, 20∶3 and 20∶4
and the metabolism of 20∶4. 相似文献
6.
This study examined the effect on the plasma lipids and plasma phospholipid and cholesteryl ester fatty acids of changing
from a typical western diet to a very low fat (VLF) vegetarian diet containing one egg/day. The effect of the addition of
saturated, monounsaturated or polyunsaturated fat (PUFA) to the VLF diet was also examined. Three groups of 10 subjects (6
women, 4 men) were fed the VLF diet (10% energy as fat) for two weeks, and then in the next two weeks the dietary fat in each
group was increased by 10% energy/week using butter, olive oil or safflower oil. The fat replaced dietary carbohydrate. The
VLF diet reduced both the low density lipoprotein (LDL)-and high density lipoprotein (HDL)-cholesterol levels; addition of
the monounsaturated fats and PUFA increased the HDL-cholesterol levels, whereas butter increased the cholesterol levels in
both the LDL- and HDL-fractions. The VLF diet led to significant reductions in the proportion of linoleic acid (18∶2ω6) and
eicosapentaenoic acid (20∶5ω3) and to increases in palmitoleic (16∶1), eicosatrienoic (20∶3ω6) and arachidonic acids (20∶4ω6)
in both phospholipids and cholesteryl esters. Addition of butter reversed the changes seen on the VLF diet, with the exception
of 16∶1, which remained elevated. Addition of olive oil resulted in a significant rise in the proportion of 18∶1 and significant
decreases in all ω3 PUFA except 22∶6 compared with the usual diet. The addition of safflower oil resulted in significant increases
in 18∶2 and 20∶4ω6 and significant decreases in 18∶1, 20∶5ω3 and 22∶5ω3. These results indicate that the reduction of saturated
fat content of the diet (<6% dietary energy), either by reducing the total fat content of the diet or by exchanging saturated
fat with unsaturated fat, reduced the total plasma cholesterol levels by approximately 12% in normocholesterolemic subjects.
Although the VLF vegetarian diet reduced both LDL- and HDL-cholesterol levels, the long-term effects of VLF diets are unlikely
to be deteterious since populations which habitually consume these diets have low rates of coronary heart disease. The addition
of safflower oil or olive oil to a VLF diet produced favorable changes in the lipoprotein lipid profile compared with the
addition of butter. The VLF diets and diets rich in butter, olive oil or safflower oil had different effects on the 20 carbon
eicosanoid precursor fatty acids in the plasma. This suggests that advice on plasma lipid lowering should also take into account
the effect of the diet on the fatty acid profile of the plasma lipids. 相似文献
7.
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
8.
Omega-3 fatty acids influence the function of the intestinal brush border membrane. For example, the omega-3 fatty acid eicosapentaenoic
acid (20∶5ω3) has an antiabsorptive effect on jejunal uptake of glucose. This study was undertaken to determine whether the
effect of feeding α-linolenic acid (18∶3ω3) or EPA plus docosahexaenoic acid (22∶6ω3) on intestinal absorption of nutrients
was influenced by the major source of dietary lipid, hydrogenated beef tallow or safflower oil. Thein vitro intestinal uptake of glucose, fatty acids and cholesterol was examined in rats fed isocaloric diets for 2 weeks: beef tallow,
beef tallow + linolenic acid, beef tallow + eicosapentaenoic acid/docosahexaenoic acid, safflower oil, safflower oil + linolenic
acid, or safflower oil + eicosapentaenic acid/docosahexaenoic acid. Eicosapentaenoic acid/docosahexaenoic acid reduced jejunal
uptake of 10 and 20 mM glucose only when fed with beef tallow, and not when fed with safflower oil. Linolenic acid had no
effect on glucose uptake, regardless of whether it was fed with beef tallow or safflower oil. The jejunal uptake a long-chain
fatty acids (18∶0, 18∶2ω6, 18∶3ω3, 20∶4ω6, 20∶5ω3 and 22∶6ω3) and cholesterol was lower in salfflower oil than with beef tallow.
When eicosapentaenoic acid/docosahexaenoic acid was given with beef tallow (but not with safflower oil), there was lower uptake
of 18∶0, 20∶5ω3 and cholesterol. The demonstration of the inhibitory effect of linolenic acid or eicosapentaenoic acid/docosahexaenoic
acid on cholesterol uptake required the feeding of a saturated fatty acid diet (beef tallow). These changes in uptake were
not explained by differences in the animals’ food intake, body weight gain or intestinal weight. Feeding safflower oil was
associated with an approximately 25% increase in the jejunal and ileal mucosal surface area, but this increase was prevented
by combining linolenic acid or eicosapentaenoic acid/docosahexaenoic acid with safflower oil. Different inhibitory patterns
were observed when mixtures of fatty acids were present together in the incubation medium, rather than in the diet: for example,
when 18∶0 was in the incubation medium with 20∶4ω6, the uptake of 20∶4ω6 was reduced, whereas the uptake was unaffected by
18∶2ω6 or 20∶5ω3. Thus, (1) the inhibitory effect of eicosapentaenoic acid/docosahexaenoic acid on jejunal uptake of glucose,
fatty acids and cholesterol was influenced by the major dietary lipid, saturated (beef tallow) or polyunsaturated fatty acid
(safflower oil); and (2) different omega-3 fatty acids (linolenic acid versus eicosapentaenoic acid/docosahexaenoic acid)
have a variable influence on the intestinal absorption of nutrients. 相似文献
9.
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
10.
The effects of oil-derived dietary essential fatty acids on the activities of mitchondrial Mn-SOD (manganese-superoxide dismutase)
and cytosolic cupric zinc-superoxide dismutase (Cu/Zn-SOD) were investigated in rat heart. A control group of rats was fed
a stock diet for 29 d, and a second group was fed on a fat-free diet. Three other groups were fed fat-free diets that were
supplemented with (i) borage oil, which is rich in linoleic (18∶2n−6) and γ-linolenic (18∶3n−6) acids, (ii) fungal oil, which
is rich in γ-linolenic, but low in linoleic acid, or (iii) evening primrose oil, which is rich in linoleic acid and low in
γ-linolenic acid. An increase in the percentage composition of arachidonic acid (20∶4n−6) in both the choline and ethanolamine
phospholipids, together with a decrease in linoleic acid in ethanolamine phospholipids, were found in heart membranes after
feeding the rats with diets containing borage oil or fungal oil as compared to those fed the stock diet. The respective activities
of Mn-SOD in rats fed the borage or fungal oil diets were also significantly higher than in rats fed the stock diet alone.
No change in cytosolic Cn/Zn-SOD activity was observed. Dietary supply of linoleic acid-rich evening primrose oil resulted
in an increased proportion of choline phospholipid linoleic acid without any changes in arachidonic acid content or in the
activity of Mn-SOD. By contrast, a reduction in the activity of Mn-SOD was detected in rats fed a fat-free diet. These results
show that the activity of heart mitochondrial Mn-SOD is influenced by dietary essential fatty acids, whereas the activity
of cytosolic Cu/Zn-SOD remained unaffected. 相似文献
11.
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
12.
In view of the findings that ω3 fatty acids inhibit the synthesis of prostaglandins (PG) from arachidonic acid (20∶4ω6) and
that among immunologically active cells, the macrophage, is a major producer of PG, we undertook a study of the effect of
dietary α-linolenic acid (18∶3ω3) on PG synthesis in the macrophage. Rats were fed purified diets containing either 10% corn
oil (CO) or linseed oil (LO), providing either a low (1/32) or high (3.5/1) ratio of 18∶3ω3 to 18∶2ω6, respectively, for 6
weeks. Fatty acid analysis of macrophage phospholipids showed that there was an appreciable increase in the percentage of
ω3 fatty acids and a decrease in the ω6 fatty acids in macrophages from rats fed the LO diet. The changes in fatty acid composition
were associated with a significant decrease in the synthesis of prostaglandin E (PGE) by macrophages from rats fed the LO
diet. Macrophages from rats fed the 2 dietary, oils did not differ in their ability to degrade PG, thus the difference in
PG production appeared to be a consequence of decreased synthesis only. The dietarily induced changes in PGE synthesis were
readily overcome in vitro by culturing macrophages with complexes of fat-free bovine serum albumin and either 20∶4ω6 or 20∶5ω3.
Part of a dissertation submitted by Linda J. Magrum in partial fulfillment of the requirements for the Ph.D. degree in Nutritional
Sciences.
Honored Student Presentation at the AOCS 74th Annual Meeting, Chicago, 1983. 相似文献
13.
The effects of various unsaturated fatty acids such as oleic (18∶1n−9), linoleic (18∶2n−6) and arachidonic (20∶4n−6) on the
activities of fatty acid synthetase (FAS), malic enzyme (ME), glucose-6-phosphate dehydrogenase (G6PDH) and 6-phosphogluconate
dehydrogenase (6PGDH) all were determined in primary cultures of mouse hepatocytes. Activities of FAS and ME were found to
decrease with time in culture regardless of whether hepatocyte donors were fed diets containing polyunsaturated fatty acid-free
hydrogenated cottonseed oil (HCTO) or corn oil (CO). On the other hand, while G6PDH activity also declined in cultured hepatocytes
obtained from HCTO-fed mice, the activity of this enzyme increased in cells cultured from CO-fed mice. 6PGDH activity was
found to increase in hepatocytes obtained from both diet groups. Neither 18∶2 nor 20∶4 when added to media could alter FAS
or ME activities compared with those observed with either 18∶1-containing or fatty acid-free media. Since lactic dehydrogenase
activity and the rate of incorporation of [3H] leucine into FAS protein were unaltered with time in hepatocyte cultures, the decreased activities of FAS and ME cannot
be attributed to a loss in cell viability during culture but rather appear to be specific for those enzymes which respond
to diet hormones in vivo. Examination of the fatty acid contents of the cells after the culture period showed that the values
for the ratios of 16∶0/16∶1 and of 18∶0/18∶1 were elevated when either 18∶2 or 20∶4 was added to the medium even though there
was no evidence for elongation of the added 18∶2 or for 20∶4 being converted to 22∶4. This result suggest that Δ9-desaturase
activity was inhibited by these polyunsaturated fatty acids and that conversion of 18∶2 to 20∶4 was not required for such
action.
The rate of synthesis determined by the relative rate of incorporation of [3H]leucine into FAS was two to five times higher in hepatocytes prepared from mice fed the HCTO diet than in hepatocytes from
mice fed the CO diet. We have concluded that the mechanisms for long-term regulation may not be contained entirely within
the liver. 相似文献
14.
Joseph Sampugna Luise Light Mary G. Enig D. Yvonne Jones Joseph T. Judd Elaine Lanza 《Lipids》1988,23(2):131-136
Analysis of cheek cell lipids has been suggested as a noninvasive method for monitoring the fatty acid composition of diets
in humans. In a pilot study conducted to determine the validity of the method, cheek cell samples were collected from subjects
consuming a low fat (20% of calories) diet consisting of fatty acids with either a 1.0 or 0.3 P/S ratio. Neither total lipid
nor polar lipid fatty acids in cheek cells consistently reflected the P/S ratio of the diets. However, there were trends,
particularly in the nonpolar lipids, suggesting that cheek cell fatty acid ratios might be useful for monitoring the fatty
acid composition of the diets. The diet with the higher P/S ratio (1.0 vs 0.3) consistently resulted in cheek cell lipids
with lower ratios of 18∶1/saturated fatty acids and greater 18∶2/20∶4, 18∶2/18∶1 and 18∶2/18∶0 fatty acid ratios. 相似文献
15.
The effects of dietary n−3 and n−6 polyunsaturated fatty acids on the fatty acid composition of phospholipid, Ca++· Mg++ ATPase and Ca++ transport activities of mouse sarcoplasmic reticulum were investigated. Mice were fed a 2 weight percent fat diet containing
either 0.5 weight percent ethyl esters of 18∶3n−3, 20∶5n−3 or 22∶6n−3 as a source of n−3 polyusaturated fatty acid or 0.5
weight percent safflower oil as a cource of n−6 polyunsaturated fatty acid for 10 days. Olive oil (2 weight percent) was used
as a control diet. Although feeding n−6 polyunsaturated fatty acid induced very little modifications of the phospholipid sarcoplasmic
reticulum fatty acid composition, feeding n−3 polyunsaturated fatty acid altered it markedly. Inclusion of 18∶−3, 20∶5n−3
or 22∶6n−3 in the diet caused an accumulation of 22∶6n−3, which replaced 20∶4n−6 and 18∶2n−6 in phospholipid sarcoplasmic
reticulum. The saturated fatty acids were significantly increased with a concurrent reduction of 18∶1n−9. These changes in
the fatty acid composition resulted in a decrease in the values of the n−6/n−3 polyunsaturated fatty acid ratio and a decrease
in the ratio of 20 carbon to 22 carbon fatty acids esterified in the phospholipid sarcoplasmic reticulum. This was associated
with a decrease in Ca++ uptake by n−3 polyunsaturated fatty acid enriched sarcoplasmic reticulum vesicles as compared with n−6 fatty acid and control
diet sarcoplasmic reticulum vesicles. However, neither the affinity for Ca++ nor the maximal velocity of ATP hydrolysis activity of Ca++·MG++ ATPase were altered by the different diets. The data suggest that the incorporation of 22∶6n−3 and/or the decrease of 20∶4n−6
plus 18∶2n−6 in the phospholipid sarcoplasmic reticulum may affect the membrane lipid bilayer structure and make it more permeable
to Ca++. 相似文献
16.
The purpose of this study was to examine the influence of long-term feeding of dietary fat rich in either n−3 or n−6 fatty
acids on the availability of arachidonic acid (20∶4n−6) in major phospholipids of gastric mucosa in rats. Three groups of
male Wistar rats were fed either a standard diet, a cod liver oil-enriched diet (10% by weight), or a corn oil-enriched diet
(10% by weight) for 8 mon. Dietary cod liver oil significantly reduced the level of 20∶4n−6 in phosphatidylcholine (PC) and
in phosphatidylethanolamine (PE) of gastric mucosa. The loss of 20∶4n−6 was compensated for by eicosapentaenoic acid (20∶5n−3)
in PC, whereas the decrease in 20∶4n−6 in PE corresponded to the increase in three n−3 fatty acids: 20∶5n−3, docosapentaenoic
acid (22∶5n−3), and docosahexaenoic acid (22∶6n−3). The level of 20∶5n−3 was higher than the level of 22∶6n−3 both in PC and
PE of mucosa in rats fed cod liver oil. Diets supplemented with corn oil increased the level of 18∶2n−6 but decreased the
monoene fatty acids 16∶1 and 18∶1n−7 in PC but not in PE of gastric mucosa. The 20∶4n−6 levels of both PC and PE were markedly
reduced by dietary cod liver oil, to about one-third of control levels. Similar changes were also observed in the stomach
wall. Gastric erosions were observed in all rats exposed to restriction stress, but this form of stress induced twice the
number of erosions in rats fed fish oil compared to control rats or rats fed corn oil. We conclude that a diet rich in fish
oil altered the balance between n−6 and n−3 fatty acids in major gastric mucosal phospholipids, markedly reduced the availability
of 20∶4n−6, and increased the incidence of gastric erosions induced by restriction or emotional stress. 相似文献
17.
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
18.
Male weanling rats were fed semi-synthetic diets high in saturated fat (beef tallow) vs high in linoleic acid (safflower oil)
with or without high levels of α-linolenic acid (linseed oil) for a period of 28 days. The effect of feeding these diets on
cholesterol content and fatty acid composition of serum and liver lipids was examined. Feeding linseed oil with beef tallow
or safflower oil had no significant effect on serum levels of cholesterol. Serum cholesterol concentration was higher in animals
fed the safflower oil diet than in animals fed the beef tallow diet without linseed oil. Feeding linseed oil lowered the cholesterol
content in liver tissue for all dietary treatments tested. Consumption of linseed oil reduced the arachidonic acid content
with concomitant increase in linoleic acid in serum and liver lipid fractions only when fed in combination with beef tallow,
but not when fed with safflower oil. Similarly, ω3 fatty acids (18∶3ω3, 20∶5ω3, 22∶5ω3, 22∶6ω3) replaced ω6 fatty acids (20∶4ω6,
22∶4ω6) in serum and liver lipid fractions to a greater extent when linseed oil was fed with beef tallow than with safflower
oil. The results suggest that the dietary ratio of linoleic acid to saturated fatty acids or of 18∶3ω3 to 18∶2ω6 may be important
to determine the cholesterol and arachidonic acid lowering effect of dietary α-linolenic acid. 相似文献
19.
The mammary tumor-promoting effect of a high-fat diet containing 20% evening primrose oil (PO) was compared to that of a 20%
corn oil (CO) diet. Mammary tumors were induced in female Sprague-Dawley rats using 10 mg (Study 1) and 5 mg (Study 2) 7,12-dimethylbenz(a)anthracene
(DMBA). The 10 mg dose of DMBA gave a total mammary tumor incidence of 47% in rats fed the PO diet and 80% for those fed the
CO diet. When only adenocarcinomas were counted, the malignant mammary tumor incidences were 41% in rats fed the PO diet and
73% in rats fed the CO diet. In a second study using 5 mg DMBA to induce mammary tumors, total tumor incidences were 50% for
PO-fed rats and 63% for those receiving a CO diet. Again, when only adenocarcinomas were counted, tumor incidences were 27%
for PO- and 63% for CO-dieted rats. Analysis of plasma fatty acid profiles indicated that animals fed a 20% PO diet showed
significant increases in 18∶3 and 20∶4 fatty acids and significant decreases in 16∶0 and 18∶1 compared to animals fed a 20%
CO diet. These results indicate that the mammary tumor promoting effect of a diet containing 20% fat can be diminished by
substituting PO for CO. Moreover, the promoting effect on mammary cancer by a high-fat diet could be depressed by feeding
a source of γ-linolenic acid (GLA). 相似文献
20.
To test the possibility that dietary palmitic acid (16∶0) may be lithogenic, different fats were blended to exchange 18∶1
in olive oil with either 16∶0 in palm stearin, 12∶0+14∶0 in coconut oil, or 14∶0+16∶0 in butterfat. Dietary 18∶2 was held
constant at 1.2% energy (en) (with extra safflower oil as needed) in these four purified diets containing low fat (11% of
total energy) and 0.4% cholesterol. A fifth, high-fat diet provided 40% of the total energy as the 16∶0-rich blend. All hamsters
fed the low-fat, 16∶0-rich blend for six weeks developed cholesterol gallstones (8/8). Although the gallstone incidence was
lower for the 12∶0+14∶0-rich diet (5/8), the severity of stone formation in affected hamsters was equal to that in the low-fat,
16∶0-rich group. Mucin accumulation in gallbladder bile was often associated with cholesterol gallstones in diets containing
16∶0, but was minimal in 18∶1-rich and 12∶0+14∶0-rich groups. Neither the lithogenic index (all>1.0), plasma lipids, nor liver
cholesterol was a selective predictor of stone formation. The high-fat, 16∶0-rich diet actually decreased cholesterol stone
incidence (3/8) and severity, but yielded a high incidence of pigment stones (5/8). Thus, saturated fat and 16∶0per se were not responsible for the exaggerated lithogenesis. Because the antilithogenic 18∶1-rich diet also normalized the 18∶2
intake (1.2% en) relative to previous butter diets (0.3% en), the potential importance of essential fatty acids (EFA) deficiency
in the model was tested in a second study by feeding graded amounts of 18∶2 (0.3, 0.6, 0.9, and 1.2% en) as safflower oil
in four low-fat, butter-rich diets (11% en as fat) without alleviating gallstone incidence or severity. These studies indicate
that substitution of 18∶1 for saturated fatty acids in low-fat diets reduces gallstone formation without affecting the lithogenic
index. Furthermore, intake of 18∶2 at or below the EFA requirement does not appear to be a major factor in this model. 相似文献