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1.
Soad H. Abou-El-Ela Keith W. Prasse Richard Carroll Adelbert E. Wade Suniti Dharwadkar Opal R. Bunce 《Lipids》1988,23(10):948-954
The comparative effects of high-fat diets (20%, w/w) on eicosanoid synthesis during mammary tumor promotion in 7,12-dimethylbenz(a)anthracene
(DMBA)-induced rats were studied using diets containing 20% primrose oil (PO), 20% menhaden oil (MO) or 20% corn oil (CO).
Sprague-Dawley rats fed the PO or MO diet had 21% or 24% fewer adenocarcinomas, respectively, than rats fed the CO diet. Histologically
(i.e., mitotic figures, inflammatory cell infiltration and necrosis), the CO-fed rats exhibited the highest frequency of changes
within tumors. Plasma fatty acid composition was significantly altered by diet, reflecting the composition of the oils which
were being fed. Only the plasma of PO-fed rats contained detectable levels of gamma-linolenic acid (GLA). Arachidonic acid
(AA) levels were significantly higher (p<0.05) in PO-fed than in CO- or MO-fed rats. MO-fed rats had significantly higher
levels of plasma palmitic acid, while palmitoleic, eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids were detected only
in MO-fed rats. As expected, linoleic acid (LA) and AA levels were lower (p<0.05) in the MO-fed rats than in PO- or CO-fed
groups. The plasma of the CO-fed rats contained significantly higher levels of oleic acid. Eicosanoid synthesis in mammary
carcinomas of rats fed the 20%-fat diets was 2–10 times higher than in mammary fat pads of control rats. The synthesis of
PGE1 and LTB4 was significantly (p<0.05) higher in PO-fed rats than in CO-fed or MO-fed rats, although PGE values were significantly (p<0.05)
higher in CO-fed rats than in Mo or PO groups. The synthesis of eicosanoids in both mammary fat pads and mammary carcinomas
of MO-fed rats was lower (p<0.05) than in tissues of rats fed either CO or PO diets due to less AA precursor being fed and/or
to competition between n−6 and n−3 fatty acids for cyclooxygenase and lipoxygenase. The ratios of monoenoic to dienoic eicosanoids
in both mammary fat pads and mammary carcinomas were higher in the PO group than in the MO or CO groups. These results suggest
that inclusion of GLA (PO feeding) or EPA and DHA (MO feeding) in the diet may decrease malignancy by altering eicosanoid
profiles. 相似文献
2.
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
3.
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
4.
Male Wistar rats were maintained for 30 days on an independent and continuous intragastric infusion of ethanol and nutritionally
defined liquid diet containing only a small amount of corn oil (CO-4.9% calories). Ethanol intake was progressively increased
from 32% to 40.4% of the total calories to maintain a high degree of intoxication during this period. Rats in the control
group were infused with an isocaloric diet in which alcohol was replaced by dextrose. The liver triglyceride (TG) content
of rats given alcohol (61.5±16.4 mg/g) was ca. 10-fold greater than that of controls (5.9±2.1 mg/g) and similar to that observed
previously in rats fed an ethanol diet containing high levels of fat (35% and 43% calories). In TG of fatty liver, the level
of 18∶2 was small (3%), even though CO in the diet contained a high level of this acid. Furthermore, 16∶1 and 16∶0 contents
were markedly elevated (16% and 40%, respectively) despite the fact that CO did not contain 16∶1 and had only a small amount
of 16∶0. Liver TG having a fatty acid (FA) composition markedly different from that of CO and the presence of high levels
of 16∶1 and 16∶0 indicate that the TG accumulated in the fatty liver originated from hepatic lipogenesis rather than from
dietary fat. 相似文献
5.
Nanna Philipson Brandorff 《Lipids》1980,15(4):276-278
During pregnancy and lactation, female rats were fed diets containing either 28% partially hydrogenated marine oil (28MO),
2% arachis oil (2AO), or no fat (FF). Milk lipid composition was examined by gas chromatographic analysis of the gastric content
of 10-day-old suckling pups. An increase to 45% in the milk content of long chain monoenoic acids, 18∶1, 20∶1 and 22∶1, reflects
the fatty acid composition of the marine oil. Milk fatty acids of medium chain length comprised 6%, 31% and 24% of total fatty
acids in the (28MO), (2AO) and (FF) groups, respectively, suggesting that a high-fat diet (28MO) inhibits the lipid synthetic
activity of mammary glands. The amount of dienoic C18-acids (6%) in the group fed (28MO) containing no essential fatty acids (EFA) was similar to the amount of 18∶2 in the group
receiving a low-fat, EFA-rich diet (2AO). However, only half the dienoic acid from the milk of the (28MO)-fed animals was
linoleic acid, which was most likely mobilized from fat depots. 相似文献
6.
Male Sprague-Dawley rats were fed for 30 days a high-fat liquid ethanol diet with dihydroxyacetone, pyruvate and riboflavin
added as supplements (AMA-). Plasma triglyceride (TG) levels were 6-fold greater in these rats than in those fed and alcohol
with without the supplements (AA-). The liver TG content in rats fed the AMA-diet was similar to that of rats fed a control
diet (CA-) in which alcohol was replaced with isocaloric amounts of dextrose. Livers of rats fed the AA- diet had 3 times
more TG than controls. Alcohol ingestion also enhanced the hepatic content of cholesteryl esters (CE) and phospholipids (PL).
These lipids were reduced to levels found in livers of rats fed the control diet (CA-) when dihydroxyacetone, pyruvate and
riboflavin were included in the alcohol diet. The fatty acid compositions of TG, CE and PL from livers of rats fed the AMA-diet
were similar to those of corresponding lipids from rats fed the control diet (CA-) but differed from compositions when fed
the alcohol diet (AA-). Regardless of the diet fed, TG had the same fatty acid composition in plasma and liver. The same was
true of PL fatty acid composition. However, the fatty acid composition of CE differed between liver and plasma. The major
fatty acid in liver CE was 18∶1 whereas in plasma it was arachidonic acid (20∶4). Reduced fatty liver was observed in an earlier
study when rats were fed ad libitum an ethanol diet containing 20∶4. In the present study, we pair-fed the same diet and fatty
liver was not reduced. Dihydroxyacetone, pyruvate and riboflavin did not prevent alcohol-induced fatty liver when 20∶4 was
included in the AMA-diet. Our results confirm that dietary dihydroxyacetone, pyruvate and riboflavin prevent alcohol-induced
fatty liver, and show that this effect may result from increased mobilization of fat from liver. 相似文献
7.
Rats were fed a diet supplemented with corn oil (n-3 deficient), soy oil, or a mixture containing 8% 22∶6n-3 ethyl ester for
6 wk. The hepatic capacities for the β-oxidation and synthesis of 22∶6n-3, in addition to the acylation of lysophosphatidate,
were tested in vitro. In rats that were fed a 22∶6n-3-enriched diet, both the β-oxidation of 22∶6n-3 and elongation of 20∶5n-3 were enhanced compared
to those in rats fed the other diets. Acylation of lysophosphatidate was also enhanced in rats fed a 22∶6n-3-enriched diet,
while the rate of dephosphorylation of phosphatidate was not changed. The amount of 22∶6n-3 in the liver was much less than
that consumed in a docosahexaenoic acid-enriched diet. These results suggest that a significant amount of dietary 22∶6n-3
was degraded via β-oxidation, and that a portion of the retroconverted 20∶5n-3 was recycled for the synthesis of 22∶6n-3. The recycling of
20∶5n-3 might contribute to the low level of 22∶6n-3 in rats fed an n-3-deficient diet. 相似文献
8.
Aspects of the lipid metabolism of male, obese and lean Zucker rats were compared using animals which had been fed ad libitum
for 32 days on a diet (HS) which contained 200 g sunflowerseed oil/kg or one (LS) which contained 50 g/kg of the oil. When
compared with the LS diet, the HS diet decreased the characteristic lipid accretion in the liver of obese rats from 126 mg
(LS) to 81 mg (HS)/g wet weight; corresponding values for the lean rats were 39 mg and 56 mg/g wet weight of liver, respectively.
The HS diet depressed lipid synthesis de novo by liver homogenates and decreased the Δ9-desaturase activity of liver microsomes
from obese and clean rats by about 50%. Δ9-Desaturase activity in vitro was also depressed by the addition of linoleic acid
to liver microsomes from both obese and lean rats fed ad libitum on a standard laboratory diet. Depressed Δ9-desaturase activity,
due to ingestion of the HS diet, was reflected in lower ratios of 16∶1/16∶0 and 18∶1/18∶0 fatty acids in tissue lipids from
obese and lean rats. Ingestion of the HS compared with the LS diet resulted in increased proportions of 18∶2ω6 in liver lipids
and adipose tissue triacylglycerols of obese and lean rats. The HS diet also increased the proportions of 20∶4ω6 in adipose
triacylglycerols of obese and lean rats and in liver lipids of obese animals but not in their lean littermates. 相似文献
9.
Male Sprague-Dawley rats were fed for 8 weeks a corn oil (CO) diet or a hydrogenated coconut oil (HCNO) diet. These diets
were fed in the absence or presence of eicosa-5,8,11,14-tetraynoic acid (TYA). The inclusion of TYA in the HCNO diet reduced
the levels of 12∶0 and 14∶0 in the total fatty acids of livers and plasma. With either diet, the presence of TYA caused an
alteration in the fatty acid composition of these tissues so as to reduce the values of the ratios: 16∶1/16∶0, 18∶1/18∶0,
and 20∶4/18∶2. These results suggest that dietary TYA can influence the hepatic metabolism of medium chain fatty acids and
that it may inhibit the desaturase enzyme involved in the synthesis of not only 20∶4 but also of monoenoic fatty acids. 相似文献
10.
Effect of varying proportions of dietary menhaden and corn oil on experimental rat mammary tumor promotion 总被引:2,自引:0,他引:2
Dose-related effects of long-chain highly unsaturated n−3 fatty acids on the development ofN-nitrosomethylurea (NMU)-induced rat mammary tumors were assessed in female F344 rats. Four test groups (36 rats/group) were
fed the following high-fat (HF) diets (23% fat, w/w): Group 1, 18% menhaden oil (MO) and 5% corn oil (CO); Group 2, 11% MO
and 11.8% CO; Group 3,5% MO and 18% CO; Group 4, CO alone. A fifth group, serving as an internal control, was fed a low-fat
diet containing 5% CO alone. Experimental diets were begun after initiation with NMU, and the experiment was terminated 31
wk later. Total tumor numbers in the five groups were 28, 16, 32, 26 and 11, respectively, indicating that the promotion phase
of NMU-induced carcinogenesis was significantly suppressed only when equal parts of CO and MO (Group 2) were fed or when CO
alone was fed at 5% (w/w). At high (Group 1) or low (Group 3) levels of MO, tumor numbers were indistinguishable from the
HF CO group (Group 4). The same pattern was observed when assessed in terms of cumulative tumor incidence and multiplicity.
However, when expressed in terms of final tumor incidence, dietary MO did not suppress tumor promotion in a statistically
significant fashion at any concentration. Animals fed MO gained weight at the same rate as those fed CO, indicating that the
presence of MO in the diet did not result in food avoidance behavior. Measurement of total serum cholesterol indicated an
inverse trend with respect to the MO content of the diet. Analysis of serum fatty acid profiles indicated that the proportion
of n−3 and n−6 polyun-saturated fatty acids (PUFA) in the serum reflected that of the diet. These results support the hypothesis
that the relative proportions of dietary n−3/n−6 fatty acids play an important role in the suppression of experimental mammary
tumorigenesis and suggest that changes in circulating cholesterol or n−3 PUFA levels, induced by dietary MO, are not directly
related to tumor development.
Presented in part at the 81st Annual Meeting of the American Association for Cancer Research, Washington, D.C., May 1990 相似文献
11.
We fed young male Sprague-Dawley rats for 4 wk ad libitum liquid diets containing 34% of the calories as ethanol and 35% as
fat with (AA+) and without (AA−) arachidonic acid (20∶4). Additional rats in the control groups were fed similar diets made
isocaloric with dextrose with (CA+) and without (CA−) 20∶4. The liver triglyceride (TG) content of rats in the AA+ group was
reduced ca. 3-fold over that of rats in the AA-group. The diet consumption and body wts of rats in the AA+ group were significantly
greater than those of rats fed alcohol without the 20∶4 supplement (AA−). Also livers from rats in the AA+ group were as large
as those from rats in control groups (CA+, CA−) and ca. twice as large as those from rats in the AA-group. The fatty acid
composition of liver TG in rats fed the alcohol diet was similar to that of dietary fat. Levels of 20∶4 and docosatetraenoic
acid (22∶4) in liver TG fatty acids from rats fed diets without arachidonate (AA−, CA−) were low (trace to 1.6%). After ingestion
of arachidonic acid, 20∶4 increased to ca. 10% and 22∶4 to ca. 5%. The content of liver phospholipids was higher in livers
of rats fed ethanol (AA−) than in those of controls (CA−).
Presented at the ISF/AOCS World Congress, April 27-May 1, 1980, New York City. 相似文献
12.
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
13.
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
14.
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
15.
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
16.
The influence of diet on the kinetics of the overt form of rat liver mitochondrial carnitine palmitoyltransferase (CPT I;
EC 2.3.1.21) was studied using rats fed either a low-fat diet (3% w/w fat), or diets which were supplemented with either olive
oil (OO), safflower oil (SO) or menhaden (fish) oil (MO) to 20% w/w of fat (high fat diets). When animals were fed each of
these four diets for 10 days, the order of the apparent maximal activity (Vmax) of CPT I toward various individual fatty acyl CoA, when measured under a fixed molar ratio of acyl CoA/albumin, was 16∶1n−7>18∶1n−9>18∶2n−6>16∶0>22∶6n−3,
and was thus not affected by the fat composition of the diet. However, in all but one case, the SO and MO diets elicited a
higher Vmax for each substrate than either the LF diet or the high fat OO diet. The apparent K
0.5 for the different acyl CoA esters was generally lowest in LF-fed animals, and highest in those fed the high-fat SO diet.
Moreover, when compared with the situation of animals fed high-fat diets, the K
0.5 values of CPT I in LF-fed animals for palmitoyl CoA and oleoyl CoA were low. This possession by CPT I of a high “affinity”
toward these nonessential fatty acyl CoAs, but a lower “affinity” toward linoleoyl CoA, the ester of an essential fatty acid,
may enable this latter fatty acid to be spared from oxidation when its concentration in the diet is low. The data also emphasize
that palmitoleoyl CoA, if available in the diet, is likely to be utilized by CPT I at a high rate. 相似文献
17.
The metabolism of α-linolenic acid from canola oil was studied in eight normolipidemic men. The 42-day study was divided into
three periods: a 6-day pre-experimental and two 18-day experimental. Approximately 75% of the dietary fat (28% of total energy)
was provided by a mixture of fats during the pre-experimental period and either canola oil (CO) or sunflower oil (SO) during
the experimental periods. The CO and SO diets were fed in a cross-over design. The ratios of linoleic to linolenic acid were
2.6∶1 and 73.9∶1 in the CO and SO diets, respectively. Dietary fat source had an effect on plasma phospholipid fatty acids:
18∶1n−9, 18∶3n−3 and 20∶5n−3 were higher (p<0.05), and 18∶2n−6 was lower in the phosphatidylcholine fraction; 18∶1n−9 was
higher and 20∶4n−6 lower in the phosphatidyl-ethanolamine fraction; and 18∶1n−9 and 20∶5n−3 were higher and 20∶4n−6 and 22∶6n−3
were lower in the alkenylacyl-ethanolamine phospholipid fraction on the CO diet as compared to the SO diet. Consumption of
the canola oil diet resulted in higher n−3 fatty acid levels and lower n−6 fatty acid levels in plasma phospholipids than
consumption of the sunflower oil diet. 相似文献
18.
Two groups of rats were fed diets containing 20% by weight of either partially hydrogenated marine oil supplemented with sunflower
seed oil (PHMO) or palm oil (PO) for 8 wk. Using a liver perfusion system, the effect of dietary long chain monoenoic fatty
acids on the uptake and metabolism of [14-14C]erucic acid was studied. The perfusion times were 15 and 60 min, respectively. The two groups showed equal ability for erucic
acid uptake in the liver but differed in the channeling of the fatty acids into various metabolic pathways. A higher metabolic
turnover of 22∶1 in the PHMO livers relative to the PO livers was demonstrated by an increased recovery of total [14C]labeling in the triglyceride (TG) and phospholipid (PL) fractions, already evident after 15 min of perfusion. The chainshortening
capacity was highest in the PHMO group, reflected by a higher [14C]18∶1 incorporation in both TG and PL, and increasing from 15 to 60 min of perfusion. The amount of [14C]18∶1 found in PL and TG after 60 min of perfusion of livers from rats fed PO corresponded to that shown for the PHMO group
after 15 min. The PL demonstrated a discrimination against 22∶1 compared to TG, and, when available, 18∶1 was highly preferred
for PL-synthesis.
The total fatty acid distribution in the TG, as determined by gas liquid chromatography (GLC), reflected the composition of
the dietary fats. In the total liver PL, 22∶1 and 20∶1 were present in negligible amounts, although the PHMO diet contained
12–13% of both 22∶1 and 20∶1. In the free fatty acid fraction (FFA), the major part of the radioactivity (≈80%) was [14-14C]erucic acid, and only small amounts of [14C]18∶1(<2%) were presents, even after 60 min of perfusion. The shortened-chain 18∶1 was readily removed from the FFA pool
and preferentially used for lipid esterification. 相似文献
19.
Studies are reported on the capacity of isolated rat renal papilla (inner medulla) to synthesize and release prostaglandin
(PG) E from endogenous and exogenous precursor(s) during development of an essential fatty acid (EFA) deficiency in the rat.
Weanling (21-day-old) male Sprague-Dawley rats were fed a fat-free diet supplemented with either 5% hydrogenated coconut oil
(HCO) or 5% safflower oil (SO). At approximately 3, 6 and 7 weeks (6, 9 and 10 weeks of age), groups of animals fed each diet
were killed for studies of PGE synthesis in the renal papillae. Differences in the fatty acid composition of the papillae
lipids of the animals of each group were also determined. The in vitro production of PGE from endogenous precursor(s) was
significantly reduced in the papillae from the 6-week-old rats fed the HCO diet compared to the control (SO) rats, and appeared
to be near maximally depressed in the 10-week-old animals compared to that of animals fed an EFA deficient diet for over a
year in an accessory experiment. Analyses of the fatty acids of the papillae lipids of the HCO groups showed that the levels
of 18∶2 and 20∶4 were markedly reduced, and those of 16∶1, 18∶1 and 20∶3 were elevated compared to the controls even in the
6-week-old animals, typical of an EFA deficiency. The papillae lipids of the animals fed the HCO diet were also depleted of
their stores of 22∶4ω6. A fatty acid believed to be derived by chain elongation of 20∶3ω9, 22∶3, was found in large concentrations
in the papillae triglycerides of the EFA deficient rats. Incubations of exogenous arachidonic acid (20∶4) in homogenates and
tissue slices of the papillae of the HCO dietary groups showed that the PG synthetase was not impaired by an EFA deficiency.
The rate of PGE synthesis in the papillae of the EFA deficient animals was generally enhanced when exogenous 20∶4 was added,
indicating that the concentration of available precursor(s) is a primary factor in the control of PGE synthesis in the papilla
of the rat. 相似文献
20.
The essential fatty acid requirement for the development of intestinal carcinogenesis was determined and compared to the overall
essential fatty acid status of the animals as measured by the triene/tetraene ratio in the plasma, liver and colon. To induce
tumors, male Sprague-Dawley rats were given two weekly injections (20 mg/kg body wt) of azoxymethane. Two weeks after the
last injection, the rats were divided into groups of 25 and given one of six diets containing various levels of essential
fatty acids (as linoleate). The diets contained 5% total fat and were prepared by mixing safflower oil (high essential fatty
acids, beef fat (low essential fatty acids), and medium chain triglyceride oil (no essential fatty acids). One group of rats
was fed a 20% beef fat diet. The range of essential fatty acids was from <0.03% to 1.28% (w/w). Twenty-six weeks after the
first azoxymethane injection, the animals were killed and intestinal tumor incidence and multiplicty were determined. Samples
of plasma, liver and colon were also taken for measurement of the triene/tetraene ratio by gas chromatography.
Large bowel tumor incidence showed a dependence on the essential fatty acid content of the diet. The results were as follows:
(percent essential fatty acids: percent tumor incidence) Group A (1.28∶ 72.4), Group B (0.60∶ 73.3), Group C (0.11∶ 55.2),
Group D (0.08∶ 39.3), Group E (<0.03∶ 37.9) and Group F, which was fed 20% beef fat, (0.34∶ 88.5). These data suggest the
essential fatty acid requirement for colon tumorigenesis is much lower than values previously reported for tumorigenesis in
the breast and pancreas. The plasma and liver triene/tetraene ratios showed clear-cut essential fatty acid deficiency (ratio
>0.4) in Groups D and E, although no clinical symptoms were evident. In all dietary groups, the triene/tetraene ratio in the
colon was lower than 0.3. In addition in the colon, the percentage of fatty acids present as 20 carbon polyunsaturated fatty
acids was lower than in the plasma and liver. These data suggest the colon possesses low levels of the fatty acid desaturase
and elongase needed for conversion of linoleate to 20 carbon fatty acids, and therefore, that the colonic requirement for
essential fatty acids may be low. Furthermore, in the absence of other clinical symptoms, the reduced tumorigenesis observed
in the groups fed low essential fatty acids suggests the essential fatty acid requirement of tumor tissue may be higher than
that of normal colon mucosa. 相似文献