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1.
Diets rich in polyunsaturated fatty acids (PUFA) are well known to suppress hepatic lipogenic enzymes compared to fat-free
diets or diets rich in saturated fatty acids. However, the mechanism underlying suppression of lipogenic enzymes is not quite
clear. The present study was undertaken to investigate whether lipid peroxidation products are involved in suppression of
lipogenic enzymes. Therefore, an experiment with growing male rats assigned to six groups over a period of 40 d was carried
out. Rats received semisynthetic diets containing 9.5% coconut oil and 0.5% fresh soybean oil (coconut oil diet, peroxide
value 5.1 meq O2/kg oil), 10% fresh soybean oil (fresh soybean oil diet, peroxide value 0.5 meq O2/kg oil), or 10% thermally treated soybean oil (oxidized soybean oil diet, peroxide value 74 meq O2/kg oil). To modify the antioxidant state of the rats, we varied the vitamin E supply (11 and 511 mg α-tocopherol equivalents
per kg of diet) according to a bi-factorial design. Food intake and body weight gain were not influenced by dietary fat and
vitamin E supply. Activities of hepatic lipogenic enzymes were markedly influenced by the dietary fat. Feeding either fresh
or oxidized soybean oil diets markedly reduced activities of fatty acid synthase, (FAS), acetyl CoA-carboxylase, (AcCX), glucose-6-phosphate
dehydrogenase, (G6PDH), 6-phosphogluconate dehydrogenase, and ATP citrate lyase (ACL) relative to feeding the coconut oil
diet. Moreover, feeding oxidized soybean oil slightly, but significantly, lowered activities of FAS, AcCX, and ACL compared
to feeding fresh soybean oil. Activities of hepatic lipogenic enzymes were reflected by concentrations of triglycerides in
liver and plasma. Rats fed the coconut oil diet had markedly higher triglyceride concentrations in liver and plasma than rats
consuming fresh or oxidized soybean oil diets, and rats fed oxidized soybean oil had lower concentrations than rats fed fresh
soybean oil. The vitamin E supply of the rats markedly influenced concentrations of thiobarbituric acid-reactive substances
in liver, but it did not influence activities of hepatic lipogenic enzymes. Because the vitamin E supply had no effect, and
ingestion of an oxidized oil had only a minor effect, on activities of hepatic lipogenic enzymes, it is strongly suggested
that neither exogenous nor endogenous lipid peroxidation products play a significant role in the suppression of hepatic lipogenic
enzymes by diets rich in PUFA. Therefore, we assumed that dietary PUFA themselves are involved in regulatio of hepatic lipogenic
enzymes. Nevertheless, the study shows that ingestion of oxidized oils, regardless of the vitamin E supply, also affects hepatic
lipogenesis, and hence influences triglyceride levels in liver and plasma. 相似文献
2.
In previous studies, zinc-deficient rats force-fed a diet with coconut oil as the major dietary fat developed a fatty liver,
whereas zinc-deficient rats force-fed a diet with linseed oil did not. The present study was conducted to elucidate the reason
for this phenomenon. In a bifactorial experiment, rats were fed zinc-adequate or zinc-deficient diets containing either a
mixture of coconut oil (70 g/kg) and safflower oil (10 g/kg) (“coconut oil diet”) or linseed oil (80 g/kg) (“linseed oil diet”)
as a source of dietary fat, and activities of lipogenic and glycolytic enzymes in liver were determined. In order to ensure
adequate food intake, all the rats were force-fed. Zinc-deficient rats on the coconut oil diet developed a fatty liver, characterized
by elevated levels of triglycerides with saturated and monounsaturated fatty acids. These rats also had markedly elevated
activities of the lipogenic enzymes acetyl-CoA carboxylase, fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH),
6-phosphogluconate dehydrogenase (6PGDH), and citrate cleavage enzyme, whereas activities of malic enzyme and glycolytic enzymes
were not different compared with zinc-adequate rats on the coconut oil diet. In contrast, rats receiving the linseed oil diet
had similar triglyceride concentrations regardless of zinc status, and activities of lipogenic enzymes and glycolytic enzymes
were not different between the two groups. Zinc-deficient rats fed either type of dietary fat exhibited statistically significant
correlations between activities of FAS, G6PDH, 6PGDH and concentrations of saturated and monounsaturated fatty acids in liver.
The concentrations of serum lipids were elevated in zinc-deficient rats fed either type of dietary fat. These results demonstrate
that fatty liver in zinc-deficient rats on the coconut oil diet is caused by elevated activities of lipogenic enzymes, and
not by disturbed lipid secretion from liver. Dietary linseed oil prevents both the elevation of lipogenic enzyme activity
and fatty liver in zinc-deficient rats. 相似文献
3.
Effects of dietary vitamin E,selenium, and polyunsaturated fats on in vivo lipid peroxidation in the rat as measured by pentane production 总被引:1,自引:0,他引:1
Starting at 21 days of age, groups of six rats each were fed a basal Torula yeast diet supplemented with 0,4% L-methionine
and varying amounts of vitamin E as dl-alpha tocopherol acetate, selenium as sodium selenite, and with either 10% stripped
corn oil, stripped lard, or coconut oil. By 7 wk, pentane production by rats fed a corn oil diet deficient in both vitamin
E and selenium was twice that by rats fed 0.1 or 1 mg of selenium per kg of the same basal diet. Blood glutathione peroxidase
activity after 7 wk was proportional to the logarithm of dietary selenium. Groups of rats fed the vitamin E- and selenium-deficient
diets with lard or coconut oil had one-half the pentane production of rats fed the vitamin E- and selenium-deficient corn
oil diets. The plasma level of linoleic plus arachidonic acid was 1.8 times greater on a wt % basis in rats fed corn oil than
in rats fed lard or coconut oil as the fat source. Pentane production by rats fed 40 i.u. dl-alpha tocopherol acetate per
kg of the selenium-deficient corn oil diet was one-sixth of that by rats fed the same diet without vitamin E; the plasma of
the rats fed the vitamin E-supplemented corn oil diet had a level of vitamin E that was about six times greater than that
of the rats fed the vitamin E-deficient corn oil diet. 相似文献
4.
Dietary fats and energy levels differently affect tissue lipogenic enzyme activity in finishing pigs
Giuseppe Bee Ruth Messikommer Stefan Gebert 《European Journal of Lipid Science and Technology》1999,101(9):336-342
The aim of the present study was to determine the relationship between high and low digestible energy levels (9.5 vs. 15.4 MJ ME/kg) and either tallow or soy oil supplementation (5%rpar; on lipogenic activities and fatty acid profile of the backfat tissue outer layer and liver tissue in finishing pigs. Twenty Large White pigs averaging 30 (initial) to 106 kg (final) live weight were allocated into four dietary groups and fed the diets ad libitum. The lipid content and fatty acid composition of the tissues were determined and glucose-6-phosphate dehydrogenase (G6PDH), malic enzyme (ME), and fatty acid synthase (FAS) activity were measured. Growth performance and carcass measurements were affected by the dietary energy levels but not by the fat sources. Lipid deposition rate of animals fed the low energy diets was lowered regardless whether tallow or soy oil was supplemented. Unlike lipid deposition, fatty acid profile was influenced by both dietary factors. Pigs fed the low energy diet supplemented with soy oil exhibited the lowest level of saturated (P<0.001), monounsaturated (P<0.001), and the highest level of polyenic fatty acids in the backfat, the opposite was the case for the pigs fed the high energy diet supplemented with beef tallow. The fatty acid profile of the adipose tissue of animals fed the other two diets were intermediate, but clear distinction of the profile due to diets was visible. Independent of dietary treatments, lipogenic activities were up to 10 times higher in the backfat than in the liver. G6PDH activity was higher (P<0.05) due to high energy diet, whereas the activities of ME and FAS were not affected. Animals fed the high energy diet either supplemented with tallow or soy oil exhibited higher ME activity lpar;P<0.05) in the backfat, without any effects on G6PDH activity. In contrast, dietary fat sources affected the FAS activity, with lower activity lpar;P<0.05) exhibited in the backfat of animals fed the soy oil diets. The present results indicate that dietary manipulation, which change the flux through the pathway of lipogenesis and pentose-phosphate must affect differently the activities of the involved enzymes. The effect of the dietary energy level was stronger and overwhelmed the inducing effect of the PUFA on the activities of the collateral enzymes. In contrast the immediately involved lipogenic enzyme FAS responded more to dietary PUFA stimulation than to the energy supply. 相似文献
5.
The objective of this study was to evaluate the effects of dietary heated fats from a commercial deep-fat frying operation
on rat liver enzyme activity. The fats, partially hydrogenated soybean oil (PHSBO) used for four days and for 7 days (7-DH)
for frying foodstuffs in a commercial restaurant, were fed to rats in either free access to food or by pair-feeding graded
doses. All diets were isocaloric and contained 15 g/100 g of diet. Experiments were conducted with control rats fed nonheated
(NH) PHSBO diet. Animals fed 7-DH diet in each set of experiments had larger amounts of cytochromes P450 and b5 and greater activity of NADPH-cytochrome P450 reductase when compared to controls. The activities of carnitine palmitoyltransferase-I and isocitrate dehydrogenase were
significantly lower in rats fed test diets in comparison to controls. A significantly depressed activity of glucose 6-phosphate
dehydrogenase was also noticed for these animals when compared to those fed NH. In addition, liver and microsomal protein
concentrations were significantly greater in rats fed the used oils in comparison to controls, and liver glycogen was significantly
lower. 相似文献
6.
Male Wistar rats were fed for 4 wk on diets containing 2% oxidized corn oil. Liver tissue was then studied to determine the
effect of feeding peroxidized oil on lipogenic enzymes. Although substances which reacted with thiobarbituric acid increased
in liver microsomes and mitochondria with increasing peroxide values of the dietary corn oil fed, the activities of glucose-6-phosphate
dehydrogenase, malic enzyme and acetyl-CoA carboxylase in liver were unchanged. However, when rats were fed for 2 wk on diets
containing 10% fat, of which 0.5, 5 or 10% was unoxidized corn oil and the remainder was hydrogenated beef tallow filler,
the lipogenic enzyme activities and also the liver triglyceride levels were observed to decrease with increasing amounts of
dietary corn oil. Therefore, although a synthetic diet containing corn oil was easy to oxidize spontaneously, the reductions
of lipogenic enzymes in rats fed the diet would not have been caused by lipid peroxides but by unsaturated fatty acids themselves. 相似文献
7.
Minocher C. Reporter Robert S. Harris 《Journal of the American Oil Chemists' Society》1961,38(1):47-51
Three lots of cold-pressed soybean oil were treated with bubbling oxygen for 70, 80, and 180 hrs. at 70°C. and fed to rats
at a level of 18% in diets which were nutritionally adequate but devoid of vitamin A. Untreated soybean oil was fed in similar
control diets. Subgroups of 15 weanling rats each were given graded injections of vitamin A acetate intramuscularly each week.
Diarrhea developed in the rats fed the diets containing oxidized oil. This condition soon subsided in the groups receiving
vitamin A injections but not in the vitamin A-free group. Diarrhea was not noted in the rats receiving the untreated soybean
oil, without respect to the amount of vitamin A they received.
The rats on the vitamin A-free diets developed deficiency more rapidly when the diet contained oxidized rather than the untreated
oil. The food efficiencies of the groups fed the oxidized oils were lower than the controls. The intestines of the groups
receiving the oxidized oils were distended with fluid and were hemorrhagic. Enlarged kidneys were noted in the vitamin A-deficient
control as well as in test rats.
The retroperitoneal lipids of the groups on the oxidized oil were less unsaturated, had lower refractive indices, higher peroxide
values, and higher carbonyl values than comparable groups fed the control oil.
Vitamin A deficiency decreased the unsaturation of the kidney and liver lipids but increased that of the retroperitoneal lipids.
Injections of increasing amounts of vitamin A produced increases in the unsaturation of the body lipids.
The kidney lipids of the groups on the oxidized oil diets were less unsaturated and contained more peroxidic compounds than
the controls. Vitamin A deficiency increased the peroxidic compounds in the kidney and liver lipids, even in rats fed the
control oil. The liver lipids of the groups fed oxidized oil were less unsaturated, lower in vitamin A content, and higher
in peroxide compounds than the controls.
The vitamin A content of the whole blood varied in relation to the amounts injected. The content of tocopherol in the tissues
were not affected significantly by the oxidized oil in the diet.
The evidence indicates that severely oxidized oil may destroy vitamin A in the tissue of the rat, thereby hastening the development
of deficiency on vitamin A-free diets, reducing the storage of injected vitamin A, and increasing the vitamin A requirement.
These effects are with abused oil and should not be interpreted to mean that the mildly oxidized oils and fats, such as those
in the diets of human beings in this country are toxic.
1 Read in part at the 36th Fall meeting. American Oil Chemists' society, Chicago, October 20–22, 1958.
2 Assisted by a grant from the Roche Anniversary, Fund, Hoffmann LaRoche Inc.
3 Contribution No. 414 from the Department of Nutrition. Food Science and Technology, Massachusetts Institute of Technology,
Cambridge, Mass. 相似文献
8.
This study was conducted to investigate the effects of dietary cyclic fatty acid monomers (CFAM), contained in heated fat
from a commercial deep-fat frying operation, on rat liver enzyme activity. A partially hydrogenated soybean oil (PHSBO) used
7 d (7-DH) for frying foodstuffs, or 0.15% methylated CFAM diets was fed to male weanling rats in comparison to a control
group fed a nonheated PHSBO (NH) diet in a 10-wk experiment. All diets were isocaloric with 15% fat. Animals fed either CFAM
or 7-DH diets showed increased hepatic content of cytochrome (cyt.) b5 and P450 and increased activity of (E.C. 1.6.2.4) NADPH-cyt. P450 reductase in comparison to the control rats. In addition, the activities of (E.C. 2.3.1.21) carnitine palmitoyltransferase-l
and (E.C. 1.1.1.42) isocitrate dehydrogenase were significantly decreased when compared to that of rats fed the NH diet. A
significantly depressed activity of (E.C. 1.1.1.49) glucose 6-phosphate dehydrogenase was also observed for these animals
compared to the control rats fed NH diet. Moreover, liver and microsomal proteins were significantly increased when CFAM or
7-DH diets were fed to animals in comparison to controls while liver glycogen was decreased significantly in experimental
groups of rats. The results obtained in this study indicate that the CFAM in the diet from either synthetic sources or used
fats increase the activity of liver enzyme systems that detoxify them. 相似文献
9.
Fresh and oxidized cotton seed oil (CO) olive oil (OO), chicken fat (CF) and beef fat (BF) were fed to male weanling rats
for 33 to 108 weeks. Groups fed oxidized fats except OO showed a higher death rate than those fed the corresponding fresh
fats. Groups fed oxidized CO and BF had the highest death rate. Histological studies of animals dying from natural causes
showed more pronounced cardiac lesions in the animals fed oxidized CO. Serum, liver and brain cholesterol levels were not
influenced by oxidized fats. Fatty acid composition of depot fats and of heart and liver lipids did not show significant differences
between groups fed fresh and the corresponding oxidized fats.
Presented at the Spring Meeting of the AOCS 1964. 相似文献
10.
Malondialdehyde (MDA) production and cytosolic aldehyde dehydrogenase (ALDH) response were examined in rat liver tissues after
feeding different levels of dietary vitamin E and/or selenium and polyunsaturated fat for 12–38 wk. MDA production was significantly
increased by vitamin E deficiency or by high levels of polyunsaturated fat intake, but not by selenium deficiency. The activity
of cytosolic ALDH increased upon increased production of MDA after 12–16 wk of feeding the lipid peroxidation-inducing diets.
However, ALDH activity was suppressed after 38 wk of feeding the vitamin E-deficient diet. The results indicate that the hepatic
cytosolic ALDH may be involved in the metabolism of MDA during a relatively short-term increase inin vivo lipid peroxidation, but that ALDH activity becomes suppressed after more severein vivo lipid peroxidation has been produced. Hepatic and plasma α-tocopherol levels and lipid peroxidation products were measured
for the various dietary groups. 相似文献
11.
Klaus Eder Manfred Kirchgessner 《European Journal of Lipid Science and Technology》1999,101(5):178-184
Several studies demonstrated that dietary oxidized oils markedly affect the vitamin E status and alter the fatty acid composition of tissue lipids in animals. It must however be emphasized that highly oxidized oils reduce the feed intake of animals, which makes it difficult to interpret the results. Therefore, the present study used a moderately thermoxidized soybean oil (peroxide value: 75 mEq O2/kg), having a similar fatty acid composition as fresh soybean oil (peroxide value: 9.5 mEq O2/kg) which was used as control. Moreover, according to a bifactorial design, two different vitamin E supplementary levels (11 vs. 511 mg α-to-copherol equivalents per kg diet) were used. The experiment was conducted with male Sprague-Dawley rats. The feeding period lasted for 40 days. In order to assess the vitamin E status, the vitamin E concentrations in plasma, liver, heart, kidney, and adipose tissue were determined. The vitamin E supply had a pronounced effect on the vitamin E concentrations of those tissues whereas the type of fat had only a slight effect. The fatty acid composition of total lipids from liver, erythrocytes, and low-density lipoproteins was also only slightly influenced by the oxidized fat. The osmotic fragility of erythrocytes was even reduced by feeding the oxidized oil. With a low vitamin E supply, the in vitro susceptibility of low-density lipoproteins to lipid peroxidation was slightly increased by feeding the oxidized oil. In contrast, with a high vitamin E supply, there was no adverse effect of the dietary oxidized oil on the susceptibility of low-density lipoproteins to lipid peroxidation. Feeding the oxidized oil, however, increased the concentrations of malondialdehyde in low-density lipoproteins suggesting an increased in vivo lipid peroxidation. Therefore, it cannot be ruled out that moderately oxidized dietary fats increase the atherogenicity of low-density lipoproteins. In contrast, a moderately oxidized oil scarcely affected the vitamin E status and the fatty acid composition of tissue lipids. 相似文献
12.
Studies are reported on the relative effects of in vivo oxidation produced by diets devoid of vitamin E and the consumption
of oxidized fat. Rats of the Sprague-Dawley strain were raised from weaning on a sucrose-casein diet containing minerals and
vitamins in the required amounts, supplemented with 10% of safflower oil, menhaden oil, hydrogenated coconut oil or no fat.
Animals of ca. 185 g of the group fed the 10% safflower oil were then switched for 4 weeks to safflower or menhaden oil-supplemented
diets that were allowed to oxidize by exposing them to room temperature in the dark for 2–8 days. For comparison with effects
of in vivo oxidation, animals were raised from weaning on similar fresh diets devoid of vitamin E. Consumption of oxidized
fat was accompanied by loss of weight, effects on the size of the organs, changes in triglyceride levels and production of
TBA-reacting substances in the tissues. There was no effect on the induced swelling of liver mitochondria or the susceptibility
of erythrocytes to hemolysis in these animals. Growth was also suppressed in the animals fed the vitamin E-free diets, and
in vivo oxidation in these animals produced marked effects on the membrane properties of erythrocytes and liver mitochondria. 相似文献
13.
Corn oil and olive oil were thermally oxidized, and the free fatty acids from the fresh fats, and from the distillable non-urea-adductable
(DNUA) fractions of the thermally oxidized fats were prepared. These were added as emulsions to the medium of primary cultures
of heart endothelial and muscle cells from neonatal rats. After exposure for 24 hr, the fatty acid composition of the triacylglycerol
(TC) and phospholipid (PL) fractions of the cells was determined. Reflecting the nature of the fat used, the corn oil treatment
produced relatively higher concentrations of linoleic acid in the TG and PL fractions compared to the olive oil treatment,
in which case the oleic acid level was influenced. Treatment of the cultured cells with components derived from oxidized corn
oil or oxidized olive oil resulted in lower concentrations of linoleic and arachidonic acids in the PL moieties compared to
the fresh fat controls. However, there were marked increases in arachidonic acid in the TG fractions of both the endothelial
and muscle cells. These changes due to the DNUA from thermally oxidized fats indicate a distinct metabolic response to the
derivatives formed during thermal oxidation of the fats. 相似文献
14.
The effects of vitamin E and selenium intake on oxidative stress and plasma lipids in hamsters fed fish oil 总被引:5,自引:0,他引:5
The aim of the present work was to test the effects of large-dose supplementation of vitamin E (Vit E) and selenium (Se),
either singly or in combination, on fish oil (FO)-induced tissue lipid peroxidation and hyperlipidemia. The supplementation
of Se has been shown to lower blood cholesterol and increase tissue concentrations of the antioxidant glutathione (GSH); however,
the effects of Se supplementation, either alone or in combination with supplemental Vit E, on FO-induced oxidative stress
and hyperlipidemia have not been studied. Male Syrian hamsters received FO-based diets that contained 14.3 wt% fat and 0.46
wt% cholesterol supplemented with Vit E (129 IU d-α-tocopheryl acetate/kg diet) and/or Se (3.4 ppm as sodium selenate) or that contained basal requirements of both nutrients.
The cardiac tissue of hamsters fed supplemental Se showed increased concentrations of lipid hydroperoxides (LPO) but decreased
oxidized glutathione (GSSG) concentrations. The higher concentrations of LPO in the hearts of Se-supplemented hamsters were
not lowered with concurrent Vit E supplementation. In the liver, Se supplementation was associated with higher Se-dependent
glutathione peroxidase activity and an increase in the GSH/GSSG ratio, whereas a lower hepatic non-Se-dependent glutathione
peroxidase activity was seen with Vit E supplementation. Supplemental intake of Se was associated with lower plasma concentrations
of total cholesterol and low density lipoprotein cholesterol plus very low density lipoprotein cholesterol. In view of the
pro-oxidative effects of Se supplementation on cardiac tissue, a cautionary approach needs to be taken regarding the plasma
lipid-lowering properties of supplemental Se. 相似文献
15.
Rat plasma high density lipoproteins (HDL) are comprised of two major particle size subpopulations, HDL1 (255 Å?140 Å) and HDL2 (140 Å?84 Å), in which the proportion of arachidonate in fatty acids of cholesteryl esters is greater than 50%. To determine whether decreased availability of arachidonate for cholesterol esterification would alter the distribution and/or amounts of the HDL subpopulations, we compared HDL subpopulations in EFA-deficient and control rats. To separate the effects of EFA deficiency and fat deficiency and to evaluate effects of different saturated fats, we used EFA-deficient diets that were fat-free or that contained 5% saturated fat. The control diets were the EFA-deficient diets plus 1% safflower oil. The saturated fats were hydrogenated coconut oil, hydrogenated cottonseed oil and saturated medium-chain triglycerides. All EFA-deficient diets decreased the proportion of the HDL1 subpopulation and the peak diameter of the HDL2 subpopulation. These changes appeared after quite brief EFA depletion in young rats and may be related to the increased liver cholesteryl ester concentrations typical of EFA-deficient rats. 相似文献
16.
A semisynthetic diet containing 15% by weight of dietary fat was fed to six groups of male Wistar rats for 28 days. Two groups
received the distilable fraction of fresh corn oil (DCO) or fresh olive oil (DOO), two groups the distillable fraction of
the thermally oxidized fats (OCO,OOO), and two groups received the respective fresh fats as controls (FCO, FOO). Substantial
changes in the fatty acid composition occurred in the fats upon thermal oxidation. Only the rats that received OOO showed
overt symptoms of heated fat toxicity. This was reflected in the histological scores of these animals, with the liver sustaining
the most numerous and severe lesions. Tissue fatty acid changes of any significance were confined largely to the polar liver
lipids of the rats that were fed OCO or OOO. The results of this study would suggest that the relatively greater toxicity
of OOO, compared to OCO, may in part be due to the high oleic:linoleic acid ratio of the fresh olive oil and in part to a
higher tocopherol content of the corn oil. 相似文献
17.
In an effort to reduce the deleterious nutritional effects of oxidation products generated in heated fats, a partially hydrogenated
soybean oil (PHSBO) used 7 d (7-DH) for frying foodstuffs was obtained from a commercial deep-fat frying operation. The used
fat was treated with magnesium silicate (T-7DH). Isocaloric diets containing 15% of either 7-DH or T-7-DH fats were prepared
and fed to male weanling rats for 10 wk in a pair-feeding experiment and compared to control rats fed nonheated PHSBO (NH).
Animals fed the 7-DH diet showed higher liver enzyme cytochrome b5 and P450 activity than the T-7DH diet compared to the NH group, suggesting a positive effect of the treatment. These results suggested
the presence of lower amounts of harmful compounds in the diet containing the heated used oil which had been treated with
the active adsorbent. 相似文献
18.
The impact of a moderate Zn deficiency on growth and plasma and liver lipids was investigated in two 4-week experiments with
male weanling rats fed fat-enriched diets. Semisynthetic, approximately isocaloric diets containing 3% soybean oil were supplemented
with either 7 or 100 mg Zn/kg diet and with 22% beef tallow (BT) or sunflower oil (SF). In Experiment 1, which compared the
dietary fat level and the fat source in a factorial design of treatments, all diets were fed ad libitum to 6 × 8 animals,
whereas intake of the high-Zn BT and SF diets was restricted in Experiment 2 (5 × 6 rats) to the level of intake of the respective
low-Zn diets. The low-Zn SF diet consistently depressed food intake and final live weights of the animals to a greater extent
than the other low-Zn diets, while intake and growth were comparable among the animals fed the high-Zn diets. The marginal
Zn deficit per se did not alter plasma triglyceride and cholesterol concentrations nor hepatic concentrations of triglyceride,
cholesterol and phospholipids. The fatty acid pattern of liver phospholipids did not indicate that chain elongation and desaturation
of fatty acids was impaired by a lack of zinc. It was concluded that dietary energy and fat intake, and fat source have a
greater effect on plasma and liver lipids than a moderate Zn deficiency. Marginally Zn-deficient diets enriched with sunflower
oil as a major energy source cause a greater growth retardation than diets rich in carbohydrates or beef tallow. 相似文献
19.
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
20.
J. C. Alexander 《Journal of the American Oil Chemists' Society》1978,55(10):711-717
In deep-fat frying the fat is used over and over again, and moisture and air are mixed into the hot oil. Substantial quantities
of the heated fat are absorbed into the fried foods. Many reports from experimental observations with animals fed these fats
have shown biological effects ranging from a slight depression in growth, all the way to very poor growth, diminished feed
efficiency, increased liver size, fatty necrosis of the liver, and various other organ lesions. Obviously, certain fat constituents
may be changed by frying conditions, and the adverse biological effects are relative. We are at the stage in studying these
heated fats where selected techniques including biochemical parameters, histopathological evaluations, and tissue culture
in monolayers can be good indicators of some of the specific effects on biological tissues. Isolated fractions from heated
fat samples, which contained concentrations of cyclic monomer and dimer derivatives, were used in animal studies. Incorporation
of the above materials into rat diets produced distended flatulent stomachs and intestines, gastric ulcers, and multiple focal
hemorrhages. Histological evaluation of heart, liver, and kidney tissue sections indicated extensive cellular damage. Livers
and kidneys exhibited the most severe lesions. Neonatal heart cells established as monolayers on glass cover slips were exposed
to fractions from heated or fresh fats. Cellular damage including pyknosis, vacuolization of the cytoplasm, and mitotic aberrations
were observed. Uptake of14C-labeled fatty acid by the triglyceride fraction of the cells was increased with heated fats. 相似文献