The effect of dietary vitamin E supply and a moderately oxidized oil on activities of hepatic lipogenic enzymes in rats

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.     

Effect of oxidized oil on lipogenic enzymes

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.     

Long-term feeding of dietary oils alters lipid metabolism, lipid peroxidation, and antioxidant enzyme activities in a teleost (Anabas testudineus bloch)

Anabas testudineus (climbing perch), average body weight 21±1 g, were maintained in culture tanks and fed a 35% protein feed plus an additional supplementation of three dietary oils (20% each of coconut oil, palm oil, or cod liver oil). Body weight gain was similar among all groups. However, several hepatic lipogenic enzymes such as malic enzyme (ME), NADP-isocitrate dehydrogenase (ICDH), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH) and β-hydroxy-β-methyl glutaryl CoA reductase (HMG CoA reductase) were assayed, and they responded differently. Hepatic ME and G6PDH activities showed a significant decrease in the coconut oil and palm oil groups, but there was no significant change in ICDH activity. The 6PGDH activities were reduced, whereas HMG CoA reductase activity was increased in the palm oil-treated group. Cholesterol synthesis in the liver and muscle increased in the palm oil-treated group, but liver phospholipids did not show any significant change in fish supplemented with oils rich in saturated fatty acids. Triacyl-glycerol and free fatty acid concentrations were high in the coconut oil- and palm oil-supplemented groups. Lipid peroxidation products such as thiobarbituric acid-reactive substances and conjugated dienes decreased in the same two groups. Antioxidant potential was high in all groups as evidenced by increased activity of superoxide dismutase, glutathione peroxidase, and glutathione content. The results of this study indicate that in fish, dietary lipids depress hepatic lipogenic activity as well as lipid peroxidation products by maintaining high levels of antioxidant enzymes.     

Levels of polyunsaturated fatty acids in tissues from zinc-deficient rats fed a linseed oil diet

The effect of zinc deficiency on the levels of n−6 and n−3 polyunsaturated fatty acids (PUFA) in lipids from tissues of rats fed a diet containing linseed oil was investigated. Rats were fed either a control diet (25 mg Zn/kg) or a zinc-deficient diet (0.8 mg Zn/kg) for 10 d. To avoid energy and nutrient deficiency, 11.6 g of diet per day was administered by gastric tube. At the end of the experiment, rats fed the zinc-deficient diet had drastically reduced plasma zinc concentration and alkaline phosphatase activity consistent with severe zinc deficiency in these rats. Zinc-deficient rats had higher levels of n−3 PUFA, in particular eicosapentaenoic acid (EPA), and lower levels of n−6 PUFA, in particular linoleic acid, in liver and plasma phosphatidylcholine (PC) and in erythrocyte membrane total lipids than did control rats. By contrast, the levels of n−3 PUFA in PC from testes and heart, and in phosphatidylethanolamine (PE) from liver, testes and heart, were only slightly different between zinc-deficient and control rats. The study suggests that desaturation of α-linolenic acid is not inhibited by zinc deficiency, and that in zinc-deficient rats, n−3 PUFA preferentially incorporated into phospholipids at the expense of n−6 PUFA, especially EPA into PC. The study also shows that the effect of zinc deficiency on PUFA levels is different for PC and PE in rat tissues.     

Differential effects of dietary linoleic and α-linolenic acid on lipid metabolism in rat tissues

Comparative effects of feeding dietary linoleic (safflower oil) and α-linolenic (linseed oil) acids on the cholesterol content and fatty acid composition of plasma, liver, heart and epididymal fat pads of rats were examined. Animals fed hydrogenated beef tallow were used as isocaloric controls. Plasma cholesterol concentration was lower and the cholesterol level in liver increased in animals fed the safflower oil diet. Feeding the linseed oil diet was more effective in lowering plasma cholesterol content and did not result in cholesterol accumulation in the liver. The cholesterol concentration in heart and the epididymal fat pad was not affected by the type of dietary fatty acid fed. Arachidonic acid content of plasma lipids was significantly elevated in animals fed the safflower oil diet and remained unchanged by feeding the linseed oil diet, when compared with the isocaloric control animals fed hydrogenated beef tallow. Arachidonic acid content of liver and heart lipids was lower in animals fed diets containing safflower oil or linseed oil. Replacement of 50% of the safflower oil in the diet with linseed oil increased α-linolenic, docosapentaenoic and docosahexaenoic acids in plasma, liver, heart and epididymal fat pad lipids. These results suggest that dietary 18∶2ω6 shifts cholesterol from plasma to liver pools followed by redistribution of 20∶4ω6 from tissue to plasma pools. This redistribution pattern was not apparent when 18∶3ω3 was included in the diet.     

Fish oil prevents change in arachidonic acid and cholesterol content in rat caused by dietary cholesterol

Rats were fed diets high in either saturated fat (beef tallow) or α-linolenic acid (linseed oil) or eicosapentaenoic and docosahexaenoic acids (fish oil) with or without 2% cholesterol supplementation. Consumption of linseed oil and fish oil diets for 28 days lowered arachidonic acid content of plasma, liver and heart phospholipids. Addition of 2% cholesterol to diets containing beef tallow or linseed oil lowered 20∶4ω6 levels but failed to reduce 20∶4ω6 levels when fed in combination with fish oil. Feeding ω3 fatty acids lowered plasma cholesterol levels. Addition of 2% cholesterol to the beef tallow or linseed oil diet increased plasma cholesterol concentrations but not when fish oil was fed. Feeding the fish oil diet reduced the cholesterol content of liver, whereas feeding the linseed oil diet did not. Dietary cholesterol supplementation elevated the cholesterol concentration in liver in the order: linseed oil > beef tallow > fish oil (8.6-, 5.5-, 2.6-fold, respectively). Feeding fish oil and cholesterol apparently reduced 20∶4ω6 levels in plasma and tissue lipids. Fish oil accentuates the 20∶4ω6 lowering effect of dietary cholesterol and appears to prevent accumulation of cholesterol in plasma and tissue lipids under a high dietary load of cholesterol.     

Dietary saturated fat level alters the competition between α-linolenic and linoleic acid

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.     

Influence of dietary fats on butyrylcholinesterase and esterase-1 (ES-1) activity in plasma of rats

We studied the effects of dietary fats, especially fish oil, on the activities of esterase-1 (ES-1) and butyrylcholine-sterase in the plasma of rats. The identification of nutritional determinants of these enzymes could provide clues as to their physiological function. Fish oil, when compared with corn oil, consistently caused increased activities of both enzymes. Plasma ES-1 activity, but not butyrylcholinesterase activity, was increased after isocaloric replacement of carbohydrates by coconut fat. Dietary medium-chain triglycerides, when compared with corn oil, produced decreased and increased activities of butyrylcholinesterase and ES-1, respectively. Various plant fats, such as corn oil, linseed oil, coconut fat, palm oil, palm kernel oil, soybean oil and rapeseed oil, did not differentially influence butyrylcholinesterase activities. Plasma triglyceride concentrations were lowered by fish oil and increased by coconut fat and palm kernel oil. For individual rats in 5 out of 6 experiments, weak, negative correlation coefficients of the order of 0.3 were found between the changes in plasma butyrylcholinesterase activities and in plasma triglyceride concentrations.     

Effects of dietary thermoxidized fats on expression and activities of hepatic lipogenic enzymes in rats

This study was undertaken to investigate the effect of dietary oxidized fats on the relative mRNA concentrations and the activities of fatty acid synthase (FAS) and glucose-6-phosphate dehydrogenase (G6PDH) in the liver of rats treated with vitamin E or selenium. Two experiments with male Sprague-Dawley rats were carried out. The first experiment included eight groups of rats fed diets with either fresh fat or three different types of oxidized fat, preparated by heating at temperatures of 50, 105, or 190°C, over a period of 6 wk. The diets contained either 25 or 250 mg α-tocopherol equivalents per kg. The second experiment included four groups of rats fed diets with fresh fat or oxidized fat, heated at a temperature of 55°C, containing either 70 or 570 μg selenium per kg, over a period of 8 wk. Feeding the diets with oxidized fats led to a significant overall reduction of the relative mRNA concentrations and the activities of FAS and G6PDH in both experiments. The effects of the oxidized fats on mRNA concentrations and activities of these enzymes were independent of the dietary concentrations of vitamin E or selenium. Moreover, in both experiments the rats whose diet contained the oxidized fats had significantly lower concentrations of TG in liver, plasma, and VLDL than the rats whose diet contained fresh fat. The study suggests that oxidized fats contain substances that suppress gene expression of lipogenic enzymes in the liver.     

Incorporation of n−3 fatty acids into plasma and liver lipids of rats: Importance of background dietary fat

The health benefits of long-chain n−3 PUFA (20∶5n−3 and 22∶6n−3) depend on the extent of incorporation of these FA into plasma and tissue lipids. This study aimed to investigate the effect of the background dietary fat (saturated, monounsaturated, or n−6 polyunsaturated) on the quantitative incorporation of dietary 18∶3n−3 and its elongated and desaturated products into the plasma and the liver lipids of rats. Female weanling Wistar rats (n=54) were randomly assigned to six diet groups (n=9). The fat added to the semipurified diets was tallow (SFA), tallow plus linseed oil (SFA-LNA), sunola oil (MUFA), sunola oil plus linseed oil (MUFA-LNA), sunflower oil (PUFA), or sunflower oil plus linseed oil (PUFA-LNA). At the completion of the 4-wk feeding period, quantitative FA analysis of the liver and plasma was undertaken by GC. The inclusion of linseed oil in the rat diets increased the level of 18∶3n−3, 20∶5n−3, and, to a smaller degree, 22∶6n−3 in plasma and liver lipids regardless of the background dietary fat. The extent of incorporation of 18∶3n−3, 20∶5n−3, and 22∶5n−3 followed the order SFA-LNA>MUFA-LNA>PUFA-LNA. Levels of 22∶6n−3 were increased to a similar extent regardless of the type of major fat in the rat diets. This indicates that the background diet affects the incorporation in liver and plasma FA pools of the n−3 PUFA with the exception of 22∶6n−3 and therefore the background diet has the potential to influence the already established health benefits of long-chain n−3 fatty acids.     

Effect of dietary fats on some membrane-bound enzyme activities,membrane lipid composition and fatty acid profiles of rat heart sarcolemma

The effect of various dietary fats on membrane lipid composition, fatty acid profiles and membrane-bound enzyme activities of rat cardiac sarcolemma was assessed. Four groups of male weanling Charles Foster Young rats were fed diets containing 20% of groundnut, coconut, safflower or mustard oil for 16 weeks. Cardiac sarcolemma was prepared from each group and the activities of Na⁺,K⁺-ATPase, 5′-nucleotidase, Ca²⁺-ATPase and acetylcholinesterase were examined. ATPase activities were similar in all groups except the one fed coconut oil, which had the highest activities. Acetylcholinesterase activity was also similar in all the groups, however, it was significantly higher in the group fed mustard oil. No significant changes were observed among the groups in 5′-nucleotidase activity, in the cholesterol-to-phospholipid molar ratio and in sialic acid content. The coconut, safflower and mustard oil diets significantly increased cholesterol and phospholipid contents and the lipid-to-protein ratio of cardiac sarcolemma as compared to feeding the groundnut oil diet. The fatty acid composition of membrane lipids was quite different among the various groups, reflecting the type of dietary fat given. The total unsaturated-to-saturated fatty acid ratio was not different among the various groups; however, the levels of some major fatty acids such as palmitic (16∶0), oleic (18∶1) and linoleic (18∶2) acids were significantly different. Cardiac sarcolemma of the group fed safflower oil had the highest polyunsaturated fatty acid content. The results suggest that dietary fats induce changes not only in the fatty acid composition of the component lipids but also in the activities of sarcolemmal enzymes involved in the regulation of cardiac function.     

Dietary fats and energy levels differently affect tissue lipogenic enzyme activity in finishing pigs

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.     

Interrelationship between dietarytrans fatty acids and the 6- and 9-desaturases in the rat

Studies are reported on the effects of dietarytrans fatty acids on the 6- and 9-acyl desaturase activities in the liver microsomes of rats fed essential fatty acid (EFA)-deficient and non-FFA-deficient diets. In experiment I, weanling male rats were fed a semisynthetic diet with either 10% safflower oil (SAF) or 10% hydrogenated coconut oil (HCO). At the age of one year, half of the dietary fat was replaced by a supplement containing elaidate, linolelaidate andcis,trans-trans,cis-18∶2 (TRANS) for 12 weeks. In experiment II, male rats which were kept from weaning on a 10% SAF diet for one year received one of the following fat supplements for a 12-week period: 10% HCO, 9% HCO+1% TRANS, or 5% HCO+5% TRANS. Feeding TRANS depressed the 6-desaturase activity in the liver microsomes, especially in the EFA-deficient rats (HCO+TRANS group of experiment I). Unlike the 6-deaturase activity, the 9-desaturase activity was not inhibited by the dietarytrans fatty acids and was significantly stimulated in the non-EFA-deficient rats (SAF+TRANS group of experiment I and HCO+TRANS groups of experiment II). This was evidenced by incubation reactions and by comparisons of fatty acid consumptions and microsomal fatty acid levels, showing extra biosynthesis of 16∶1 and 18∶1 when TRANS was fed. The biosynthesis of essential (n−6) fatty acids was depressed by the TRANS supplement in EFA-deficient as well as in non-EFA-deficient animals.     

Effect of high fat corn oil,olive oil and fish oil on phospholipid fatty acid composition in male F344 rats

Epidemiological and laboratory animal model studies have provided evidence that the effect of dietary fat on colon tumorigenesis depends on the amount of fat and its composition. Because of the importance of the composition of dietary fat and of tissue membrane fatty acid composition in tumor promotion, experiments were designed to investigate the relative effects of high fat diets rich in ω3, ω6 and ω9 fatty acids and colon carcinogen on the phospholipid fatty acid composition of liver, colon, small intestine, erythrocytes and blood plasma. At 6 wk of age, groups of animals were fed diets containing 5% corn oil (LFCO), 23.5% corn oil (HFCO), 23.5% olive oil (HFOO), and 20.5% fish oil plus 3% corn oil (HFFO). Two weeks later all the animals except the vehicle-treated animals received azoxymethanes.c. once weekly for 2 wk at a dose rate of 15 mg/kg body weight. Animals were sacrificed 5 d later and liver, colon, small intestine and erythrocytes and blood plasma were analyzed for phospholipid fatty acids. The results indicate that the phospholipid fatty acid composition of liver, colon and small intestine of HFCO diet fed animals, were not significantly different from those fed the LFCO diet. The levels of palmitoleic acid and linoleic acid were increased in erythrocytes and blood plasma of the animals fed the HFCO diet compared to those fed the LFCO diet. Feeding the HFCO diet significantly increased the oleic acid content and decreased the linoleic acid and arachidonic acid levels in various organs when compared to the HFCO diet. Animals fed the HFFO diet showed a marked increase in eicosapentaenoic acid and docosahexaenoic acid and a decrease in linoleic acid and arachidonic acid levels as compared to those fed the HFCO diet. The results also indicate that carcinogen treatment had only a minimal effect on the phospholipid fatty acid composition.     

Digestion and absorption of free and esterified fish oil fatty acids in rats

This study was designed to test the hypotheses that digestibility and post-absorption metabolism of fish oil are influenced by impaired lipolysis and by the stereospecific composition of its triacylglycerols. Male Wistar rats were fed nonpurified diets containing one of the following fat sources: 9% native fish oil (NFO), 9% autorandomized fish oil (RFO), 8.1% fish oil-derived free fatty acids (FO-FFA) plus 0.9% glycerol, or 9% soybean oil (SO) as a reference fat. In a 24-day balance study, apparent digestibility of total dietary fat averaged 93.1% in the SO, NFO and RFO groups, and 90.9% in the FO-FFA group. Randomization of fish oil had no effect on apparent digestibility of individual fatty acids. In rats fed FO-FFA, apparent absorption of saturated and monounsaturated fatty acids was lower when compared to the NFO and RFO groups. Feeding the FO-FFA diet tended to increase plasma triglyceride content. The hypocholesterolemic effect of polyunsaturated n−3 fatty acids was not influenced by the dietary source. Similar effects on fatty acid profiles of plasma and liver phospholipids were caused by the NFO, RFO and the FO-FFA diets. We conclude that once polyunsaturated n−3 fatty acids are absorbed, their effect on lipid metabolism is not determined by the dietary source.     

Dietary cod liver oil decreases arachidonic acid in rat gastric mucosa and increases stress-induced gastric erosions

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.     

The hypercholesterolemic effect of dietary coconut fatversus corn oil in hypo- or hyperresponsive rabbits is not exerted through influencing cholesterol absorption

In two inbred strains of rabbits with high or low response of plasma cholesterol to dietary saturatedversus polyunsaturated fatty acids, the efficiency of intestinal cholesterol absorption was measured. The feeding of a cholesterol-free purified diet containing saturated fatty acids in the form of coconut fat, when compared with a diet containing corn oil as polyunsaturated fatty acids, did not influence the efficiency of cholesterol absorption in the two rabbit strains. Irrespective of the dietary fat source, the hyperresponsive rabbits absorbed cholesterol more efficiently. It is concluded that the hypercholesterolemic effect of dietary coconut fatversus corn oil is not exerted by influencing cholesterol absorption.     

The ratio of n-6 to n-3 polyunsaturated fatty acids in the rat diet alters serum lipid levels and lymphocyte functions

Previous studies have reported that feeding rats diets rich in fish oils, which contain high proportions of the n-3 polyunsaturated fatty acids (PUFA) eicosapentaenoic and docosahexaenoic acids, results in lowering of blood lipid levels and suppression of lymphocyte functions testedex vivo andin vivo. The effects of other n-3 PUFA, such as α-linolenic acid, which is found in high proportions in linseed oil, are not as well documented. Therefore, in the present study, weanling male rats were fed for six weeks on one of five high-fat (20% by weight) diets made by mixing together sunflower and linseed oils; the resulting blends had n-6/n-3 PUFA ratios of 112.5:1 (pure sunflower oil), 14.8:1, 6.5:1, 0.8:1, and 0.33:1 (pure linseed oil); the levels of all other components in the diet were identical. The final body weight and total dissectable fat were lowest in rats fed the pure linseed oil diet. Serum cholesterol, triacylglycerol and nonesterified fatty acid concentrations decreased as the n-6/n-3 PUFA ratio of the diet decreased. The fatty acid composition of the serum and of spleen lymphocytes was influenced by the diet fed-there was a progressive decrease in the proportions of linoleic and arachidonic acids and a progressive increase in the proportion of α-linolenic acid as the n-6/n-3 PUFA ratio of the diet decreased. Eicosapentaenoic and docosahexaenoic acids were detected in the serum but not in spleen lymphocytes. Inclusion of α-linolenic acid in the diet resulted in significant suppression of spleen lymphocyte proliferation in response to the T-cell mitogen concanavalin A and in spleen lymphocyte natural killer cell activity, both measuredex vivo. The localized graft vs. host response, a measure of cellmediated immunityin vivo, progressively decreased as the n-6/n-3 PUFA ratio of the diet decreased. Thus, this study shows that dietary α-linolenic acid results in lowered blood lipid levels and suppressed lymphocyte functionsex vivo andin vivo. With respect to these effects, α-linolenic acid is as potent as dietary fish oil.     

Fish Oil Normalizes Plasma Glucose Levels and Improves Liver Carbohydrate Metabolism in Rats Fed a Sucrose-Rich Diet

A sucrose-rich diet (SRD) induces insulin resistance and dyslipidemia with impaired hepatic glucose production and gluconeogenesis, accompanied by altered post-receptor insulin signaling steps. The aim of this study was to examine the effectiveness of fish oil (FO) to reverse or improve the impaired hepatic glucose metabolism once installed in rats fed 8 months a SRD. In the liver of rats fed SRD in which FO replaced corn-oil during the last 2 months, as dietary fat, several key enzyme activities and metabolites involved in glucose metabolisms (phosphorylation, glycolysis, gluconeogenesis and oxidative and non oxidative glucose pathway) were measured. The protein mass levels of IRS-1 and αp85 PI-3K at basal conditions were also analyzed. FO improved the altered activities of some enzymes involved in the glycolytic and oxidative pathways observed in the liver of SRD fed rats but was unable to restore the impaired capacity of glucose phosphorylation. Moreover, FO reversed the increase in PEPCK and G-6-Pase and reduced the G-6-Pase/GK ratio. Glycogen concentration and GSa activity returned to levels similar to those observed in the liver of the control-fed rats. Besides, FO did not modify the altered protein mass levels of IRS-1 and αp85 PI-3K. Finally, dietary FO was effective in reversing or improving the impaired activities of several key enzymes of hepatic carbohydrate metabolism contributing, at least in part, to the normalization of plasma glucose levels in the SRD-fed rats. However, these positive effects of FO were not observed under basal conditions in the early steps of insulin signaling transduction.     

Dietary protein deficiency affects n−3 and n−6 polyunsaturated fatty acids hepatic storage and very low density lipoprotein transport in rats on different diets

Fatty livers and the similarity between the skin lesions in kwashiorkor and those described in experimental essential fatty acid (EFA) deficiency have led to the hypothesis that protein and EFA deficiencies may both occur in chronic malnutrition. The relationship between serum very low density lipoprotein (VLDL) and hepatic lipid composition was studied after 28 d of protein depletion to determine the interactions between dietary protein levels and EFA availability. Rats were fed purified diets containing 20 or 2% casein and 5% fat as either soybean oil rich in EFA, or salmon oil rich in eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, or hydrogenated coconut, oil poor in EFA. Animals were divided into six groups, SOC (20% casein +5% soybean oil), SOd (2% casein +5% soybean oil), COC (20% casein +5% hydrogenated coconut oil), COd (2% casein + 5% hydrogenated coconut oil), SAC (20% casein +5% salmon oil) and SAd (2% casein +5% salmon oil). After 28 d, liver steatosis and reduced VLDL-phospholipid contents (P<0.001) were observed in protein-deficient rats. In protein deficiency, triacylglycerol and phospholipid fatty acid compositions in both liver and VLDL showed a decreased polyunsaturated-to-saturated fatty acid ratio. This ratio was higher with the salmon oil diets and lower with the hydrogenated coconut oil diets. Furthermore, independent of the oil in the diet, protein deficiency decreased linoleic and arachidonic acids in VLDL phospholipids. Conversely, despite decreased proportions of EPA at low protein levels, DHA levels remained higher in rats fed salmon oil diets. While in rats fed the hydrogenated coconut oil-fed diets the amount of 22∶5n−6 was lower in liver, it was higher in VLDL lipids at low protein levels. Both EPA and arachidonic acid are precursors of eicosanoids and their diminution may be related to certain clinical symptoms seen in infants suffering from kwashiorkor.