Comparative hypocholesterolemic effects of six dietary oils in cholesterol-fed rats after long-term feeding

Rats (8 wk of age) fed a conventional diet were shifted to diets containing 10% Oenothera biennis Linn oil (OBLO, linoleic acid +γ-linolenic acid) from a wild plant, evening primrose oil (EPO, linoleic acid +γ-linolenic acid) from a cultivated plant, bio-γ-linolenic acid oil from mold (BIO, palmitic acid+oleic acid+linoleic acid+γ-linolenic acid), safflower oil (linoleic acid), palm oil (PLO, palmitic acid+oleic acid+linoleic acid), or soybean oil (linoleic acid+α-linolenic acid) with 0.5% cholesterol for 13 wk. Though there were no significant differences in the food intake among the groups, the body weight gain of the OBLO group was significantly lower than that of other groups except for the BIO and PLO groups, and that of the EPO and SPO groups were the highest among the groups. The liver weight of the OBLO group was significantly lower than that of other groups, and that of the PLO group was the highest among the groups. The serum total cholesterol and very low density lipoprotein (VLDL)+intermediate density lipoprotein (IDL)+low density lipoprotein (LDL) cholesterol concentrations of the OBLO and EPO groups were consistently lower than those in the other groups. However, those of the BIO group were higher than those in the OBLO and EPO groups. The liver cholesterol concentration of the PLO group was the highest among all groups except for the EPO group. The fecal neutral sterol and bile acid extraction of the BIO group tended to increase compared to other groups. The results of this study demonstrate that OBLO and EPO inhibit the increasing of serum total cholesterol and VLDL+IDL+LDL-cholesterol concentrations in the presence of excess cholesterol in the diet compared with the other dietary oils.     

Effects of diets enriched in n−6 or n−3 fatty acids on cholesterol metabolism in older rats chronically fed a cholesterol-enriched diet

Hypocholesterolemic effects in older animals after long-term feeding are unknown. Therefore, aged rats (24 wk of age) fed a conventional diet were shifted to diets containing 10% perilla oil [PEO; oleic acid+linoleic acid+α-linolenic acid; n−6/n−3, 0.3; polyunsaturated fatty acid/saturated fatty acid (P/S), 9.6], borage oil [oleic acid+linoleic acid+α-linolenic acid; n−6/n−3, 15.1; P/S, 5.3], evening primrose oil (FPO; linoleic acid+γ-linolenic acid; P/S, 10.5), mixed oil (MIO; oleic acid+linoleic acid+γ-linolenic acid+α-linolenic acid; n−6/n−3, 1.7; P/S, 6.7), or palm oil (PLO; palmitic acid+oleic acid+linoleic acid; n−6/n−3, 25.3; P/S, 0.2) with 0.5% cholesterol for 15 wk in this experiment. There were no significant differences in the food intake and body weight gain among the groups. The liver weight in the PEO (n−6/n−3, 0.3) group was significantly higher than those of other groups in aged rats. The serum total cholesterol and very low density lipoprotein (VLDL) +intermediate density lipoprotein (IDL)+low density lipoprotein (LDL)-cholesterol concentrations of the PLO (25.3) group were consistently higher than those in the other groups. The serum high density lipoprotein cholesterol concentrations of the PEO (0.3) and EPO groups were significantly lower than in the other groups at the end of the 15-wk feeding period. The liver cholesterol concentration of the PLO (25.3) group was significantly higher than those of other groups. There were no significant differences in the hepatic LDL receptor mRNA level among the groups. Hepatic apolipoprotein (apo) B mRNA levels were not affected by the experimental conditions. The fecal neutral steroid excretion of the PLO (25.3) group tended to be low compared to the other groups. The results of this study demonstrate that both n\t-6 fatty acid and n\t-3 fatty acids such as \gg-linolenic acid and \ga-linolenic acid inhibit the increase of serum total cholesterol and VLDL+IDL+LDL-cholesterol concentrations of aged rats in the presence of excess cholesterol in the diet compared with dietary saturated fatty acid.     

Comparative hypocholesterolemic effects of capybara (Hydrochoerus hydrochaeris dabbenei) oil, horse oil, and sardine oil in cholesterol-fed rats

The hypocholesterolemic efficacy of various polyunsaturated fatty acids was compared in rats given cholesterol-enriched diets. Capybara oil (CO, linoleic+α-linolenic acids), horse oil (HO, α-linolenic acid), and sardine oil (SO, eicosapentaenoic+docosahexaenoic acids) were added to diets at 50 g/kg. The weight gain, food intake, and liver weight in the CO-fed group were significantly higher than those in other groups during the 6-wk experimental period. The serum total and very low density lipoprotein (VLDL)+intermediate density lipoprotein (IDL)+low density lipoprotein (LDL) cholesterol concentrations of the CO-fed and SO-fed groups were significantly lower than in the HO-fed group after 6 wk. The serum high density lipoprotein cholesterol concentration in the SO-fed group was significantly higher than that in the CO-fed and HO-fed groups. The fecal neutral sterol concentration in the CO-fed group was reduced significantly compared with the other groups, and the fecal bile acid concentration in the HO-fed group was significantly higher than that in the SO-fed group. The results of this study demonstrate that CO lowers the serum total cholesterol and VLDL+IDL+LDL-cholesterol concentrations in the presence of excess cholesterol in the diet as well as SO.     

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.     

Acyl group distributions in tissue lipids of rats fed evening primrose oil (λ-linolenic plus linoleic acid) or soybean oil (α-linolenic plus linoleic acid)

Three groups of rats were fed diets with either 10 weight percent (wt%) of evening primrose oil, safflower oil or soybean oil for 11 weeks. Diets contained 7.1 wt% linoleic acid +0.8 wt% γ-linolenic acid, 7.6 wt% linoleic acid, or 5.3 wt% linoleic acid +0.7 wt% α-linolenic acid, respectively. In liver mitochondria as well as in heart, dietary γ-linolenic acid did not affect the fatty acid profiles of phosphatidylcholnes (PC), phosphatidylethanolamines (PE) or cardiolipins (CL), whereas dietary α-linolenic acid caused an increased formation of (n−3) polyunsaturated fatty acids (PUFA). The liver Δ6− and Δ5-desaturase activities determined in vitro were not affected by the dietary fats. In brain PE, which are rich in C22− and C20-(n−3) PUFA, as well as in testes PC and PE, which are rich in (n−6) PUFA, no effects were found from a partial replacement of dietary linoleic acid with γ-linolenic acid or α-linolenic acid. In kidney PC, PE, phosphatidylinositol (PI) and CL, 20∶3(n−6) was moderately elevated to ca. 1% following intake of γ-linolenic acid, whereas partial replacement of linoleic acid with α-linolenic acid was followed by increased deposition of 22∶6(n−3) in PC and PE of testes and kidney. Thus, no general effect of evening primrose oil on the content of (n−6) PUFA in rat tissue phospholipids was observed, wheras a significant incorporation of γ-linolenic acid into liver and adipose tissue triglycerides was found.     

Dietary linoleic, α-linolenic and oleic acids are oxidized at similar rates in rats fed a diet containing these acids in equal proportions

The objective of this study was to examine whether whole body oxidation rates of dietary linoleic, α-linolenic and oleic acids differ when the acids are provided in identical quantities. Male rats were fed for 10 wk a 15% fat (w/w) diet containing equal amounts of linoleic, α-linolenic and oleic acids (22.7, 23.0 and 23.2% of total fatty acids, respectively). At week 10, after overnight fasting, rats were intragastrically administered 20 μCi of either [1-¹⁴C]-labelled linoleic, α-linolenic or oleic acid in a 200-μL bolus of oil containing equal quantities of each fatty acid. The appearance of¹⁴CO₂ in expired air was then monitored hourly for 12h for each animal. A preliminary study had shown that growth and food consumption patterns in animals consuming the oil containing equal quantities of each of the fatty acids paralleled the patterns of animals that were self-selecting among separate diets, each of which contained one of the component oils. The appearance of¹⁴C, expressed as percent dose administered, peaked at 2–3 h post-dose for¹⁴C-labelled linoleic (5.28±0.37%/h), α-linolenic (6.92±0.51%/h) and oleic (5.98±0.44%/h) acids. Statistically these values were not significantly different. Cumulative¹⁴CO₂ excretion rates over 12 h were also similar for linoleic (27.2±0.9%), α-linolenic (26.8±1.2%) and oleic (25.9±1.2%) acids. The results suggest that the rat's capacity to oxidize 18-carbon unsaturated fatty acids is not affected by fatty acid unsaturation when these fatty acids are provided at equal dietary levels.     

Effects of dietary linseed oil and marine oil on lipid peroxidation in monkey liverin vivo andin vitro

Diets rich in linoleic acid (CO) from corn oil, or in linoleic acid and either α-linolenic acid (LO) based on linseed oil or n−3 fatty acids (MO) from menhaden oil were fed to male and female Cynomolgus monkeys for 15 wk. In the liver a 40% reduction of α-tocopherol occurred in the MO group relative to the CO and LO groups followed by increased formation of lipofuscinin vivo. A four-fold increase of α-tocopherol in the MO diet (MO+E) brought the level in the liver to that found with CO and LO. The increased peroxidation in the MO group in the liver phospholipids was associated with the replacement of 60% of the n−6 fatty acids by n−3 fatty acids from menhaden oil. Similar fatty acid profiles were found in groups fed MO and MO+E, respectively. Compared to the CO fed group, feeding α-linolenic acid only resulted in a slight incorporation of n−3 fatty acids in the liver membranes mainly due to a direct incorporation of α-linolenic acid. However, in monkeys fed menhaden oil more than 30% of the total fatty acids in the liver phospholipids were n−3 fatty acids. The various diets did not influence the activity of liver catalase (EC 1.11.1.6) nor superoxide dismutase (EC 1.15.1.1), but glutathione-peroxidase activity (EC 1.11.1.9) was higher in monkeys fed the MO diet. The catalase activity in females was 20% higher than in males. In anin vitro assay, liver microsomes from monkeys fed the MO diet or the MO diet supplemented with tocopherol produced similar amounts of thiobarbituric acid reactive substances and at a much higher rate than microsomes from the CO and LO groups. It appeared that α-tocopherol did not protect long-chain n−3 C₂₀ and C₂₂ fatty acids as well as n−6 fattya acids against peroxidation. The present data showed that monkeys were not fully able to compensate for increased peroxidative stress but a four-fold supplement of vitamin E to the diets reduced the oxidation.     

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.     

Microbial conversion of an oil containing α-linolenic acid to an oil containing eicosapentaenoic acid

Mycelia of arachidonic acid-producing fungi belonging to the genusMortierella were found to convert an oil containing α-linolenic acid to an oil containing 5,8,11,14,17-cis-eicosapentaenoic acid (EPA). This conversion was observed when they were grown in a medium containing the oil, glucose and yeast extract at 28 C. On the screening of various oils, linseed oil, in which α-linolenic acid amounts to about 60% of the total fatty acids, was found to be the most suitable for EPA production. Under the optimal culture conditions, a selected strain,Mortierella alpina 20-17, converted 5.1% of the α-linolenic acid in the added oil into EPA, the EPA production reaching 1.35 g/l of culture broth (41.5 mg/g dry mycelia). This value corresponded to 7.1% (by weight) of the total fatty acids in the extracted lipids. The lipid was also found to be rich in arachidonic acid (12.3%). Other major fatty acids in the lipid were palmitic acid (4.4%), stearic acid (3.2%), oleic acid (13.5%), linoleic acid (13.7%), α-linolenic acid (38.5%) and γ-linolenic acid (0.9%).     

γ-tocotrienol as a hypocholesterolemic and antioxidant agent in rats fed atherogenic diets

This study was designed to determine whether incorporation of γ-tocotrienol or α-tocopherol in an atherogenic diet would reduce the concentration of plasma cholesterol, triglycerides and fatty acid peroxides, and attenuate platelet aggregability in rats. For six weeks, male Wistar rats (n=90) were fed AIN76A semisynthetic test diets containing cholesterol (2% by weight), providing fat as partially hydrogenated soybean oil (20% by weight), menhaden oil (20%) or corn oil (2%). Feeding the ration with menhaden oil resulted in the highest concentrations of plasma cholesterol, low and very low density lipoprotein cholesterol, triglycerides, thiobarbituric acid reactive substances and fatty acid hydroperoxides. Consumption of the ration containing γ-tocotrienol (50 μ/kg) and α-tocopherol (500 mg/kg) for six weeks led to decreased plasma lipid concentrations. Plasma cholesterol, low and very low density lipoprotein cholesterol, and triglycerides each decreased significantly (P<0.001). Plasma thiobarbituric acid reactive substances decreased significantly (P<0.01), as did the fatty acid hydroperoxides (P<0.05), when the diet contained both chromanols. Supplementation with γ-tocotrienol resulted in similar, though quantitatively smaller, decrements in these plasma values. Plasma α-tocopherol concentrations were lowest in rats fed menhaden oil without either chromanol. Though plasma α-tocopherol did not rise with γ-tocotrienol supplementation at 50 mg/kg, γ-tocotrienol at 100 mg/kg of ration spared plasma α-tocopherol, which rose from 0.60±0.2 to 1.34±0.4 mg/dL (P<0.05). The highest concentration of α-tocopherol was measured in plasma of animals fed a ration supplemented with α-tocopherol at 500 mg/kg. In response to added collagen, the partially hydrogenated soybean oil diet without supplementary cholesterol led to reduced platelet aggregation as compared with the cholesterol-supplemented diet. However, γ-tocotrienol at a level of 50 mg/kg in the cholesterol-supplemented diet did not significantly reduce platelet aggregation. Platelets from animals fed the menhaden oil diet released less adenosine triphosphate than the ones from any other diet group. The data suggest that the combination of γ-tocotrienol and α-tocopherol, as present in palm oil distillates, deserves further evaluation as a potential hypolipemic agent in hyperlipemic humans at atherogenic risk.     

Changes in lipid composition of liver microsomes and fatty acyl-CoA desaturase activities induced by medium chain triglyceride feeding

Changes in fatty acid composition, microsomal Δ⁹- and Δ⁶-desaturase activities and liver contents of cholesterol and phospholipids were studied in rats fed medium chain triglyceride-supplemented diets. Weanling rats were divided into four groups and fed for three weeks a basal diet with different 10%-fat supplements: corn oil, medium chain triglyceride-corn oil, olive oil and medium chain triglyceride-olive oil. The highest relative content of saturated fatty acids corresponded to corn oil-fed animals. Both monounsaturated fatty acid content and Δ⁹-desaturase activity were higher in the animals fed olive oil diets than in corn oil-fed rats. The long chain polyunsaturated fatty acids of the n−3 series were increased in the olive oil and medium chain triglyceride-olive oil-fed groups probably due to the lower linoleic/α-linolenic ratios found in these two diets. The cholesterol/phospholipid molar ratio was unaffected by diet and the unsaturation index was only slightly changed in the four groups. Thus, some mechanism may be operative under these conditions to maintain the homeostasis of the membrane.     

A diet containing myristoleic plus palmitoleic acids elevates plasma cholesterol in young growing swine

The objective of this study was to test the effect of a novel fatty acid mixture, enriched with myristoleic and palmitoleic acids, on plasma lipoprotein cholesterol concentrations. Weanling pigs were assigned to one of six groups and each group received a diet differing in fatty acid composition. Diets were fed for 35 days and contained 10 g added cornstarch/100 g (to provide baseline data) or 10 g added fatty acids/100 g. For those diets containing added fatty acids, extracted lipids contained 36% myristoleic plus palmitoleic acid combined (14∶1/16∶1 diet), 52% palmitic acid (16∶0 diet), 51% stearic acid (18∶0 diet), 47% oleic acid (18∶1 diet), or 38% linoleic acid (18∶2 diet). Witht the exception of the cornstarch diet, all diets contained approximately 30% myristic acid. There were no significant differences in weight gain across treatment groups (P=0.22). All diets caused a significant increase in triglycerides and in total, low density lipoprotein, high density lipoprotein, and very low density lipoprotein cholesterol. The increase in total plasma cholesterol from pretreatment values was greatest in pigs fed the 14∶1/16∶1 and 18∶1 diets. However, the increase in low density lipoprotein cholesterol from the pretreatment concentration was greatest in the 14∶1/16∶1-fed pigs. Increases in very low density lipoprotein cholesterol above pretreatment concentrations were lowest in 16∶0-fed pigs and greatest in 18∶1-fed pigs. Dietary fatty acids elicited changes in plasma fatty acids which generally were reflective of the diets, although the 18∶0 diet did not alter plasma fatty acid concentrations and the 16∶0 diet increased plasma 16∶0 only at the end of the study. These results demonstrated that the combination of myristoleic plus palmitoleic acids increased plasma cholesterol in young pigs, suggesting that fatty acid chain length, rather than degree of unsaturation, is primarily responsible for the effects of fatty acids on circulating lipoprotein cholesterol concentrations.     

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 fatty acids regulate cholesterol induction of liver CYP7α1 expression and bile acid production

In the present study we investigated the effects of dietary fats containing predominantly PUFA, monounsaturated FA (MUFA), or saturated FA (SFA) on lipid profile and liver cholesterol 7α-hydroxylase (CYP7α1) mRNA expression and bile acid production in C57BL/6J mice. The animals (n=75) were randomly divided into five groups and fed a basic chow diet (AIN-93G) (BC diet), a chow diet with 1g/100g of cholesterol (Chol diet), a chow diet with 1g/100g of cholesterol and 14g/100g of safflower oil (Chol+PUFA diet), a chow diet with 1g/100g of cholesterol and olive oil (Chol+MUFA diet), or a chow diet with 1g/100g of cholesterol and myristic acid (Chol+SFA diet) for 6 wk. The results showed that the Chol+SFA diet decreased CYP7α1 gene expression and bile acid pool size, resulting in increased blood and liver cholesterol levels. Addition of PUFA and MUFA to a 1% cholesterol diet increased the bile acid pool production or bile acid excretion and simultaneously decreased liver cholesterol accumulation despite decreased CYP7α1 mRNA expression. The results indicate that the decreased bile acid pool size induced by the SFA diet is related to inhibition of the liver CYP7α1 gene expression, but an increased bile acid pool size and improved cholesterol homeostasis are disassociated from the liver CYP7α1 gene expression.     

Prevention of cholesterol cholelithiasis by dietary unsaturated fats in hormone-treated female hamsters

We examined the effect of diet on gallstone incidence and the composition of biliary phosphatidylcholines in methyltestosterone-treated female hamsters. These hamsters were fed a nutritionally adequate purified lithogenic diet containing 2% corn oil, 4% butterfat, 0.3% cholesterol, and 0.05% methyltestosterone, resulting in a cholesterol gallstone incidence of 86%. This incidence was lowered when mono-and polyunsaturated fats or fatty acids were added to the diet: 2.5% oleic acid resulted in total prevention of cholesterol cholelithiasis, 2.5% linoleic acid, and 4% safflower oil (78% linoleic acid content) reduced gallstone incidence to 26 and 8%, respectively. An additional 4% butterfat (29% oleic acid content) produced gallstones in 50% of the animals. At the end of the 6-wk feeding period, the bile of all hamsters was supersaturated with cholesterol. The major biliary phosphatidylcholine species in all groups were (sn-1-sn-2): 16:0–18:2, 16:0–18:1, 18:0–18:2, 16:0–20:4, and 18:2–18:2. The safflower oil-and linoleic acidfed hamsters exhibited an enrichment of 16:0–18:2 (16–18%); added butterfat or oleic acid increased the proportion of 16:0–18:1 (9 and 25%, respectively). We conclude that the phosphatidylcholine molecular species in female hamster bile can be altered by dietary fats/fatty acids and that mono-and polyunsaturated fatty acids play a role in suppressing the induced cholelithiasis.     

Dietary comparison of conjugated linolenic acid (9 cis, 11 trans, 13 trans) and α-tocopherol effects on blood lipids and lipid peroxidation in alloxan-induced diabetes mellitus in rats

The present study investigated the dietary effect of conjugated linolenic acid (CLnA) on lipid profiles and lipid peroxidations in alloxan-induced diabetes mellitus in rats. Diabetic rats were fed with 20% sunflower oil (diabetic control), sunflower oil supplemented with 0.5% CLnA, sunflower oil supplemented with 0.15% α-tocopherol, and sunflower oil containing 0.25% CLnA+0.15% α-tocopherol. The results demonstrated that 0.5% CLnA, 0.15% α-tocopherol, and 0.25% CLnA+0.15% α-tocopherol each on supplementation significantly lowered total cholesterol and non-HDL-cholesterol in comparison with the diabetic control group. The TAG level was significantly lowered in both the 0.15% α-tocopherol and 0.25% CLnA+0.15% α-tocopherol groups. LDL lipid peroxidation and erythrocyte membrane lipid peroxidation were reduced significantly in each of the experimental groups vs. the control group. The CLnA+α-tocopherol diet induced a greater reduction in membrane lipid and liver lipid peroxidation than the α-tocopherol diet alone. In conclusion, dietary CLnA exerts antioxidant activity as evidenced by reduced lipid peroxidation in chemically induced diabetes mellitus.     

Comparative effects of flaxseed and sesame seed on vitamin E and cholesterol levels in rats

Flaxseed and sesame seed both contain more than 40% fat, about 20% protein, and vitamin E, mostly γ-tocopherol. Furthermore, both contain considerable amounts of plant lignans. However, flaxseed contains 54% α-linolenic acid, but sesame seed only 0.6%, and the chemical structures of flaxseed and sesame lignans are different. In this study, we investigated the differential effects of flaxseed and sesame seed on plasma and tissue γ-tocopherol, TBARS, and cholesterol concentrations. Rats were fed experimental diets for 4 wk: vitamin E-free, (-VE), γ-tocopherol, flaxseed (FS), sesame seed (SS), flaxseed oil (FO), FO with sesamin (FOS), and defatted flaxseed (DFF). SS and FOS diets induced significantly higher γ-tocopherol concentrations in plasma and liver compared with FS, FO, and DFF diets. Groups fed FS, FO, and FOS showed lower plasma total cholesterol compared with the SS and DFF groups. Higher TBARS concentrations in plasma and liver were observed in the FS and FO groups but not in the FOS groups. These results suggest that sesame seed and its lignans induced higher γ-tocopherol and lower TBARS concentrations, whereas flaxseed lignans had no such effects. Further, α-linolenic acid produced strong plasma cholesterol-lowering effects and higher TBARS concentrations.     

Dietary cholesterol modulates Δ6 and Δ9 desaturase mRNAs and enzymatic activity in rats fed a low-EFA diet

The effects of a 1% addition of cholesterol to a diet low in EFA on FA desaturases were examined. The administration of cholesterol markedly increased the esterified cholesterol content in microsomes and total liver lipids from the first day, whereas the proportion of free cholesterol remained unaltered throughout the treatment. An excellent homeostasis in the free cholesterol content was apparently evoked by the acyl-CoA cholesterol acyltransferase. The cholesterol esters were mainly oleate, palmitate, and stearate, and the addition of cholesterol increased the relative proportions of cholesterol palmitoleate and oleate. The addition of cholesterol to a low-EFA diet induced, as in animals fed a high-FFA diet, a marked increase in liver stearoyl-CoA desaturase-1 mRNA and enzyme activity. This increased activity apparently evoked a similar enhancement of palmitoleic and oleic acids in total and microsomal liver lipids. The cholesterol-rich diet depressed the liver Δ6 and Δ5 desaturase activity. However, the abundance of Δ6 desaturase mRNA was not modified throughout the treatment. This indicates that the depressive effect is evoked at a step beyond that controlled by the mRNA level. The depression of both enzymatic activities was consistent with the decrease in the percentages of arachidonic acid and DHA in total and microsomal liver lipids. Taken together, these results indicate that through its modulating effect on the desaturases, dietary cholesterol may lead an animal or humaan fed low-EFA diet to a true deficiency by the decreased synthesis of the highly polyunsaturated acids derived from linoleic and α-linolenic acids.     

Olive oil and modulation of cell signaling in disease prevention

Epidemiological studies show that populations consuming a predominantly plant-based Mediterranean-style diet exhibit lower incidences of chronic diseases than those eating a northern European or North American diet. This observation has been attributed to the greater consumption of fruits and vegetables and the lower consumption of animal products, particularly fat. Although total fat intake in Mediterranean populations can be higher than in other regions (ca. 40% of calories), the greater proportion is derived from olive oil and not animals. Increased olive oil consumption is implicated in a reduction in cardiovascular disease, rheumatoid arthritis, and, to a lesser extent, a variety of cancers. Olive oil intake also has been shown to modulate immune function, particularly the inflammatory processes associated with the immune system. Olive oil is a nonoxidative dietary component, and the attenuation of the in-flammatory process it elicits could explain its beneficial effects on disease risk since oxidative and inflammatory stresses appear to be underlying factors in the etiology of these diseases in man. The antioxidant effects of olive oil are probably due to a combination of its high oleic acid content (low oxidation potential compared with linoleic acid) and its content of a variety of plant antioxidants, particularly oleuropein, hydroxytyrosol, and tyrosol. It is also possible that the high oleic acid content and a proportionate reduction in linoleic acid intake would allow a greater conversion of α-linolenic acid (18∶3n−3) to longer-chain n−3 PUFA, which have characteristic health benefits. Adoption of a Mediterranean diet could confer health benefits in high-risk populations.     

1-14C-Linoleic acid distribution in various tissue lipids of guinea pigs following an oral dose

A recent study on the metabolism of 1-¹⁴C-α-linolenic acid in the guinea pig revealed that the fur had the highest specific activity of all tissues examined, 48 h after dosing. The present study investigated the pattern of tissue lipid labeling following an oral dose of 1-¹⁴C-linoleic acid after the animals had been dosed for the same time as above. Guinea pigs were fed one of two diets with a constant linoleic acid content (18% total fatty acids) and a different content of α-linolenic acid (0.3 or 17.3%) from weaning for 3 wk and 1-¹⁴C-linoleic acid was given orally to each animal for 48 h prior to sacrifice. The most highly labeled tissues (dpm/mg of linoleic acid) were liver, followed by brain, lung and spleen, heart, kidney and adrenal and intestines, in both diet groups. The liver had almost a three-fold higher specific activity than skin and fur which was more extensively labeled than the adipose and carcass. Approximately two-thirds of the label in skin plus fur was found in the fur which, because of a low lipid mass, would indicate that the fur was highly labeled. All tissues derived from animals on the diet with the low α-linolenic acid level were significantly more labeled than the tissues from the animals on the high α-linolenic acid diet, by a factor of 1.5 to 3. The phospholipid fraction was the most highly labeled fraction in the liver, free fatty acids were the most labeled fraction in skin & fur, while triacyglycerols were the most labeled in the carcass and adipose tissue. In these tissues, more than 90% of the radioactivity was found in fatty acids with 2-double bonds in the tissue lipids. These data indicate that the majority of label found in guinea pig tissues 48 h after dosing was still associated with a fatty acid fraction with 2-double bonds, which suggests there was little metabolism of linoleic acid to more highly unsaturated fatty acids in this time frame. In this study, the labeling of guinea pig tissues with linoleic acid, 48 h after dosing, was quite different from the labeling with α-linolenic acid reported previously. The retention of the administered radioactivity from ¹⁴C-linoleic acid in the whole body lipids was 1.6 times higher in the group fed the low α-linolenic acid diet (diet contained a total of 1.8 g PUFA/100 g diet)compared with the group fed the high α-linolenic acid diet (diet contained 3.6 g PUFA/100 g diet). The lack of retention of ¹⁴C-labeled lipids in the whole body would be consistent with an increased rate of β-oxidation of the labeled fatty acid on the diet rich in PUFA, a result supported by other studies using direct measurement of labeled carbon dioxide.