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.     

Effect of flaxseed processing on engineering properties and fatty acids profiles of pasta

Flaxseed contains numerous bioactive compounds which induce various biological effects. Among bioactive compounds, flaxseed contains 38–45% oil, of which up to 59% is α-linolenic acid. Focus has recently been put on the technical difficulties of processing flaxseed pasta and studies have shown that flaxseed could tolerate some processing conditions. A close link between pasta processing conditions and the in vitro digestion of the food matrix has also been identified. The aim of this study were (1) to understand the impact of flaxseed processing and content on engineering properties of pasta after the extrusion, the drying and the cooking process; (2) to characterize the fatty acids profile of flaxseed-enriched pasta during the processing and after the in vitro digestion. Two processes were considered prior to the incorporation of flaxseed into pasta at levels of 15% and 30% (dry basis): (Process A) conditioning and milling of flaxseed; (Process B) conditioning of flaxseed, oil pressing, milling of flaxseed cake and reformulation. Results showed that pressing oil from flaxseed and then milling the flaxseed cake (Process B) allowed obtaining an average particle size smaller than milling the whole flaxseed (Process A) which doubled the flaxseed-to-semolina particles ratio. Flaxseed processing, prior to the incorporation into pasta, and content had impacts on engineering properties after the extrusion, the drying and the cooking process and, affected the protection and the release of free fatty acids during in vitro digestion. While free fatty acids profiles remained relatively stable through all steps of pasta processing, they were affected by the in vitro digestion. Decrease in the proportion of omega-3 fatty acid (C18:3) was more important for the Process A compared to the Process B.     

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.     

Lipid and fatty acid profiles in rats consuming different high-fat ketogenic diets

High-fat ketogenic diets are used to treat intractable seizures in children, but little is known of the mechanism by which these diets work or whether fats rich in n−3 polyunsaturates might be beneficial. Tissue lipid and fatty acid profiles were determined in rats consuming very high fat (80 weight%), low-carbohydrate ketogenic diets containing either medium-chain triglyceride, flaxseed oil, butter, or an equal combination of these three fat sources. Ketogenic diets containing butter markedly raised liver triglyceride but had no effect on plasma cholesterol. Unlike the other fats, flaxseed oil in the ketogenic diet did not raise brain cholesterol. Brain total and free fatty acid profiles remained similar in all groups, but there was an increase in the proportion of arachidonate in brain total lipids in the medium-chain triglyceride group, while the two groups consuming flaxseed oil had significantly lower arachidonate in brain, liver, and plasma. The very high dietary intake of α-linolenate in the flaxseed group did not change docosahexaenoate levels in the brain. Our previous report based on these diets showed that although ketosis is higher in rats consuming a ketogenic diet based on medium-chain triglyceride oil, seizure resistance in the pentylenetetrazol model is not clearly related to the degree of ketosis achieved. In combination with our present data from the same seizure study, it appears that ketogenic diets with widely differing effects on tissue lipids and fatty acid profiles can confer a similar amount of seizure protection.     

Effects of dietary n−3 fatty acid-enriched chicken eggs on plasma and tissue cholesterol and fatty acid composition of rats

The purpose of this study was to examine the effects of feeding n−3 polyunsaturated fatty acid (PUFA)-enriched chicken eggs on plasma and liver cholesterol levels and fatty acid composition in rats. Eggs were collected from laying hens fed diets containing 10% flax seed (Hn−3), 12% sunflower seed (Hn−6), or wheat and soybean meal control (CON). Yolk powders were prepared and fed at the 15% level to weanling female Sprague-Dawley rats for 28 days. Consumption of n−3 PUFA-enriched yolks significantly reduced both plasma and liver total cholesterol. Liver total lipids and phospholipids of rats fed Hn−3 diet were enriched with linolenic, eicosapentaenoic, and docosahexaenoic acids with a concomitant reduction of arachidonic acid in liver phospholipids. The plasma cholesterol of rats fed yolk powders enriched with n−6 PUFA (mainly linoleic acid) was reduced to the same extent as in those fed the n−3 enriched, but the liver cholesterol was significantly increased, indicating differential effects of dietary n−3 and n−6 PUFA. The results demonstrated that the cholesterolemic and tissue lipid modulating properties of chicken eggs could be modified in a favorable way by altering the fatty acid composition of yolk lipids through manipulation of laying hen diets.     

Effects of flaxseed derivatives in experimental polycystic kidney disease vary with animal gender

Flaxseed derivatives, including both oil and flax lignan, modify progression of renal injury in animal models, including Han:SPRD-cy polycystic kidney disease (PKD). Gender is a significant factor in the rates of progression of many forms of human renal disease, but the role of gender in the response to nutrition intervention in renal disease is unexplored. In this study, male and female Han:SPRD-cy rats or normal littermates were fed either corn oil (CO) or flax oil (FO) diets, with or without 20 mg/kg of the diet flax lignan secoisolaricinoresinol dyglycoside (SDG). Renal injury was assessed morphometrically and biochemically. Renal and hepatic PUFA composition was assessed by GC and renal PGE₂ release by ELISA. FO preserved body weight in PKD males, with no effect in females. SDG reduced weight in both normal and PKD females. FO reduced proteinuria in both male and female PKD. FO reduced cystic change and renal inflammation in PKD males but reduced cystic change, fibrosis, renal inflammation, tissue lipid peroxides, and epithelial proliferation in PKD females. SDG reduced renal inflammation in all animals and lipid peroxides in PKD fenales. A strong interaction between SDG and FO was observed in renal FA composition of female kidneys only, suggesting increased conversion of C₁₈ PUFA to C₂₀ PUFA. FO reduced renal release of PGE₂ in both genders. Gender influences the effects of flaxseed derivatives in Han:SPRD-cy rats. Gender-based responses to environmental factors, such as dietary lipid sources and micronutrients, may contribute to gender-based differences in disease progression rates.     

Inclusion of Flaxseed in Hay- and Barley Silage Diets Increases Alpha-Linolenic Acid in Cow Plasma Independent of Forage Type

Feeding flaxseed to cattle may be a means of increasing omega-3 fatty acid levels in ruminant products, but possible interactions with conserved forages have not been investigated. Twelve Holstein cows were used in a replicated 4 × 4 Latin Square experiment. Cows were fed one of four 50:50 forage:concentrate diets (DM basis): hay (hay control, HC), hay plus 15% ground flaxseed (hay-flaxseed, HF), barley silage (silage control, SC), and barley silage plus 15% ground flaxseed (silage-flaxseed, SF). Plasma concentrations of alpha-linolenic acid (ALA) did not differ between SC and HC diets. Flaxseed increased ALA (P < 0.05), but levels were not influenced by forage type. Flaxseed slightly increased 18:2n-6 (P < 0.05) and some n-6 and n-3 elongation and desaturation products, particularly arachidonic acid (ARA) and eicosapentaenoic acid (EPA). Flaxseed also increased C18:0 (P < 0.05) with this increase being greater (P < 0.01) for cows fed SF than HF. Feeding flaxseed also increased plasma C18:1-trans isomers (P < 0.01), predominantly vaccenic acid (VAA, 18:1-t11), with this increase being greater (P < 0.05) in cows fed HF than SF. Although conjugated linoleic acid (CLA) was increased (P < 0.001) with flaxseed it was not influenced by forage type (P = 0.06). Overall, feeding flaxseed increased plasma ALA, EPA, ARA and CLA independently of forage type. Feeding flaxseed with silage, however, resulted in more 18:0, while feeding flaxseed with hay resulted in greater accumulations of plasma 18:1-trans isomers mainly in the form of VAA.     

Severe fatty liver in rats fed a fat-free ethanol diet,and its prevention by small amounts of dietary arachidonate

Rats were fed ethanol and a fat-free diet for 30 days to determine whether dietary fat is needed for the development of fatty liver. The severity of fatty liver was similar to that of rats fed an isocaloric diet with 35% fat. Small amounts (29 mg/day) of dietary arachidonic acid prevented alcoholic fatty liver. Rats fed either the alcohol (AF) or control (CF) fat-free diets developed essential fatty acid deficiency (EFAD) as measured by the triene/tetraene ratio of liver and plasma lipids. Rats fed arachidonic acid (AA, alcohol and CA, control diets) did not develop EFAD. Although EFAD alone did not cause the development of fatty liver, the combination of dietary ethanol and EFAD did. The ratios of 16∶1/16∶0 and 18∶1/18∶0 in liver lipids indicated that desaturase enzymes were less active and lipogenesis was reduced in rats fed the AA diet compared to those fed the AF diet. In contrast, stimulated lipogenesis appears to have been the cause of fatty liver in rats fed the AF diet. Presented at the XII International Congress of Nutrition, San Diego, CA, August 1981. Abbreviations: Diets are indicated as fat-free with ethanol (AF), fat-free without ethanol (CF), or similar diets with 0.9% of the calories as arachidonic acid with (AA) or without (CA) ethanol. The composition of these diets is discribed in the text and Table 1.     

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.     

Increase of Serum Cholesterol Levels by Heat-Moisture-Treated High-Amylose Cornstarch in Rats Fed a High-Cholesterol Diet

The effects of four cornstarches containing various contents of resistant starch on serum and liver cholesterol levels in rats fed a high-cholesterol diet were investigated. Male Sprague Dawley rats (aged 4 weeks) were divided into four groups (n = 7) and fed high-cholesterol diets containing 15% of cornstarch (CS), heat-moisture-treated CS (HCS), high-amylose CS (HA), or heat-moisture-treated HA (HHA) for 21 days. The results showed that the serum and hepatic level of total cholesterol, LDL-cholesterol, and triglyceride in rats of the HHA group and their arteriosclerosis index were significantly higher, suggesting that HHA increases the risk of arteriosclerosis under a high-cholesterol dietary condition. No significant between-group differences were noted in the levels of plasma mevalonic acid and hepatic HMG-CoA reductase mRNA, whereas fecal cholesterol excretion was significantly higher in the HHA group, indicating that the elevation of the serum and liver cholesterol levels was not due to the promotion of liver cholesterol synthesis and cholesterol absorption in the intestine.     

Hypolipidemic and Antioxidant Effects of Dietary Curcumin and Capsaicin in Induced Hypercholesterolemic Rats

Health beneficial hypolipidemic and antioxidant influences of dietary spice principles—curcumin, capsaicin alone and in combination included in the diet for 8 weeks were evaluated in induced hypercholesterolemic rats, in order to verify if there is any additive or synergistic effect of these two bioactive compounds. Dietary curcumin (0.2%), capsaicin (0.015%) or their combination significantly countered the hypercholesterolemia brought about by high cholesterol feeding. Hepatic cholesterol was lowered by dietary spice principles only in normal rats. Liver triglyceride levels were lowered in both normal and hypercholesterolemic rats by capsaicin. Curcumin and capsaicin lowered hepatic and blood lipid peroxides in hypercholesterolemic rats, while the effect in blood was additive with their combination. Hepatic ascorbic acid was enhanced by dietary spice principles in normal rats; glutathione was enhanced by their combination only in hypercholesterolemic rats. Activities of serum glutathione reductase, glutathione transferase and catalase and hepatic glutathione reductase in normal rats and serum glutathione peroxidase in hypercholesterolemic rats were enhanced by dietary spice principles. While dietary curcumin and capsaicin normalized the changes in the levels of antioxidant molecules and activities of antioxidant enzymes to a significant extent, this effect was not generally additive when given in combination, and was higher than the individual effects only in a few instances.     

The effect of feeding di-(2-ethylhexyl) phthalate (DEHP) on the lipid metabolism of laying hens

Di-(2-ethylhexyl)phthalate (DEHP), a commonly used plasticizer, is now seen as an environmental pollutant. DEHP has been found to inhibit lipid and sterol synthesis in rats and mice. The effects of DEHP on various aspects of lipid metabolism were examined in chickens. White Leghorn laying hens were fed either a standard laying mash control diet (C) or the control diet containing 1% DEHP (DEHP) or 1% DEHP and 5% tallow (DEHP-T) for 28 days. DEHP and DEHP-T lowered feed consumption 10% but did not significantly affect body weight. After 3 weeks on the diets, egg production was 15–20% less in DEHP-T than in C and DEHP hens. No differences were observed in egg weight, percent shell, white or yolk among the groups. DEHP and DEHP-T did not alter egg lipid or egg cholesterol concentrations. DEHP and DEHP-T lowered plasma lipid concentration about 20% and free and total cholesterol 20–30%. Liver weights increased, being 30, 34 and 39 g for C, DEHP and DEHP-T hens, respectively, after 28 days. Total liver lipid and cholesterol increased 19% and 26% in DEHP hens and 54% and 79% in DEHP-T hens when compared to controls. In contrast, the fat content of pectoralis major muscle decreased significantly in DEHP and DEHP-T hens. These results, in showing that DEHP alters plasma and tissue cholesterol but not yolk cholesterol, demonstrate again that egg cholesterol is remarkably resistant to alteration by dietary means.     

Effect of dietary fat on phospholipid class distribution and fatty acid composition in rat fat cell plasma membrane

The effect of dietary fats on phospholipid class distribution and fatty acid composition was studied in rat fat cell plasma membrane. Three groups of male Wistar weanling rats were fed for 8 wk three diets differing in the amount and nature of the fats: 1.5% sunflower oil (low fat control; LFC), 10% sunflower oil (high fat, unsaturated; HFU), 1.5% sunflower oil+8.5% cocoa butter (high fat, saturated; HFS). Plasma membranes were prepared from epididymal adipocytes. The amount and type of dietary fat significantly altered membrane phospholipid distribution. Phospholipid content was lowered with HFU as compared to LFC or HFS diets, but no changes were observed for cholesterol. Phosphatidylinositol (PI) and phosphatidylserine (PS) were less affected by dietary changes than were other phospholipid classes. Major changes were detected for phosphatidylcholine (PC), phosphatidylethanolamine (PE) and sphingomyelin (SM) contents. No large changes in PC and PE fatty acid compositions were observed between the LFC and HFS groups, but the HFU diet induced several changes. Correlations with plasma membrane 5′-nucleotidase activities are discussed.     

Changes in lipids in liver and serum of rats fed a histidine-excess diet or cholesterol-supplemented diets

The influence of dietary excess (5%) L-histidine on serum and liver lipids was examined in rats. Feeding a histidine-excess diet for 3, 6, 14 or 30 days caused growth retardation, hepatomegaly and decreased liver lipids throughout the period of the experiment. Hypercholesterolemia was observed after feeding a histidine-excess diet for 6 days; then serum cholesterol continuously increased for 30 days. Serum triglyceride on day 30 in rats fed the histidine-excess diet showed a significant decrease compared to rats fed the basal diet. Serum phospholipids of rats fed the histidine-excess diet for 7 or 14 days showed a significant increase compared to rats fed the basal diet. When rats were fed a basal, histidine-excess or cholesterol-supplemented diet (0.5% and 1.0% cholesterol) for 6 days, the distribution of serum high density (HDL), low density (LDL) and very low density lipoprotein cholesterol in rats fed the histidine-excess diet was similar to that of rats fed the basal diet, whereas LDL-cholesterol increased and HDL-cholesterol decreased in rats fed the cholesterol-supplemented diet.     

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.     

Effect of age and dietary fat (fish,corn and coconut oils) on tocopherol status of C57BL/6Nia mice

The effect of age and dietary fat type on tocopherol status was investigated using young and old C57BL/6Nia mice fed semipurified diets containing 5% (by weight) fish, corn or coconut oils and supplemented with 30, 100 or 500 ppm dl-α-tocopheryl acetate for 6 wk. Tocopherol levels in the diets, plasma, liver, kidney and lung were measured by high performance liquid chromatography following appropriate extractions. The results indicate that mice fed fish oil maintain lower plasma and tissue tocopherol concentrations than those fed corn and cononut oils (fish<corn oil<coconut oil). The difference was not due to a loss of tocopherol prior to consumption, but rather appeared to occur during the absorption process. Old mice had lower plasma and liver tocopherol concentrations than young mice. Old mice fed fish oil, however, maintained plasma tocopherol levels better than young mice fed fish oil, presumably due to their larger tocopherol pool. No age effect was detected on kidney and lung tocopherol levels. It is concluded that tocopherol status is affected by age and dietary fat type, especially fish oil.     

Screw pressing of whole and dehulled flaxseed for organic oil

Flaxseed oil, a rich source of dietary n−3 FA, is commonly obtained by cold pressing whole seed. Furthermore, flaxseed hulls are emerging as a valuable lignan-rich product for functional food use; therefore, the pressing characteristics of dehulled seed need to be understood. Screw press performance was measured for pressing of whole and dehulled flaxseed. When whole Omega flaxseed was pressed through a 6-mm choke, an inverse relationship between seed moisture content (6.1–11.6% range) and oil recovery (70.1–85.7%) was observed. However, peak oil recovery from pressing dehulled Omega flaxseed of 72.0% was found at 10.5% moisture content in the moisture content range of 7.7–11.2%. Although oil recovery from dehulled Omega flaxseed was lower than from whole Omega flaxseed, the weight of oil produced from dehulled Omega flaxseed per unit time was higher. The dependence of capacity on moisture content was less evident with the 6-mm choke than with the 8-mm choke. An inverse relationship between moisture content of whole flaxseed and oil and meal temperature was observed. The oil and meal temperatures from pressing dehulled flaxseed were significantly lower than those from whole flaxseed. Therefore, pressing dehulled flaxseed appears to offer advantages in organic flaxseed oil production.     

Effect of dietary fat upon aflatoxicosis in rats fed torula yeast containing diet

This study was designed to study the possible interrelationships between Torula yeast, vitamin E, and the dietary fat source on aflatoxin-induced tumors. Rats were fed Torula yeast-containing basal diets which included 1.7 ppm aflatoxin B₁ with either lard, corn oil or no fat, and with or without vitamin E supplements for 3 months. Thereafter, the respective diets without aflatoxin were fed for ca. 9 months. Animals receiving the vitamin E-deficient diets had a high mortality. Although the vitamin E-deficient, aflatoxin-treated rats had lower wt gains than did the vitamin E-deficient controls, they lived twice as long. In addition, regardless of the dietary fat source, the kidneys and adrenals of these vitamin E-deficient, aflatoxin-supplemented rats were found to be significantly heavier than the controls, and plasma cholesterol levels were elevated. Increased amounts of liver lipid were observed in response to aflatoxin in both corn oil-fed and fat-deficient rats. No such differences were observed in the responses of the vitamin E-supplemented groups to aflatoxin. On the corn oil diet, aflatoxin administration resulted in an increased deposition of polyunsaturated fatty acids in cholesteryl ester and phospholipid fractions in livers of vitamin E-deficient rats and the phospholipid fraction of vitamin E-sufficient rats. The vitamin E-deficient rats exhibited necrosis of the liver, which was alleviated when aflatoxin was included in the diet, and calcification of the kidneys, which was potentiated by the dietary aflatoxin. No tumors were observed in these animals. In animals maintained on vitamin E-sufficient diets for 1 year, growth was depressed as a result of aflatoxin administration with the greatest depression occurring in the group fed corn oil. Spleen wt were decreased in all groups given aflatoxin. However, there were no changes in either plasma or liver cholesterol or total liver lipids which could be attributed to aflatoxin administration. When aflatoxin was fed with lard, the cholesteryl ester, triglyceride, and free fatty acid fractions of plasma had decreased amounts of the C20:4 acid. In the cholesteryl ester fraction only, this change was accompanied by increased levels of C16:0, C18:0, and C18:1 acids. In the liver phospholipids, there were increased levels of mono- and polyunsaturated fatty acids and decreases in the saturated fatty acids. All of the animals receiving aflatoxin exhibited severe necrosis and tumor formation in the kidneys; the animals fed lard had the highest level of involvement and those in the fat-free group the least. Liver pathology was the least marked among the rats fed the fat-free diet. Since aflatoxin-induced tumors are rich in lipids, the fat-free diet may be protective to the animal.     

Stimulation of lipid absorption in young rats by cholesterol: Early time changes and effects on pentobarbital sleeping time

Four groups of young male and female rats were fed a chow diet (0), chow plus 10% corn oil (F), chow plus 1% cholesterol (C), or chow plus 1% cholesterol plus 10% corn oil (CF) for 1, 2, 4 and 8 days. After 2 dats, male F, C and CF rats exhibited a shorter anesthesia period (−20 to −30%) when given pentobarbital. By 4 days, male F and C rats had pentobarbital sleeping times (PB-ST) 20% less than 0 rats. These effects were additive and CF rats had 40% shorter PB-ST. Reduction of PB-ST by cholesterol and corn oil was similar but slightly less in female rats. Liver lipid content doubled in 4 days in CF rats, and liver cholesterol was 4 times that of 0 rats. These changes and the increases in metabolism of barbiturate suggested changes in liver microsomal enzyme activities. Serum glutamic oxaloacetic and glutamic pyruvic transaminase, two enzymes reflective of liver damage, did not increase after 8 days on C, F or CF diets. Our results suggest that consumption of an animal sterol and a high lipid diet by laboratory rats, normally consuming a diet low in fat (3–4%), increases the ability of the animal to detoxify a barbiturate. Storage of absorbed dietary cholesterol in the liver may represent a major mechanism for maintaining extra hepatic cholesterol homeostasis.