The effect of different proportions of casein in semipurified diets on the concentration of serum cholesterol and the lipoprotein composition in rabbits

The effect of different proportions of casein in semipurified diets on the concentation of serum cholesterol and the lipoprotein composition was studied in rabbits. Low-casein diets (10% w/w) resulted in serum cholesterol levels and growth rates that were lower than high-casein diets (40%). An intermediate proportion of casein (20%) produced intermediate concentrations ofserum cholesterol, but only minor differences in food intake and weight gain, compared with the high-casein group. In the animals with the highest values of total serum cholesterol (the 40% casein group), most of the serum cholesterol was transported in the very low density lipoproteins, whereas with moderate hypercholesterolemia (the 20% casein group), the low density lipoproteins were the main carriers of cholesterol. Elevation in lipoprotein cholesterol was associated in all groups with an increased ratio of cholesterol to protein, suggesting the formation of particles relatively rich in cholesterol. When the rabbits on the diet containing 10% casein were subsequently transferred to the 40% casein diet, a steep increase in the level of serum cholesterol occurred. Conversely, switching the rabbits on the 40% casein diet to the 10% casein diet resulted in a decrease in the level of serum cholesterol.     

Plasma high density lipoprotein subgroup distribution in rats fed diets with varying amounts of sucrose and sunflower oil

The effect of varying the dietary sunflower oil/sucrose (SO/SU) ratio on rat plasma lipid concentration and lipoprotein distribution was studied. Four groups of 10 rats were fed for 4 weeks diets with varying SO/SU ratios. Lipoprotein components were then estimated in whole plasma and after cumulative density ultracentrifugation. Whole plasma triacylglycerol (TG), total cholesterol (TC) and free cholesterol (FC) decreased with increasing SO/SU ratio; the CE/FC ratio increased, because CE remained virtually unaltered. Plasma TG-lowering was due to a decrease in VLDL and LDL-TG. Protein, CE and FC in d=1.063–1.100 g/ml (HDL_2b) and d=1.100–1.125 g/ml (HDL_2a) lipoproteins decreased upon increasing the SO/SU ratio. In contrast, in d=1.125–1.200 g/ml (HDL₃) lipoproteins, there was a concomitant increase in these components. Although increasing the SO/SU ratio effected more protein and CE transportation in HDL₃ and less in HDL₂, the total amount of these components in high density lipoproteins (d=1.063–1.200 g/ml) remained constant. Apo A-I and apo C-III decreased in HDL₂ but increased in HDL₃ upon increasing the SO/SU ratio. Also, HDL₂ apo E, and the apo C-II/apo C-III and small apo B/large apo B ratios in VLDL and LDL were lowered by increasing the SO/SU ratio. The hepatic VLDL-TG output during isolated liver perfusion was lowest in rats fed the diet with the highest SO/SU ratio. In perfusate, like in plasma, the VLDL and LDL apo C-II/apo C-III ratio, as well as the small apo B/large apo B ratio, decreased upon increasing the dietary SO/SU ratio. The results indicate that there can be appreciable diet-dependent variations in plasma HDL subgroup distribution in spite of unchanged total HDL levels.     

Oxidative susceptibility of low density lipoprotein from rabbits fed atherogenic diets containing coconut,palm, or soybean oils

The oxidative susceptibilities of low density lipoproteins (LDL) isolated from rabbits fed high-fat atherogenic diets containing coconut, palm, or soybean oils were investigated. New Zealand white rabbits were fed atherogenic semisynthetic diets containing 0.5% cholesterol and either (i) 13% coconut oil and 2% corn oil (CNO), (ii) 15% refined, bleached, and deodorized palm olein (RBDPO), (iii) 15% crude palm olein (CPO), (iv) 15% soybean oil (SO), or (v) 15% refined, bleached, and deodorized palm olein without cholesterol supplementation [RBDPO(wc)], for a period of twelve weeks. Total fatty acid compositions of the plasma and LDL were found to be modulated (but not too drastically) by the nature of the dietary fats. Cholesterol supplementation significantly increased the plasma level of vitamin E and effectively altered the plasma composition of long-chain fatty acids in favor of increasing oleic acid. Oxidative susceptibilities of LDL samples were determined by Cu²⁺-catalyzed oxidation which provide the lag times and lag-phase slopes. The plasma LDL from all palm oil diets [RBDPO, CPO, and RBDPO(wc)] were shown to be equally resistant to the oxidation, and the LDL from SO-fed rabbits were most susceptible, followed by the LDL from the CNO-fed rabbits. These results reflect a relationship between the oxidative susceptibility of LDL due to a combination of the levels of polyun-saturated fatty acids and vitamin E. Based on a paper presented at the PORIM International Palm Oil Congress (PIPOC) held in Kuala Lumpur, Malaysia, 1993.     

Serum lipoproteins of rabbits fed semi-purified diets varying in protein and carbohydrate source

The effect of dietary protein and carbohydrate type on the composition and properties of serum lipoproteins in rabbits was studied. The animals were pair-fed either casein-sucrose and soy protein-sucrose or casein-dextrose and soy protein-dextrose-containing low fat, low cholesterol, semi-purified diets for 84 days. Main effects due to protein and carbohydrate type were observed to be altered lipoprotein class compositions. These effects were due primarily to the presence of casein which resulted in cholesterol-rich, triglyceride-poor lipoproteins among all isolated classes. Increases in serum low and high density lipoprotein cholesterol and protein concentrations, as well as lipoprotein total mass, were also observed with casein feeding. Carbohydrate effects due to dietary sucrose were elevated high density lipoprotein phospholipid and protein concentrations, independent of protein source. When casein was included, sucrose-containing diets resulted in increased intermediate density lipoprotein cholesterol; when soy protein was used, low density lipoprotein cholesterol elevations were observed. Dietary interactions were also found especially between casein and sucrose, resulting in increased intermediate lipoprotein mass and total lipoprotein concentrations. Comparisons of lipoprotein class particle size among rabbits indicated similar particle diameters among animals in all dietary groups. Evidence that casein feeding caused increased lipoprotein particle number in addition to compositional differences was obtained. It was concluded that lipoprotein structure within a given class is maintained in spite of compositional variations due to dietary protein or carbohydrate source.     

Plasma and lipoprotein lipid peroxidation in humans on sunflower and rapessed oil diets

The effects of natural mixed diets on lipid peroxidation were investigated in humans. In the first study, 59 subjects were fed a rapeseed oil-based diet rich in monounsaturated fatty acids (MUFA) and a sunflower oil-based diet rich in polyunsaturated fatty acids (PUFA) in a cross-over manner for three and a half weeks. The lipid peroxidation products in plasma were determined by measuring conjugated dienes and malondialdehyde (MDA). In a second study, plasma thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides, and the susceptibility of very low density lipoprotein + low-density lipoprotein (LDL) toin vitro oxidation were measured from subjects fed similar MUFA and PUFA diets for six week diets. No significant differences in plasma MDA or conjugated diene concentrations were found after the rapeseed oil diet or the sunflower oil diet in Study 1. In the second study, a small but significant decrease (P<0.05) in both lipid hydroperoxides and TBARS was observed in the LDL fraction after the sunflower oil diet. Thein vitro oxidation gave opposite results, showing increased oxidation after the sunflower oil diet. Despite a high intake of α-tocopherol during the oil peroids, no increase in plasma α-tocopherol was noticed in either study. The results suggest that moderate changes in the fatty acid composition in the Western-type diet may be adequate to affect lipoprotein susceptibility to oxidationin vitro, but there is considerable disparity with some indices ofin vivo lipid peroxidation.     

Hematological and lipid changes in newborn piglets fed milk-replacer diets containing erucic acid

Canola oil is not presently permitted in infant formulations in the United States because of lack of information concenring the effects of feeding canola oil to the newborn. We have previously reported a transient decrease in platelet counts and an increase in platelet size in newborn piglets fed canola oil for 4 wk, and have confirmed this in the present study. In canola oil-fed piglets, changes in platelet size and number were overcome by adding either long-chain saturated fatty acids from cocoa butter (16:0 and 18:0), or shorter-chain saturates from coconut oil (12:0 and 14:0). Feeding a high erucic acid rapeseed (HEAR) oil, with 20% 22:1n−9, led to an even greater platelet reduction and increased platelet size throughout the 4-wk trial. Bleeding times were longer in piglets fed canola oil or HEAR oil compared to sow-reared and soybean oil-fed piglets. There were no other diet-related changes. Diet-induced platelet changes were not related to platelet lipid class composition, but there were fatty acid changes. The incorporation of 22:1n−9 into platelet phospholipids of piglets fed canola oil was low (0.2–1.2%), and even for the HEAR oil group ranged from only 0.2% in phosphatidylinositol to 2.4% in phosphatidylserine. A much greater change was observed in the concentration of 24:1n−9 and in the 24:1n−9/24:0 ratio in platelet sphingomyelin (SM). The 24:1n−9 increased to 49% in the HEAR oil group compared to about 12% in animals fed the control diets (sow-reared piglets and soybean oil-fed group), while the 24:1n−9/24:0 ratio increased from about 1 to 12. Even feeding canola oil, prepared to contain 2% 22:1n−9, led to a marked increase in 24:1n−9 to 29% and had a 24:1n−9/24:0 ratio of 5. The canola oil/cocoa butter group, which also contained 2% 22:1n−9, showed a lower level of 24:1n−9 (20%) and the 24:1n−9/24:0 ratio (3) compared to the canola oil group. The results suggest that the diet-related platelet changes in newborn piglets may be related to an increase in 24:1n−9 in platelet SM, resulting from chain elongation of 22:1n−9. The inclusion of canola oil as the sole source of fat in the milk-replacer diets of newborn piglets resulted in significant platelet and lipid changes.     

Plasma esterase-1 (ES-1) activity is increased in rats fed high-fat diets

The question addressed is whether the amount and type of dietary fat affects esterases in plasma. Rats were fed semipurified diets containing 2.0 to 19.4% (w/w) of fat in the form of coconut fat or corn oil. Fat was added to the diets at the expense of isocaloric amounts of carbohydrates. Plasma total esterase activities measured with 4-nitrophenylacetate as substrate were slightly increased with increasing fat intakes. However, an increase in fat concentration of the diet was associated with a pronounced increase in the activity of the so-called ES-1 isozyme in plasma. ES-1, which represents very little plasma total esterase activity, was quantified densitometrically as the high-mobility, anodal esterase band on polyacrylamide gel electrophoresis. The positive association between amount of dietary fat and ES-1 activity was identical for coconut fat and corn oil.     

Short-Term changes in hepatic HMG-CoA reductase in rats fed diets containing cholesterol or oat bran

In vivo regulation of hepatic HMG-CoA reductase (HMGR) (mevalonate: NADP⁺ oxidoreductase [acylating CoA]; EC 1.1.1.34] by phosphorylation/dephosphorylation has not been demonstrated. Rats were meal-fed semipurified diets; effects of inclusion of cholesterol (2%) or oat bran (15%) in a single meal on expressed (phosphorylated) and total (dephosphorylated) activities of HMGR were measured from 15 min to 4 hr after presentation of the meal. Expressed activity was not significantly altered in response to the control diet during the time periods examined, while total HMGR activity declined by 15 min and increased through 4 hr to an activity about 1.5 times control levels. Addition of cholesterol resulted in little change in expressed activity but a greater and more sustained reduction in total activity. Oat bran caused reductions in both total and expressed activities, which were maintained through 4 hr. Total HMGR activity was best correlated with apparent demand for cholesterol synthesis.     

l-Carnitine effects on chemical composition of plasma lipoproteins of rabbits fed with normal and high cholesterol diets

l-Carnitine plays an important role in the mitochondrial uptake of long-chain fatty acids in mammals. It has recently been shown that this compound has a marked hypo-cholesterolemic effect when used in conjunction with lipid-rich diets. The aim of this study was to investigate the effects of l-carnitine on the fatty acid composition of plasma lipoproteins in rabbits fed with different diets. Four different groups were investigated: group I (standard diet), group II (standard diet supplemented with l-carnitine at 80 mg/kg), group III (standard diet supplemented with 0.5% cholesterol), and group IV (standard diet supplemented with 0.5% cholesterol plus l-carnitine at 80 mg/kg). The feeding period was 126 d. Total plasma cholesterol was indistinguishable in groups I and II, but increased nearly 40-fold in group III. This increment was reduced by 50% in group IV. Correspondingly, total cholesterol content in lipoprotein fractions [very low density lipoprotein (VLDL), low density lipoprotein (LDL), high density lipoprotein (HDL) separated by agarose gel chromatography was the same for groups I and II, while for animals fed a cholesterol-rich diet (III) total cholesterol in VLDL+LDL increased nearly 100-fold when compared with groups I and II but, again, the increment was reduced by 50% in group IV. In contrast, total cholesterol in HDL increased only fivefold for both groups III and IV when compared with groups I and II, indicating no effects of l-carnitine on this parameter. The reduction of total cholesterol in VLDL+LDL particles in animals fed a cholesterol-rich diet plus l-carnitine was associated with a marked decrease in the ratio of cholesteryl ester to free cholesterol and a dramatic increase in their phospholipid content; opposite effects were observed for HDL. l-Carnitine induced a marked decrease in the saturated to unsaturated C₁₆+C₁₈ fatty acid ratio in cholesteryl esters associated with VLDL and LDL from animals fed with both normal and cholesterol-rich diets. The opposite effect (a large increase in the saturated to unsaturated fatty acid ratio) was observed for both cholesteryl esters and phospholipids associated with HDL in animals fed with both diets. The results suggested that the hypocholesterolemic effects of l-carnitine could be associated with increased systemic breakdown of cholesteryl esters, a probable increase in reverse cholesterol transport, and the stabilization of a phospholipid-based structure of VLDL+LDL particles.     

Very low density lipoprotein secretion by cultured hepatocytes of rabbits fed purified or autoxidized cholesterol

The main objectives of this study were to compare the effects of dietary commercial cholesterol (containing 5% of oxidized cholesterol derivatives) and purified cholesterol on the secretion rate of very low density lipoprotein apolipoproteins and lipids by cultured rabbit hepatocytes and to verify the hypothesis that products of cholesterol autoxidation stimulate the rapid development of hypercholesterolemia. Rabbits fed dietary (old) commercial cholesterol for six weeks showed a fivefold increase in the serum concentration of cholesterol compared with that in purified cholesterol-fed rabbits. The secretion rates of very low density lipoprotein total protein and very low density lipoprotein [³H]apolipoproteins were similar for the hepatocytes of these two cholesterol-fed groups of animals and were two- and threefold greater, respectively, than for cells from control rabbits. Cholesteryl ester content of the hepatocytes from dietary (old) commercial cholesterol-fed rabbits was dramatically increased in comparison with hepatocytes from control and purified cholesterol-fed rabbits. The elevated intracellular cholesteryl ester content is assumed to account for such an increase of very low density lipoprotein-cholesteryl ester secretion by cells prepared from dietary (old) commercial cholesterol-fed rabbits. These effects appear to be caused by activation of cholesterol esterification by oxidized cholesterol derivatives. The rapid development of hypercholesterolemia induced by dietary (old) commercial cholesterol is associated, at least in part, with the stimulated production of hepatic very low density lipoprotein apolipoproteins and cholesteryl esters.     

Hypercholesterolemia in rats fed cholesterol in agar gel diets

Female (Exp. I) or male (Exp. II) weanling rats were fed diets containing either 2% Solka-Floc or 2% agar for 28-day periods. Some groups received 1% cholesterol, either added in crystalline form or first dispersed in the oil portion of the diet, and some agar groups received their diet in a gelled form. Feces were collected for a 3-day period after 2 weeks (Exp. II) or during the fourth week (Exp. I) of experimentation. Serum and liver cholesterol, total liver lipids, fecal lipids, and fecal sterols were determined. The results indicated that cholesterol feeding increased serum cholesterol, total liver, and fecal lipids, liver cholesterol, and fecal sterols. Substitution of agar for Solka-Floc in dry (nongelled) diets further increased total liver lipids (Exp. I), but had no significant effect upon any other measured parameter. Gelling of 1% cholesterol agar diets, in contrast to the 1% cholesterol dry agar diet, resulted in reduced liver cholesterol in both experiments. Gelling significantly increased fecal sterols after 2 weeks feeding (Exp. II), but no significant differences were observed after 4 weeks feeding (Exp. I) when compared to 1% cholesterol-fed groups. Small, nonsignificant increases of liver cholesterol and total liver lipids with similar reduction of fecal sterols resulted from dispersing the cholesterol in the oil portion of the diet prior to mixing. The results indicate that (a) inclusion of 2% agar in rat diets and (b) dispersing cholesterol in oil had little effect upon serum, liver, or fecal lipids in cholesterol-fed rats. However, gelling the agar diets reduced liver cholesterol, possibly by initial reduction of dietary cholesterol absorption.     

Mammary tumorigenesis in rats fed diets high in lard

Studies were performed to examine the effect of a lard diet on tumorigenesis by 7,12-dimethylbenzanthracene (DMBA), given parenterally rather than by gavage, to eliminate any effect of the high lard diet on carcinogen absorption. In addition, the effect of low dietary levels of the antioxidants butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) in the tumor model was evaluated. The lards fed were analyzed for fatty acid composition and content of certain potential contaminants. DMBA induced tumors when given by intravenous or subcutaneous injection. The high lard diet appeared to enhance tumorigenesis in rats given a dose of 0.25 mg (10% of the gavage dose) by injection into the mammary gland, although the effect was not statistically significant. In other experiments using lard from different sources and DMBA given by gavage, significant enhancement of tumorigenesis was limited to groups fed the high lard diets throughout the experiment or beginning after DMBA exposure. In contrast to earlier results, there was no demonstrable effect of feeding the high lard diets before DMBA administration. Addition of BHA and BHT to the lard at the concentration assayed in commercial lard samples or at the maximum concentration permitted did not influence the tumorigenesis. In groups in which tumorigenesis was enhanced by the high lard diet, the incidence of malignant, invasive tumors was higher than in other groups.     

Atherogenesis in swine fed several types of lipid-cholesterol diets

Eighteen-month-old Nebraska strain minipigs were fed diets containing 2% cholesterol and 20% corn oil, lard, or coconut oil for 12 to 18 months. Concentrations of serum total lipid, total cholesterol, and total phospholipid increased 200 to 300% with each diet. Changes in serum concentrations of S_f 20+ and S_f 0–20 lipoproteins varied with diets fed. Serum concentration of high density lipoprotein was increased in all cases. Intima concentration of S_f 0–20 lipoprotein fraction was elevated by feeding the corn oil diet. There was no development of atherosclerosis as a result of feeding the corn oil-cholesterol diet, but there was an increase in atherosclerosis as a result of feeding the lard or coconut oil diet. There were no correlations between fatty acid patterns of several lipid fractions from serum and corresponding lipid fractions from aortic intima of corn oil fed animals. Deceased.     

Liver lipid alterations in rats fed arginine deficient diets

Arginine deficiency is associated with a marked increase in liver lipids in the rat. Triglyceride accumulation accounts for most of the fatty infiltration. Cholesterol concentration per gram of liver increased approximately 280% above control rats receiving dietary arginine. The percentage of phospholipids was significantly decreased in the arginine-deficient rat liver compared to controls. The fatty acid composition revealed a significant reduction in the percentage of palmitic, palmitoleic, oleic, and linoleic acids. However, both stearic and arachidonic acids were increased approximately 250 and 160%, respectively, in arginine-deficient livers compared to controls. Arginine deficiency in the rat causes a marked alteration in lipid metabolism similar to that observed with orotic acid feeding. The similarities of arginine deficiency and orotic acid feeding are discussed.     

Myocardial changes in newborn piglets fed sow milk or milk replacer diets containing different levels of erucic acid

This study was undertaken to determine whether the neonate was more susceptible to the effects of dietary erucic acid (22∶1n−9) than the adult. Newborn piglets were used to assess the safety of different levels of 22∶1n−9 on lipid and histological changes in the heart. Newborn piglets showed no myocardial lipidosis as assessed by oil red 0 staining, but lipidosis appeared with consumption of sow milk and disappeared by seven days of age. Milk replacer diets containing soybean oil, or rapeseed oil mixtures with up to 5% 22∶1n−9 in the oil, or 1.25% in the diet, gave trace myocardial lipidosis. Rapeseed oil mixtures with 7 to 42.9% 22∶1n−9 showed definite myocardial lipidosis in newborn piglets, which correlated to dietary 22∶1n−9, showing a maximum after one week on diet. The severity of the lipidosis was greater than observed previously with weaned pigs. There were no significant differences among diets in cardiac lipid classes except for triacylglycerol (TAG), which increased in piglets fed a repeseed oil with 42.9% 22∶1n−9. TAG showed the highest incorporation of 22∶1n−9, the concentration of 22∶1n−9 in TAG was similar to that present in the dietary oil. Among the cardiac phospholipids, sphingomyelin and phosphatidylserine had the highest, and diphosphatidylglycerol (DPG) the lowest level of 22∶1n−9. The low content of 22∶1n−9 in DPG of newborn piglets is not observed in weaned pigs and rats fed high erucic acid rapeseed oil. The relative concentration of saturated fatty acids was lowered in all cardiac phospholipids of piglets fed rapeseed oils, possibly due to the low content of saturated fatty acids in rapeseed oils. The results suggest that piglets fed up to 750 mg 22∶1n−9/kg body weight/day showed no adverse nutritional or cardiac effects.     

Growth, development and dental caries in rats fed two experimental diets

In order to determine the nutritional adequacy of diets MIT 200 and NIH 2000 on the growth and development of experimental animals, these two diets were fed to two groups of animals during three periods of development: 1) pregnancy; 2) lactation, and 3) post-weaning. These diets were compared with a diet that satisfied the requirements of the National Research Council for growth and maintenance. It was found that for the two experimental diets, growth was compromised due to a caloric deficit in both diets. In addition, NIH 2000 was deficient in other nutrients such as iron. Analysis of other parameters such as hemoglobin, hematocrit, salivary protein, saliva flow and weight of vital organs upon autopsy revealed a picture of iron deficiency in the NIH 2000 group. Caries formation can be precipitated by a mechanism influenced by a nutrient deficit.     

Plasma cholesterol levels in suckling and weaned kittens,puppies, and guinea pigs

Plasma cholesterol levels in kittens and puppies were low at birth, rose during the suckling period, and then decreased at about the time of weaning. The increase during the suckling period was much greater in puppies than in kittens. No significant differences in plasma cholesterol levels were observed in puppies fed two different types of diet, horse meat or dog chow, after weaning. Guinea pigs had lower plasma cholesterols than either kittens or puppies. The level was highest on the first day after birth, decreased during the next 3 wk, and then remained fairly constant after the animals were weaned.     

Plasma cholesterol levels in suckling and weaned calves,lambs, pigs and colts

Plasma cholesterol levels were determined in calves, lambs, and pigs at intervals from birth until after weaning. In each case the levels were low at birth, became elevated during the suckling period, and decreased as the animals began to eat solid feed. Results with calves fed skim milk indicated that milk lipids were largely responsible for the post-partum elevation of plasma cholesterol levels. Studies with early and late weaned pigs also indicated that the elevation of plasma cholesterol in suckling animals was related to diet rather than age. Sex and breed had no apparent effect on plasma cholesterol levels in these experiments. A limited number of observations in colts indicated that plasma cholesterol levels decreased between 2 and 7 months.     

Reduction of hepatic stearoyl-CoA desaturase activity in rats fed iron-deficient diets

The effect of feeding iron-deficient diets to rats on the hepatic stearoyl-CoA desaturase activity was examined since iron is present in the Δ9 desaturation system. Separate groups of rats were fed low iron diets without fat (FF-Fe) or containing either 14% hydrogenated coconut oil (HCNO-Fe) or 14% corn oil (CO-Fe) for 10 weeks. Diets supplemented with iron (FF+Fe, HCNO+Fe and CO+Fe) were fed to the corresponding control groups. Stearoyl-CoA desaturase activity in the liver microsomes of rats in the CO+Fe group (2.55±0.17 nmol oleate produced/min/mg protein) was about half of that in the HCNO+Fe (4.76±0.15) and FF+Fe (5.38±0.18) diet groups. In rats which were fed iron-deficient diets, hepatic desaturase levels were reduced significantly as compared to those of controls (1.0±0.06, CO-Fe; 2.11±0.13, HCNO-Fe; 3.65±0.1, FF-Fe). The hemoglobin (Hb) and hematocrit (Hct) levels in blood showed moderate iron depletion only in the CO-Fe group. Hence, dietary polyunsaturated fat promotes the onset of iron deficiency. Furthermore, even before the blood Hb and Hct values express iron depletion, the effect of feeding low iron diets was observed by the reduction of hepatic Δ9 desaturase activity in rats fed HCNO-Fe and FF-Fe diets.     

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.