Influence of dietary fats and vitamin e on plasma and hepatic vitamin a and β‐carotene levels in rats fed excess β‐carotene

Effects of different dietary lipids and excess vitamin E on plasma and hepatic concentrations of β‐carotene were evaluated in rats fed diets containing a large excess (0.2%) of β‐carotene. Male weanling Wistar Kyoto rats were fed β‐carotene‐supplemented diets containing various dietary lipids as follows: Group I, a saturated fat (coconut oil); Group II, a monounsaturated fat (olive oil); Group III, a polyunsaturated fat rich in ω‐6 fatty acids (safflower oil); Group IV, same as Group III plus vitamin E; and Group V, a polyunsaturated fat rich in ω‐3 fatty acids (menhaden oil). All diets contained 2% saf flower oil to provide sufficient amounts of linoleic acid (an essential fatty acid). Rats were killed after six weeks of feeding the various diets, and the concentrations of Q‐carotene and vitamin A were determined in plasma and liver. Plasma vitamin A levels were not altered by any of the dietary lipids or by an excess of vitamin E. The concentrations of β‐carotene in plasma were the lowest in rats fed the diet containing menhaden oil. The feeding of the diet containing an excess of vitamin E also resulted in a significant decrease in plasma β‐carotene concentration. Similarly, the hepatic β‐carotene concentration was also reduced to about one‐half in rats fed the diet containing an excess of vitamin E. Liver β‐carotene concentration was higher in Groups II and III than in the other three dietary groups. Hepatic vitamin A concentrations were also affected by the type of dietary fat. The highest levels were observed in rats fed the coconut oil diet; the lowest level of vitamin A was in rats fed menhaden oil (Group V). The results of this study suggest that the type of dietary fat and an excess of vitamin E can have a significant effect on 0‐carotene and vitamin A stores in liver and on β‐carotene content of plasma.     

Influence of dietary fats and vitamin E on plasma and hepatic vitamin A and beta-carotene levels in rats fed excess beta-carotene

Effects of different dietary lipids and excess vitamin E on plasma and hepatic concentrations of beta-carotene were evaluated in rats fed diets containing a large excess (0.2%) of beta-carotene. Male weanling Wistar Kyoto rats were fed beta-carotene-supplemented diets containing various dietary lipids as follows: Group I, a saturated fat (coconut oil); Group II, a monounsaturated fat (olive oil); Group III, a polyunsaturated fat rich in omega-6 fatty acids (safflower oil); Group IV, same as Group III plus vitamin E; and Group V, a polyunsaturated fat rich in omega-3 fatty acids (menhaden oil). All diets contained 2% safflower oil to provide sufficient amounts of linoleic acid (an essential fatty acid). Rats were killed after six weeks of feeding the various diets, and the concentrations of beta-carotene and vitamin A were determined in plasma and liver. Plasma vitamin A levels were not altered by any of the dietary lipids or by an excess of vitamin E. The concentrations of beta-carotene in plasma were the lowest in rats fed the diet containing menhaden oil. The feeding of the diet containing an excess of vitamin E also resulted in a significant decrease in plasma beta-carotene concentration. Similarly, the hepatic beta-carotene concentration was also reduced to about one-half in rats fed the diet containing an excess of vitamin E. Liver beta-carotene concentration was higher in Groups II and III than in the other three dietary groups. Hepatic vitamin A concentrations were also affected by the type of dietary fat.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of a dietary oxidized fat on cholesterol in plasma and lipoproteins and the susceptibility of low-density lipoproteins to lipid peroxidation in guinea pigs fed diets with different concentrations of vitamins E and C

To investigate the effect of a dietary oxidized fat on the concentrations of cholesterol in liver, plasma, and lipoproteins and the susceptibility of low-density lipoproteins (LDL) to lipid peroxidation, and to explore the effects of vitamins E and C, male guinea pigs were divided into five groups. Four groups were fed diets with an oxidized fat supplemented with 35 or 175 mg alpha-tocopherol equivalents/kg and 300 or 1000 mg of vitamin C/kg for 29 days. One group, used as a control, was fed the same basal diet with fresh fat with 35 mg alpha-tocopherol equivalents/kg and 300 mg of vitamin C/kg. Guinea pigs fed the oxidized-fat diets, irrespective of dietary vitamin E and C concentrations, had significantly lower concentrations of total cholesterol in the liver and a lower concentration of cholesterol in LDL than the control animals fed the fresh fat. According to the lag time before onset of lipid peroxidation, LDL of guinea pigs fed the oxidized-fat diet with 35 mg alpha-tocopherol equivalents and 300 mg vitamin C/kg were significantly more susceptible to copper-induced lipid peroxidation than those of guinea pigs fed the fresh fat diet. Within the groups fed the oxidized fat diets, increasing the dietary vitamin E concentration from 35 to 175 mg/kg significantly (p < 0.05) and increasing the dietary vitamin C concentration from 300 to 1000 mg/kg in tendency (p < 0.10) reduced the susceptibility of LDL to oxidation. LDL of guinea pigs fed the oxidized fat diets with 175 mg alpha-tocopherol equivalents/kg were even more resistant to oxidation than LDL of guinea pigs fed the fresh diet. In conclusion, the study shows that dietary oxidized fat influences the cholesterol metabolism and the susceptibility of LDL to lipid peroxidation; the latter can be modified by dietary vitamins E and C.     

Linoleate enrichment of diet and prostaglandin metabolism in rats.

Evidence that biosynthesis of prostaglandins (PG) in tissues of animals deficient in essential fatty acids is dependent on the availability of their precursors has been demonstrated. The purpose of this study was to determine the following: (1) effects of dietary linoleate enrichment on PG biosynthesis in rats; (2) effects of exogenous PGE2 and dietary linoleate on plasma free fatty acids and serum cholesterol in fed and fasted rats. Rats were fed three different concentrations of dietary linoleate as beef tallow, hydrogenated vegetable fat, or corn oil. The concentrations of PGE1 and PGF2a measured by radioimmunoassay were higher in rats fed the fed the beef tallow diet independent of energy status. A decrease in the concentration of PG between fasted and fed rats receiving hydrogenated vegetable fat is discussed in respect to the possible influence of trans isomers of unsaturated fatty acids on the biosynthesis of PG. There were significant effects of fasting on serum cholesterol concentration regardless of diet and significant interactions among effects of PGE2, fasting, and diet, suggesting regulatory effects of PGE2 on serum cholesterol concentration. The increase in plasma free fatty acids associated with fasting was prevented by PGE2 for all diets, but had the most marked effect on rats fed hydrogenated vegetable fat.     

Comparison of native and capric acid-enriched mustard oil effects on oxidative stress and antioxidant protection in rats

The present study evaluated the effect of mustard oil enriched in capric acid, a medium-chain fatty acid, on antioxidant enzyme activities in liver and brain and on the levels of malondialdehyde (MDA) in liver, brain and plasma in rats; the effect of adding cholesterol to the diet was also investigated. Charles Foster male albino rats weighing 80-100 g were fed one of four diets for 30 d (six rats per group). In the absence of added dietary cholesterol, the addition of capric acid to the diet resulted in lower plasma total cholesterol, non-HDL-cholesterol and TAG concentrations, higher HDL-cholesterol concentrations, higher antioxidant enzyme activities in liver and brain and lower MDA concentrations in liver, brain and plasma. Adding cholesterol to the diet increased plasma total cholesterol, non-HDL-cholesterol and TAG concentrations, decreased HDL-cholesterol concentration, decreased the activities of antioxidant enzymes and increased tissue and plasma MDA concentrations. Including capric acid in the diet of rats receiving cholesterol at least partly prevented the effects of the increased cholesterol. It is concluded that compared with native mustard oil, capric acid-enriched mustard oil improves blood lipids, enhances antioxidant protection and reduces lipid peroxidation.     

Regulation of plasma and liver total cholesterol levels by dietary oleic acid in rats fed a high-cholesterol diet.

The effects of diets containing fats and oils or fatty acids on the lipid metabolism were investigated in male rats of the Wistar strain fed hypercholesterolemic diets, especially focusing our attention on the correlation between dietary oleic acid (OLE) contents and the levels of plasma and liver total cholesterol (T-CHOL) or the fatty acid profiles in plasma and liver CHOL-ester. In the rats fed the free (FR)-type fatty acids, the concentrations of plasma and liver T-CHOL were high and the amounts of neutral steroids excreted into the feces were low when compared with those of rats given the triacylglycerol (TG)-type fatty acids, showing that TG-type fatty acids suppress the intestinal CHOL absorption more than the FR-type fatty acids do. The concentrations of plasma T-CHOL were highest in rats fed the oleic acid (OLE)-rich diets, followed in order by rats supplied with the palmitic acid (PAL)-rich diets, the hydrogenated coconut oil (HCO) diet, and the linoleic acid (LIN)-rich diets; the lowest was in rats given tristearin (TSTE) and linseed oil (LIS) diets. A positive correlation was obtained between the dietary OLE contents and the levels of plasma and liver T-CHOL or OLE in the plasma and liver CHOL-ester, and an inverse correlation between dietary OLE contents and the amounts of excreted neutral steroids. These results suggest that the dietary OLE contents regulate the levels of plasma and liver T-CHOL in CHOL-loaded rats.     

Lipid metabolism responses in rats fed beef tallow, native or randomized fish oil and native or randomized peanut oil

In experiments with male Wistar rats, we measured the effects of nonpurified diets containing 9.1% added fat (beef tallow, native or randomized fish oil, native or randomized peanut oil) on apparent digestibility of total fat and individual fatty acids. We also investigated the effects of the diets on plasma contents of triglyceride, cholesterolesters and free and total cholesterol as well as on the fatty acid profiles of plasma and liver phospholipids. Randomization of fish oil or peanut oil had no significant effect on any of the lipid measurements. Fat digestibility was significantly lower in the rats fed beef tallow. Apparent absorption of 18:1(n-9) and polyunsaturated fatty acids was not dependent on the fatty acid profile of the dietary fat. Apparent absorption of 16:1(n-7) and saturated fatty acids was generally highest in the rats fed fish oil. Intake of fish oil or peanut oil significantly decreased plasma triglyceride content. Intake of fish oil resulted in substantially decreased contents of total cholesterol and cholesterolesters in plasma, but intake of peanut oil did not. Efficiency of conversion of 18:2(n-6) into 20:4(n-6) was inhibited by long-chain (n-3) fatty acids.     

Acute postprandial effect of hydrogenated fish oil, palm oil and lard on plasma cholesterol, triacylglycerol and non-esterified fatty acid metabolism in normocholesterolaemic males

The majority of research has focused on the association between trans unsaturated fatty acids (TUFA) from hydrogenated vegetable oils and heart disease even though TUFA are also produced from hydrogenated fish oil. We compared the acute effect of three solid fats on postprandial cholesterol, triacylglycerol (TAG) and NEFA concentrations in normocholesterolaemic males. Eight healthy male volunteers consumed each of the three 40 g fat meals (partially hydrogenated fish oil (PHFO), palm oil and lard) in random order and blood samples were drawn at 2, 4, 6 and 8 h thereafter for lipid analysis. The postprandial response in plasma TAG, TAG-rich lipoprotein-TAG (TRL-TAG), total cholesterol and plasma NEFA, measured as the area under the postprandial curve, was not significantly different between the three meals (P>0.05), which varied in MUFA, PUFA and TUFA content. There was no marked elevation of longer-chain fatty acids (C20-22, cis or trans isomers) into the TRL-TAG fraction following the PHFO meal even though they provided 40 % of the total fatty acids in the PHFO meal. The postprandial TRL-TAG response to PHFO was expected to be higher, as it is higher in TUFA, lower in PUFA and similar in saturated fatty acid composition compared with the lard and palm oil test meals. The absence of a higher postprandial response following ingestion of PHFO could be as a result of reduced absorption and increased oxidation of long-chain fatty acids (both cis and trans isomers).     

Exchanging partially hydrogenated fat for palmitic acid in the diet increases LDL-cholesterol and endogenous cholesterol synthesis in normocholesterolemic women

Partial hydrogenation of oil results in fats containing unusual isomeric fatty acids characterized by cis and trans configurations. Hydrogenated fats containing trans fatty acids increase plasma total cholesterol (TC) and LDL-cholesterol while depressing HDL-cholesterol levels. Identifying the content of trans fatty acids by food labeling is overshadowed by a reluctance of health authorities to label saturates and trans fatty acids separately. Thus, it is pertinent to compare the effects of trans to saturated fatty acids using stable isotope methodology to establish if the mechanism of increase in TC and LDL-cholesterol is due to the increase in the rate of endogenous synthesis of cholesterol. Ten healthy normocholesterolemic female subjects consumed each of two diets containing approximately 30% of energy as fat for a fourweek period. One diet was high in palmitic acid (10.6% of energy) from palm olein and the other diet exchanged 5.6% of energy as partially hydrogenated fat for palmitic acid. This fat blend resulted in monounsaturated fatty acids decreasing by 4.9 % and polyunsaturated fats increasing by 2.7%. The hydrogenated fat diet treatment provided 3.1% of energy as elaidic acid. For each dietary treatment, the fractional synthesis rates for cholesterol were measured using deuterium-labeling procedures and blood samples were obtained for blood lipid and lipoprotein measurements. Subjects exhibited a higher total cholesterol and LDL-cholesterol level when consuming the diet containing trans fatty acids while also depressing the HDL-cholesterol level. Consuming the partially hydrogenated fat diet treatment increased the fractional synthesis rate of free cholesterol. Consumption of hydrogenated fats containing trans fatty acids in comparison to a mixtur e of palmitic and oleic acids increase plasma cholesterol levels apparently by increasing endogenous synthesis of cholesterol.     

Influence of dietary n-3 polyunsaturated fatty acids on plasma lipemic effect of vitamin B6 deficiency.

Since many connections exist between vitamin B6 and lipid metabolism, we aim to investigate the lipemic effect of different dietary intakes of polyunsaturated fatty acids in rats fed a vitamin B6 deficient diet. Diets were either vitamin B6 deficient (-B6) or vitamin B6 sufficient, pair-fed to the deficient group (PF) and ad libitum (N). The diets were combined with normal lipid (LC: soya bean-coconut-palm oils) and fish oil (FO: soya bean-fish oil). The fish oil diet with sufficient vitamin B6 content caused an increase in n-3 long chain polyunsaturated fatty acids and a decrease in arachidonic acid. In the -B6 group fed a normal lipid diet, the arachidonic acid percentage decreased and the linoleic acid percentage increased; in the -B6 group fed fish oil these changes in fatty acid composition, already consequent upon dietary intake of n-3 long chain polyunsaturated fatty acids, did not show further variations. In the dietary condition of vitamin B6 deficiency, plasma cholesterol content increased in rats fed a lipid control diet, whereas no hypocholesterolemic effect was observed in those fed a fish oil diet. Plasma triglyceride contents were not influenced by dietary lipid quality because, in all conditions, the lower food intake of the PF groups caused a decrease and vitamin B6 deficiency caused an elevation in triglyceride contents which reached those of the ad libitum groups. The study highlights the interaction between vitamin B6 and polyunsaturated fatty acids and the opportunity of dietary intake of fish oil to counterbalance some effects of vitamin B6 deficiency.     

Effects of the unsaturation of dietary fat and of arachidonate supplementation on cholesterol pool expansion in the guinea pigs.

We have studied the effects of methyl arachidonate supplementation on the lipid metabolism of guinea pigs fed cholesterol. Four groups of guinea pigs were fed a purified diet containing 9.5% hydrogenated coconut oil (HCNO), a highly saturated fat with or without the addition of 1% cholesterol, for 15 weeks. One half of the animals fed the control and the cholesterol-containing diets were supplemented with 15 mg methyl arachidonate three times per week. Supplementation with methyl arachidonate did not alter the concentration of plasma total (TC) or unesterified (FC) cholesterol, erythrocyte cholesterol and plasma phospholipid or the ratio of plasma FC/TC. Accumulation of cholesterol in the major organs of the cholesterol-fed groups was also unchanged. In both control and cholesterol-fed groups, methyl arachidonate decreased the proportion of oleic (18:1) and linoleic acids (18:2) and increased arachidonic acid (20:4) content of plasma and liver phospholipid. A comparison between the results of this study and studies using cottonseed oil showed that the type of dietary fat modifies the effects of cholesterol: plasma cholesterol levels were higher and liver cholesterol storage was lower in animals fed the saturated fat than in those fed the fat rich in polyunsaturated fatty acids (PUFA). Furthermore, in spite of similar changes in erythrocyte cholesterol content and shape abnormalities, no overt hemolytic anemia was observed in the groups fed cholesterol and saturated fat, in contrast to those fed cholesterol + PUFA-containing fat. We conclude that in guinea pigs supplementary methyl arachidonate had no hypocholesterolemic effect at the levels we fed, that circulating cholesterol levels are not a measure of cholesterol accumulation by organs and that the decrease of serum cholesterol in response of PUFA is due in part to an increase of cholesterol storage in the liver.     

A solid dietary fat containing fish oil redistributes lipoprotein subclasses without increasing oxidative stress in men

There is a demand and need for healthy solid dietary fats. However, synthetic fats can be tailored to contain specific physiologic properties. Our goal was to design dietary solid test fats that would be both beneficial to the atherogenic lipid profile and stable against lipid peroxidation. Sixteen men (age 35-75 y) substituted 80 g of their normal dietary fat intake with test fat for two periods of 21 d each in a double-blind, randomized, crossover study. Although solid, both test fats were low in cholesterol-raising SFA. Test fat "F" contained 5 g/100 g long chain (n-3) fatty acids matched by oleic acid in test fat "O." Plasma total triacylglycerol (TAG), VLDL TAG, cholesterol in VLDL, and intermediate density lipoproteins (IDL) were lower (P < 0.05), whereas apolipoprotein (apo) B of the large LDL-2 (d = 1031-1042 g/L) subclass, and cholesterol of HDL(2b) subclass, were higher after intake of F than O fat (P < 0.05). There was no difference in the effect on in vivo oxidation measured as the ratio of plasma isoprostanes F(2) to arachidonic acid and urinary isoprostanes, whereas the vitamin E activity/plasma total lipids ratio was higher after intake of F than O (P = 0.008). In conclusion, a solid dietary fat containing (n-3) PUFA decreased plasma TAG, VLDL, and IDL cholesterol, and redistributed lipoprotein subclasses in LDL and HDL, with a higher concentration of the larger and less atherogenic subfractions. These changes took place without an increase in oxidative stress as measured by in vivo markers.     

Comparative study of the atherogenecity of dietary trans, saturated and unsaturated fatty acids on swine coronary arteries

Three groups of two-month-old swine were fed on basal diets supplemented with either oleic acid-rich safflower oil, lard or hydrogenated soybean oil in order to monitor the atherogenecity of various dietary fatty acids. The level of plasma triglyceride was highest in the safflower oil group and the level of plasma cholesterol was highest in the lard group. The degree of intimal thickening of the coronary arteries was most severe in the safflower oil group and lease severe in the hydrogenated fat group. Both the lard- and safflower oil-supplemented groups displayed lipid-rich coronary arterial lesions. The thickened intima of these two groups contained numerous activated smooth muscle cells, degenerated cells with or without stainable lipid and abundant cell debris. Cellular changes were less conspicuous in the coronary arteries from the hydrogenated fat group than in those from the other two groups.     

Dietary plant proteins and vegetable oil blends increase adiposity and plasma lipids in Atlantic salmon (Salmo salar L.)

In order to study whether lipid metabolism may be affected by maximum replacement of dietary fish oil and fish meal with vegetable oils (VO) and plant proteins (PP), Atlantic salmon (Salmo salar L.) smolts were fed a control diet containing fish oil and fish meal or one of three plant-based diets through the seawater production phase for 12 months. Diets were formulated to meet all known nutrient requirements. The whole-body lipid storage pattern was measured after 12 months, as well as post-absorptive plasma, VLDL and liver TAG. To further understand the effects on lipid metabolism, expression of genes encoding for proteins involved in VLDL assembly (apoB100), fatty acid uptake (FATP1, cd36, LPL and FABP3, FABP10 and FABP11) were measured in liver and visceral adipose tissue. Maximum dietary VO and PP increased visceral lipid stores, liver TAG, and plasma VLDL and TAG concentrations. Increased plasma TAG correlated with an increased expression of apoB100, indicating increased VLDL assembly in the liver of fish fed the high-plant protein- and VO-based diet. Atlantic salmon fed intermediate replacement levels of VO or PP did not have increased body fat or visceral mass. Overall, the present results demonstrate an interaction between dietary lipids and protein on lipid metabolism, increasing overall adiposity and TAG in the body when fish meal and fish oil are replaced concomitantly at maximised levels of VO and PP.     

The effect of dietary fat saturation on plasma and hepatic lipoproteins in the rat

Semipurified diets containing 10% kilocalories from either safflower oil (SO), corn oil (CO), olive oil (OO) or palm oil (PO) were fed to weanling male rats for 2 weeks. The effects of dietary fat saturation on plasma lipids and lipoproteins were: 1) Nonfasted plasma cholesterol concentration was higher in rats fed OO (mean +/- SEM = 81.0 +/- 2.9 mg/dl) vs. CO (67.5 +/- 2.9); 2) plasma chylomicron cholesterol concentration was higher in rats fed OO vs. SO and CO, with PO values in between; and 3) the cholesterol concentration of plasma very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL) did not differ among groups. The effects of dietary fat saturation on hepatic lipoproteins (determined by liver perfusion techniques) were: 1) hepatic higher density lipoprotein (d = 1.006-1.21 g/ml) cholesterol production was greater in rats fed SO and CO vs. PO [19.1 +/- 1.2, 17.2 +/- 0.8 and 13.7 +/- 1.6 micrograms/(g liver X 1.5 hour), respectively]; 2) there was no difference in hepatic VLDL cholesterol production among groups; and 3) the ratio of cholesterol to protein of hepatic VLDL and the higher density lipoprotein fraction was higher in rats fed diets rich in polyunsaturated fatty acids versus saturated fatty acids. Dietary fat saturation had no effect on carcass and liver cholesterol concentrations. Since differences in hepatic lipoprotein production were not reflected in plasma lipoprotein patterns, these results suggest that extrahepatic lipoprotein metabolism differs in rats fed diets containing fatty acids of varying saturation.     

Dietary cholesterol-fat type combinations and carbohydrate and lipid metabolism in rats and mice

In rats fed semipurified cholesterol-free diets, dietary corn oil induced higher levels of liver cholesterol, but lower concentrations of plasma cholesterol, plasma triglycerides and blood D-3-hydroxybutyric acid, than did coconut fat. Addition of cholesterol to the diets (1%, w/w) greatly increased liver cholesterol levels but did not affect the corn oil effect upon liver and plasma cholesterol. In contrast, dietary cholesterol prevented the corn oil effects upon plasma triglycerides and blood D-3-hydroxybutyric acid. Liver glycogen levels in rats increased significantly after cholesterol feeding, the effect being independent of dietary fat type. In mice, dietary corn oil, compared to coconut fat, elevated liver cholesterol only when the diet contained cholesterol. Corn oil caused an increase of liver glycogen in mice in the presence, but not in the absence of dietary cholesterol. This study shows that dietary cholesterol-fat type combinations influence various aspects of lipid and carbohydrate metabolism in rats and mice.     

Fish oil combined with SCFA synergistically prevent tissue accumulation of NEFA during weight loss in obese mice

Based on their proposed metabolic effects, we examined whether fish oil (FO) and SCFA, alone or in combination, accelerate weight loss and the resultant metabolic improvements. Obesity was induced in male C57BL/6J mice by high-energy feeding for 10 weeks. The mice were transferred to a low-fat diet (2·5w%) for 4 weeks, the source of fat being either FO, a lard-safflower oil mix (control), or both types combined with SCFA. Weight, fasting insulin, tissue and serum lipid concentrations, as well as mRNA amount of genes related to adipose inflammation and hepatic fat oxidation were determined. All groups lost weight and showed reduced fasting insulin concentrations and reduced liver TAG. However, weight loss on the control-fat diet caused significant increase in hepatic and cardiac NEFA. Substituting 20?% of the fat with SCFA increased weight loss by 48?% and reduced fasting insulin 1·5-fold more than the no-SCFA diets. It furthermore significantly increased the amount of mRNA for PPAR-α, and decreased the mRNA amount for NF-κB in the liver and white adipose tissue. The FO diets enhanced improvement of tissue lipid levels. Thus, FO improved liver TAG and NEFA levels compared with weight loss on the control diet. Combining FO and SCFA further reduced tissue NEFA accumulation. In conclusion, we found that dietary SCFA had a significant impact on gene expression in the liver and adipose tissue, and that the effect of FO on tissue NEFA content was modified by SCFA. Thus, interactions between fatty acids should be considered when studying the effects of specific fatty acids.     

Exacerbating effect of dietary 12-keto oleic acid on vitamin E deficiency in the rat.

12-Keto oleic acid, possibly one of the oxidation products of long-chain, unsaturated fatty acids, was added to the feed of weanling male rats at the 1% level. Their growth curves, tissue weights, plasma alkaline phosphatase, GOT, and GPT activities, and plasma and liver lipid (cholesterol, triglyceride and phospholipid) levels were investigated and compared with those of weanlings fed a vitamin E deficient diet. Both the diet containing 12-keto oleic acid and the diet deficient in vitamin E decreased the growth rate of body weight and tissue weight, and increased the liver triglyceride and cholesterol levels. Parallel with these, increased hemolysis and stimulation of lipid peroxidation and fluorescent production in the liver homogenate were observed. Elevated plasma alkaline phosphatase and GOT activities which may be considered to be due to a functional disorder of the liver were also observed.     

Roles of omega 3 fatty acids and chronic ethanol in the regulation of plasma and liver lipids and plasma apoproteins A1 and E in rats

Relative effects of feeding ethanol and/or omega 3 fatty acid-rich fish oil for 6 wk on body lipids and lipoproteins were investigated. Ethanol increased plasma cholesterol (P less than 0.06) and triglycerides (P less than 0.0005), whereas fish oil decreased plasma cholesterol (P less than 0.005) and triglycerides (P less than 0.02). Liver cholesterol and triglycerides were increased by ethanol (P less than 0.0001) while fish oil decreased liver cholesterol (P less than 0.01) but not triglycerides. Based on Scheffé contrasts (P less than 0.05), fish oil blocked the increases in liver cholesterol and triglycerides caused by ethanol. Substitution of normal dietary fat with omega 3 fatty acid-rich fat in ethanol-fed animals lowered plasma cholesterol by 29% (P less than 0.001) and triglycerides by 30% (P less than 0.05) within 2 wk. Plasma apo A1 was increased by ethanol (P less than 0.001) and decreased by fish oil (P less than 0.002). Plasma total apo E was unaffected by either ethanol or fish oil. However, HDL apo E was decreased by ethanol (P less than 0.04) and increased by fish oil (P less than 0.02). Scheffé contrasts (P less than 0.05) also showed that plasma apo A was increased by ethanol regardless of whether the animals were consuming regular fat (1.72-fold) or fish oil fat (1.49-fold). Thus, omega 3 fatty acids can not only prevent but also reverse many of the lipid and lipoprotein abnormalities caused by alcohol abuse in the rat.     

Growth and lipid metabolism responses in rats fed different dietary fat sources

An experiment with male albino rats was conducted to examine the effect of dietary fat sources on growth performance and apparent digestibility of total fat and fatty acids. The effect on plasma and organ cholesterol concentrations as well as lipoproteins cholesterol and fatty acid profile of hepatic phospholipids was also examined. Forty 3 week old rats were fed purified diets containing 0.041% cholesterol and 7% fat (wt/wt) from soy oil (SO), or cow ghee (GH), or 25% fish oil (FO) plus soy oil (SF) or 25% fish oil plus 75% ghee (GF), or 50% soy oil plus 50% ghee (SG) for a period of 35 days. Final body weight, weight gain, organ weights and feed efficiency ratio showed no significant differences (P < 0.05) among the dietary treatments. The apparent digestibility of total dietary fat and saturated fatty acids in the animals fed diet containing cow ghee only or in combination with fish oil or soy oil was significantly lower than the other dietary groups. Consumption of ghee with combination of fish oil or soy oil lead to significant improvement in the fat apparent digestibility of dietary fat. Total cholesterol and triglyceride concentrations of plasma and organs as well as lipoprotein cholesterol levels were higher in animals fed diets containing ghee. For rats fed diet containing cow ghee in combination with fish oil or soy oil, the cholesterol content of total plasma, lipoprotein fractions (VLDL, LDL and HDL) and organs was decreased significantly. Furthermore, dietary fats altered the fatty acids composition of hepatic phosphlipid fatty acids composition. Feeding dietary fish oil reduced arachidonic acid (20:4) and increased linoleic acid (18:2) and eicosapentaenoic acid (20:5) contents. The reduction in the arachidonic acid was being more pronounced in animals fed dietary ghee with combination of fish oil.