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At least 19 recordsLinked to original sources

The vitamin E nutritional status of rats fed on diets high in fish oil, linseed oil or sunflower seed oil.

Twelve groups of eight rats and two control groups of sixteen rats were given semisynthetic diets with 40% energy as fat for a period of 76 d. All diets contained a minimum of 3% energy as linoleic acid and comparable basal levels of D-alpha- and D-gamma-tocopherol. The diets varied in fat composition and in the content of DL-alpha-tocopheryl acetate. The diets high in polyunsaturated fatty acids (PUFA) were either rich in fish oil (FO; groups 1-4; 10% energy as fish oil PUFA), linseed oil (LN; groups 1-4; 10% energy as alpha-linolenic acid) or sunflower seed oil (SF; groups 1-4; 10 + 3% energy as linoleic acid). The control groups were given a diet high in monounsaturated fatty acids (MUFA; CO 1; 10 + 13% energy as oleic acid) or a diet with an 'average' linoleic acid content (CO 2; 8.5% energy as linoleic acid). Of each high PUFA diet three groups were supplemented with graded levels of DL-alpha-tocopheryl acetate. Steatitis, a sensitive histopathological indicator of vitamin E deficiency in animals fed on diets rich in fatty acids with three or more double bonds, was observed only in the adipose tissue of the FO groups, even in the group with the highest DL-alpha-tocopheryl acetate supplementation. Liver and serum alpha-tocopherol levels were found to be positively correlated and liver and serum gamma-tocopherol levels negatively correlated with dietary DL-alpha-tocopheryl acetate. The groups on the FO diets had significantly reduced liver and serum tocopherol levels in comparison with the groups on the other high-PUFA diets. With the supplementation scheme used for the FO groups the liver alpha-tocopherol levels of both control groups were reached but the serum control levels were not.

Adipose Tissue↗

Short communication: Diurnal profiles of conjugated linoleic acids and trans fatty acids in ruminal fluid from cows fed a high concentrate diet supplemented with fish oil, linseed oil, or sunflower oil.

Trans-18:1 and 18:2 isomer composition in ruminal fluid during the daily feeding cycle was examined in 3 cows fed a high concentrate diet (35:65) with 5% (DM basis) sunflower oil (SO), 5% linseed oil (LO), or 2.5% fish oil (FO) in a 3 x 3 Latin square with 3 4-wk periods. Grass hay and concentrate mixtures were fed at 0900, 1300, and 1700 h daily. Ruminal fluid was collected at 0900, 1100, 1300, 1500, 1700, 2000, and 0000 h. Feeding SO resulted in the greatest mean concentrations (% of total fatty acids) of trans10,cis12-18:2 and cis9,trans11-18:2. In particular, trans10,cis12-18:2 with SO was greater at 1500 (0.29%), 2000 (0.34%), and 0000 h (0.25%) relative to 0900 h (0.07%). Cis9,trans11-18:2 concentration increased from 0.47% at 0900 h to a peak of 2.06% at 1100 h; it remained greater than the percentage determined at 0900 h at 1300 (1.4%) through 0000 h (1.1%). Concentration of trans11,cis15-18:2 was greatest with LO, ranging from 3.3% (0900 h) to a peak of 11.4% at 2000 h. Mean trans10-18:1 concentration ranked by diet was SO > FO > LO. Peak trans10-18:1 with SO was observed at 1700 h (14.9%) compared with 0900 h (5.1%). Trans11-18:1 did not differ with diet or time. Stearic acid decreased over time with all diets reaching minimum concentrations at 1700 to 2000 h relative to 0900 h. Feeding FO, however, decreased mean 18:0 concentration 4-fold compared with LO or SO. The moderate effect on concentration of trans-18:1 coupled with accumulation of 18:2 intermediates and the decrease of 18:0 over time suggest that oils reduced the biohydrogenation of 18:2 isomers to trans-18:1.

Animals↗

Zinc deficiency and activities of lipogenic and glycolytic enzymes in liver of rats fed coconut oil or linseed oil.

In previous studies, zinc-deficient rats force-fed a diet with coconut oil as the major dietary fat developed a fatty liver, whereas zinc-deficient rats force-fed a diet with linseed oil did not. The present study was conducted to elucidate the reason for this phenomenon. In a bifactorial experiment, rats were fed zinc-adequate or zinc-deficient diets containing either a mixture of coconut oil (70 g/kg) and safflower oil (10 g/kg) ("coconut oil diet") or linseed oil (80 g/kg) ("linseed oil diet") as a source of dietary fat, and activities of lipogenic and glycolytic enzymes in liver were determined. In order to ensure adequate food intake, all the rats were force-fed. Zinc-deficient rats on the coconut oil diet developed a fatty liver, characterized by elevated levels of triglycerides with saturated and monounsaturated fatty acids. These rats also had markedly elevated activities of the lipogenic enzymes acetyl-CoA carboxylase, fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), and citrate cleavage enzyme, whereas activities of malic enzyme and glycolytic enzymes were not different compared with zinc-adequate rats on the coconut oil diet. In contrast, rats receiving the linseed oil diet had similar triglyceride concentrations regardless of zinc status, and activities of lipogenic enzymes and glycolytic enzymes were not different between the two groups. Zinc-deficient rats fed either type of dietary fat exhibited statistically significant correlations between activities of FAS, G6PDH, 6PGDH and concentrations of saturated and monounsaturated fatty acids in liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Antihypertensive effect of dietary sunflowerseed oil and linseed oil in spontaneously hypertensive rats during a multigeneration feeding study.

Semisynthetic diets enriched with polyunsaturated fatty acids (30 en% sunflowerseed oil or linseed oil) reduced hypertension development in spontaneously hypertensive rats (SHR) compared with control SHR fed on a regular rat chow. The effect was most markedly expressed in the 3rd and 4th generations of a four generation feeding period. PGI2-like production from isolated, pulsatingly perfused aorta preparations was reduced in linseed oil but not in sunflowerseed oil fed rats. Effects on blood pressure and PGI2-like production were abolished when the semisynthetic diets were changed for regular chow (5th and 6th generations).

Animals↗

Chromatographic column fractionation and fatty acid composition of different lipid classes of linseed oil.

Linseed oil is fractionated on silicic acid column, with subsequent identification of different lipid classes by thin layer chromatography. Sterol esters, triglycerides, free fatty acids, sterols and phospholipids represent 0.15, 92.25, 3.30, 1.15 and 1.16%, respectively of linseed lipids. The total saturated fatty acid content of the phospholipid fraction is higher than that of the oil, the triglyceride fraction and the free fatty acid fraction. Linolenic acid, which is the major fatty acid in linseed triglycerides (47.5%), makes 18.2% of the phospholipid fatty acids. Oleic acid is the major fatty acid in the phospholipid fraction (35.2%), while it constitutes 19.3% of the triglycerides fatty acids.

Chromatography, Gel↗

[Determination of epoxidized soybean oil and linseed oil in wrapping film and cap sealing].

A determination method was developed for epoxidized soybean oil (ESBO) and epoxidized linseed oil (ELO), which are used as plasticizers and/or stabilizers, in wrapping film and cap sealings. The ESBO method reported by Castle et al. was improved. Samples were extracted with acetone-hexane (3: 7), transmethylated under alkaline conditions, then derivatized to the 1,3-dioxolanes and analyzed by GC/MS. The recoveries of spiked ESBO and ELO were between 92.6% and 104.4%. The determination limits were 0.01 mg/g for ESBO and 0.02 mg/g for ELO in the wrapping film, and 0.04 mg/g and 0.08 mg/g in the cap sealing. ESBO and ELO were surveyed in 10 samples each of wrapping film and cap sealings currently available on the Japanese market. ESBO was found at 34.7-82.8 mg/g in polyvinyl chloride (PVC) wrapping films and at 5.47-399 mg/g in cap sealings. ELO was detected at 8.6-11.4 mg/g in polyvinylidene chloride (PVDC) wrapping films, and at 46.4 mg/g in a PVC wrapping film.

Excipients↗

Activities of liver microsomal fatty acid desaturases in zinc-deficient rats force-fed diets with a coconut oil/safflower oil mixture of linseed oil.

The present study was conducted to investigate the effect of zinc deficiency on fatty acid desaturation in rats fed two different types of dietary fat, a mixture of coconut oil and safflower oil (7:1, w/w, "coconut oil diet") or linseed oil ("linseed oil diet"). In order to ensure an adequate food intake, all rats were force-fed by gastric tube. Zinc deficiency caused statistical significant reduction of delta 9-desaturase activity in liver microsomes of rats fed coconut oil diet and tendencial reduction (p < 0.15) in rats fed linseed oil diet compared with control rats fed diets with the same type of fat. In agreement with this effect, zinc deficiency in the rats fed both types of dietary fat increased the ratio between total saturated and total monounsaturated fatty in liver phospholipids and liver microsomes. Zinc deficient rats on the coconut oil diet had unchanged delta 6-desaturase activity with linoleic acid as substrate and lowered activity with alpha-linolenic acid as substrate. In contrast, zinc deficient rats on the linseed oil diet had increased delta 6-desaturase activity with linoleic acid as substrate and unchanged activity with alpha-linolenic acid. Because linoleic acid is the main substrate for delta 6-desaturase in the rats fed coconut oil diet, and alpha-linolenic acid is the main substrate in the rats fed linseed oil diet, it is concluded that in vivo delta 6-desaturation was not changed by zinc deficiency in the rats fed both types of dietary fat. Activity of delta 5-desaturase was also not changed by zinc deficiency in the rats fed both dietary fats. Levels of fatty acids in liver phospholipids and microsomes derived by delta 4-, delta 5-, and delta 6-desaturation were not consistently changed by zinc deficiency in the rats fed both types of dietary fat. Thus, the enzyme studies and also fatty acid composition data of liver phospholipids and microsomes indicate that zinc deficiency does not considerably disturb desaturation of linoleic and alpha-linolenic acid. Therefore, it is suggested that similarities between deficiencies of zinc and essential fatty acids described in literature are not due to disturbed desaturation of linoleic acid in zinc deficiency. The present study also indicates that zinc deficiency enhances incorporation of eicosapentaenoic acid into phosphatidylcholine of rats fed diets with large amounts of n-3 polyunsaturated fatty acids.

Alkaline Phosphatase↗

Effect of dietary fish oil substitution with linseed oil on the performance, tissue fatty acid profile, metabolism, and oxidative stability of Atlantic salmon.

The objective of this experiment was to test the effect of total or partial substitution of dietary fish oil (FO) by linseed oil (LO) in Atlantic salmon feeding on performance, liver and muscle fatty acid composition, selected lipogenic and lipolytic enzyme activities, and flesh oxidative stability. For 12 wk, fish (220 +/- 12 g of initial BW) were fed five experimental diets in which the FO was serially replaced by 25, 50, 75, and 100% LO. Total FO replacement by LO did not (P = 0.20) affect fish final weight, biometric indices, or i.m. fat contents. Liver and muscle neutral lipid (NL) composition responded to dietary treatments in different ways. Whereas the sum of n-3 PUFA in muscle followed a linear and quadratic pattern with increasing levels of LO, a linear (P = 0.005) effect was observed in the liver NL fraction. Total n-3 and n-6 PUFA contents in the polar lipid fraction (PL) were unaffected (P = 0.356) by dietary input of LO in muscle. Activity of liver glucose-6-P-dehydrogenase (G6PD) was greater with increasing levels of LO (P = 0.004). A time effect (P < 0.001) was observed in the concentration of lipid peroxidation products, expressed as thiobarbituric acid reactive substances, in fish flesh stored under refrigeration for 9 d; however, the progressive inclusion of LO in the feed did not affect (P = 0.125) flesh oxidation stability. In summary, LO can totally replace FO in Atlantic salmon feed without affecting growth performance and muscle susceptibility to lipid oxidation. Fatty acid metabolism in the liver was affected by LO, promoting G6PD activity and eicosatetraenoic acid accumulation; however, a 100% LO replacement decreased (P < 0.001) concentrations of eicosapentaenoic and docosahexaenoic acids in salmon muscle.

Animal Feed↗

Dietary linseed oil produces lower abdominal fat deposition but higher de novo fatty acid synthesis in broiler chickens.

Previous experiments have shown lower abdominal and body fat deposition in broilers fed polyunsaturated fatty acids (PUFA) compared with those fed saturated fatty acids (SFA) or monounsaturated fatty acids (MUFA). These changes in fat deposition may be related to different rates of lipid synthesis or lipid oxidation. In Experiment 1, in vivo lipogenesis of broilers fed different dietary fatty acid profiles (tallow, sunflower oil, or linseed oil) was investigated. In Experiment 2, liver fatty acid deposition of broilers fed a basal diet (without additional fat) or diets with added tallow, olive oil, sunflower oil, or linseed oil was studied. Results from Experiment 1 showed higher rates of de novo fatty acid synthesis in broilers fed the diet with added linseed oil (P < 0.05), compared with those fed tallow or sunflower oil. In Experiment 2, values of liver-to-dietary-fatty-acid ratios of fatty acids from endogenous synthesis (SFA, n-7 and n-9 fatty acids) were higher in broilers fed linseed oil and the basal diet. Results obtained in both experiments suggest that lower abdominal and body fat deposition of broilers fed PUFA compared with those fed SFA or monounsaturated fatty acids is mainly due to differences in lipid oxidation rates and that the higher in vivo lipogenesis found in broilers fed linseed oil would be another mechanism to dissipate energy, contributing to the lower fat deposition in these birds.

Abdomen↗

Diet-induced thermogenesis is lower in rats fed a lard diet than in those fed a high oleic acid safflower oil diet, a safflower oil diet or a linseed oil diet.

The objectives of the present study were to examine the effects of dietary fats differing in fatty acid composition on diet-induced thermogenesis, sympathetic activity in brown adipose tissue and body fat accumulation in rats. Rats were meal-fed for 12 wk an isoenergetic diet based on lard, high oleic acid safflower oil, safflower oil or linseed oil, and norepinephrine turnover rates in brown adipose tissue were then estimated. Whole-body oxygen consumption after the meal indicated that diet-induced thermogenesis was significantly lower in rats fed the lard diet than in those fed the other diets. The norepinephrine turnover rate in the interscapular brown adipose tissue was also significantly lower in the lard diet group than in the other diet groups. The carcass fat content was significantly higher in the lard diet group than in the other diet groups, whereas the abdominal adipose tissue weights were the same in all diet groups. These results suggest that the intake of animal fats rich in saturated fatty acids, compared with the intake of vegetable oils rich in monounsaturated or polyunsaturated fatty acids, decreases diet-induced thermogenesis by a decline of sympathetic activity in brown adipose tissue, resulting in the promotion of body fat accumulation.

Adipose Tissue, Brown↗

[Influence of heated linseed oil on reproduction in the female rat and on the composition of hepatic lipids in young rats].

During gestation and lactation, six month old female Wistar rats were fed diets containing 10 p. 100 by weight of various vegetable oils; thermopolymerized linseed oil at 275 degrees C for 12 hours under nitrogen atmosphere (group T), oxidized linseed oil at 200 degrees C for 100 hours under air atmosphere (group O). The two oils contain respectively 11,5 and 1,1 p. 100 of cyclic monomers (18 C). Control groups were fed either fresh linseed oil or fresh peanut oil under the same conditions. In group T, most of the newborn rats die at birth or during the first three days of life; none of them survive 13 days after birth. In group O, mortality of youngs is not so high but is still significantly higher than in control groups. Moreover, dead young rats of group T have heavier livers and higher lipid content in the organ. Cyclic monomers were detected in liver fatty acids. In surviving young rats of group O,the body growth during lactation is significantly slower than in control animals. Young rats of group O were sacrificed at the age of 14 days. Liver weight and lipid content of the organ are increased and cyclic monomers were detected. The effects are however less pronounced than in group T. One can assume that among abnormal compounds formed during heating of linseed oil, cyclic monomers are responsible for the toxic effects observed in the present experiment since they have been transmitted to the litters either during gestation or lactation.

Animals↗