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.     

Effects of oxidized soybean oil on the vitamin A nutrition of the rat

Three lots of cold-pressed soybean oil were treated with bubbling oxygen for 70, 80, and 180 hrs. at 70°C. and fed to rats at a level of 18% in diets which were nutritionally adequate but devoid of vitamin A. Untreated soybean oil was fed in similar control diets. Subgroups of 15 weanling rats each were given graded injections of vitamin A acetate intramuscularly each week. Diarrhea developed in the rats fed the diets containing oxidized oil. This condition soon subsided in the groups receiving vitamin A injections but not in the vitamin A-free group. Diarrhea was not noted in the rats receiving the untreated soybean oil, without respect to the amount of vitamin A they received. The rats on the vitamin A-free diets developed deficiency more rapidly when the diet contained oxidized rather than the untreated oil. The food efficiencies of the groups fed the oxidized oils were lower than the controls. The intestines of the groups receiving the oxidized oils were distended with fluid and were hemorrhagic. Enlarged kidneys were noted in the vitamin A-deficient control as well as in test rats. The retroperitoneal lipids of the groups on the oxidized oil were less unsaturated, had lower refractive indices, higher peroxide values, and higher carbonyl values than comparable groups fed the control oil. Vitamin A deficiency decreased the unsaturation of the kidney and liver lipids but increased that of the retroperitoneal lipids. Injections of increasing amounts of vitamin A produced increases in the unsaturation of the body lipids. The kidney lipids of the groups on the oxidized oil diets were less unsaturated and contained more peroxidic compounds than the controls. Vitamin A deficiency increased the peroxidic compounds in the kidney and liver lipids, even in rats fed the control oil. The liver lipids of the groups fed oxidized oil were less unsaturated, lower in vitamin A content, and higher in peroxide compounds than the controls. The vitamin A content of the whole blood varied in relation to the amounts injected. The content of tocopherol in the tissues were not affected significantly by the oxidized oil in the diet. The evidence indicates that severely oxidized oil may destroy vitamin A in the tissue of the rat, thereby hastening the development of deficiency on vitamin A-free diets, reducing the storage of injected vitamin A, and increasing the vitamin A requirement. These effects are with abused oil and should not be interpreted to mean that the mildly oxidized oils and fats, such as those in the diets of human beings in this country are toxic. 1 Read in part at the 36th Fall meeting. American Oil Chemists' society, Chicago, October 20–22, 1958. 2 Assisted by a grant from the Roche Anniversary, Fund, Hoffmann LaRoche Inc. 3 Contribution No. 414 from the Department of Nutrition. Food Science and Technology, Massachusetts Institute of Technology, Cambridge, Mass.     

Studies on the nutritional and physiological effects of thermally oxidized oils

Summary The present results indicated that the thermal oxidation products from the polyunsaturated fatty acids, primarily linoleic acid, are responsible for much of the loss of nutritional value in thermally oxidized edible oils. Oils which have a high linoleic acid content are more likely to undergo thermal oxidative damage than those with lower linoleic contents. Also the ratio of linoleic acid to total unsaturation has some effect on the nutritive stability of the oil when it has been thermally oxidized. An oil with a high iodine value but with a low linoleic acid value appears to be more stable to thermal oxidation than an oil with an iodine value one half as great but with most of the unsaturation in the oil caused by linoleic acid. The products formed during thermal oxidation which cause the loss of nutritional value are those which do not form urea-inclusion compounds. They are probably polymeric in nature, but thermally oxidized oils also contain carboxylic acids and carbonyl groups which might cause some of the nutritional loss observed when thermally oxidized oils are fed. The rate ofin vitro hydrolysis of the thermally oxidized corn oil by pancreatic lipase, also the rate of absorption from the intestine of the male rats, were found to be decreased. However the percentage of absorption in 24 hrs. was the same with both fresh and thermally oxidized oil. The liver-body weight ratio of rats fed a diet containing the thermally oxidized oil were found to be significantly larger than the liver-body weight ratio in animals fed diets containing fresh oil. However the livers of animals fed the thermally oxidized oil diets did not differ in lipide percentage or total solid content, and histopathological investigations did not show any abnormal conditions.     

Sesamin Supplementation Increases White Muscle Docosahexaenoic Acid (DHA) Levels in Rainbow Trout (<Emphasis Type="Italic">Oncorhynchus mykiss</Emphasis>) Fed High Alpha-Linolenic Acid (ALA) Containing Vegetable Oil: Metabolic Actions

The effects of including an equi-mixture of sesamin and episesamin in fish diets based on vegetable oils of different fatty acid composition were examined. Sesamin/episesamin (hereafter named sesamin) was included at 0.58 g/100 g diet. The oil used in the feed was either a mixture of linseed and sunflower oils (6:4, by vol) or 100% linseed oil. Addition of sesamin increased the percentages of docosahexaenoic acid (DHA) in white muscle phospholipid and triacylglycerol fraction by up to 37% but the fatty acids in red muscle and liver were not affected. The expression of the peroxisome proliferator-activated receptor PPARalpha was significantly down regulated in the liver of the fish fed sesamin and mixed oil diet (P < 0.05). Sesamin and episesamin were detected in liver and muscle tissues of the fish that had been fed sesamin. Fish fed sesamin had elevated levels of total cytochrome P450 (CYP) enzymes and EROD activity in the liver, indicating an induction of CYP1A in this tissue. Our conclusion was that supplementation of fish feed with sesamin increased the proportions of DHA in the white muscle.     

Effects of dietary oil related to the toxic oil syndrome on the lipids of guinea pig liver microsomes

The potential effects of oil specimens related to cases of toxic oil syndrome (TOS) on the liver microsomal lipid composition from guinea pigs were investigated. For four weeks, animals were fed diets supplemented with either “case oil” (oil related to cases of TOS) or “control oil” (oil unrelated to cases of TOS), either previously heated or not. Results were compared with those from guinea pigs fed the same diet with no oil. The administration of case oil produced changes in liver microsomal lipid composition. Statistically significant differences were also found between heated case and heated control oils. The cholesterol/phospholipid molar ratios and the major phospholipid class distribution were unaffected under these diet conditions. However, increases in the relative contents of linoleic and arachidonic acids and, simultaneously, a reduction in palmitic and palmitoleic acid levels were observed by diet effects. Heated oil administration decreased the saturated/unsaturated ratios in all cases. Our data suggest that changes observed in the fatty acid composition are attributable to the free fatty acid contents of administered oils. The toxic constituents of case oil seem to be able to alter the liver microsomal lipid composition.     

Nutritional evaluation of refined,heated and hydrogenatedHibiscus sabdariffa seed oil

Alkali refinedHibiscus sabdariffa seed oil (Mesta Oil) of the familyMalvales was heated and hydrogenated to eliminate the cyclopropene fatty acids (CPFA). Such processed oils were fed to weanling rats at 10% level of the diet for 4, 8 and 12 weeks. The food intake and gain in weight were found to be less in the refined oil group than in the peanut oil control group. The digestibility was found normal with all the processed oils. Serum and liver lipid composition with respect to total lipids, cholesterol and phospholipids were comparable to those fed with peanut oil. The liver architecture did not show any abnormalities withH. sabdariffa oil feeding.     

Effects of oil heated with gluten on weight-loss dieting. I

Fresh oil was heated for 20 h at 180 degrees C with amino acids or gluten. A powdered diet (AIN93G; no fat) was mixed with 7 wt% of fresh oil (control), or supernatants of the heated oils described above, and fed to male Wistar rats for 12 weeks. No gross symptoms attributable to the heated oils were observed, but the gluten group showed a slow body weight increase; a significant difference was found in the weight after age 21 weeks in spite of diet consumption comparable to that of the control group. The serum of the heated oil groups showed a tendency toward lower values on various hematological measures, especially triacylglycerol and free fatty acid and toward higher values on aspartate aminotransferase (AST) and alanine aminotransferese (ALT), than those of the control group. All the rats except one in the gluten group had the same level of AST as those of the control rats, while the amino acid group included four rats with AST over 100 IU/L, the highest value in the control group. The number of dark red patches found on the surface of the liver and histological evaluation also showed frequent damage to the livers of the amino acid group. The difference in toxicity between the two heated oils seems to be related to the molecular sizes of amino acids and gluten. Gluten or melanoidin produced during heating probably decreased or counteracted the cytotoxicity of thermally oxidized oil. It is expected that oil heated with gluten can be used as a safe and effective oil for humans on weight-reduction diets.     

Nutritional and metabolic studies of distillable fractions from fresh and thermally oxidized corn oil and olive oil

A semisynthetic diet containing 15% by weight of dietary fat was fed to six groups of male Wistar rats for 28 days. Two groups received the distilable fraction of fresh corn oil (DCO) or fresh olive oil (DOO), two groups the distillable fraction of the thermally oxidized fats (OCO,OOO), and two groups received the respective fresh fats as controls (FCO, FOO). Substantial changes in the fatty acid composition occurred in the fats upon thermal oxidation. Only the rats that received OOO showed overt symptoms of heated fat toxicity. This was reflected in the histological scores of these animals, with the liver sustaining the most numerous and severe lesions. Tissue fatty acid changes of any significance were confined largely to the polar liver lipids of the rats that were fed OCO or OOO. The results of this study would suggest that the relatively greater toxicity of OOO, compared to OCO, may in part be due to the high oleic:linoleic acid ratio of the fresh olive oil and in part to a higher tocopherol content of the corn oil.     

Major clofibrate effects on liver and plasma lipids are independent of changes in polyunsaturated fatty acid composition induced by dietary fat

The effects of clofibrate on the content and composition of liver and plasma lipids were studied in mice fed for 4 wk on diets enriched in n−6 or n−3 polyunsaturated fatty acids (PUFA) from sunflower oil (SO) or fish oil (FO), respectively; both oils were fed at 9% of the diet (dry weight basis). Only FO was hypolipidemic. Both oil regimes led to slightly increased concentrations of phospholipids (PL) and triacylglycerols (TG) in liver as compared with a standard chow diet containing 2% fat. Clofibrate promoted hypolipidemia only in animals fed SO. Its main effect was to enlarge the liver, such growth increasing the amounts of major glycerophospholipids while depleting the TG. SO and FO consumption changed the proportion of n−6 or n−3 PUFA in liver and plasma lipids in opposite ways. After clofibrate action, the PUFA of liver PL were preserved better than in the absence of oil supplementation. However, most of the drug-induced changes (e.g., increased 18∶1n−9 and 20∶3n−6, decreased 22∶6/20∶5 ratios) occurred inrrespective of lipids being rich in n−6 or n−3 PUFA. The concentration of sphingomyelin (SM), a minor liver lipid that virtually lacks PUFA, increased with the dietary oils, decreased with clofibrate, and changed its fatty acid composition in both situations. Thus. oil-increased SM had more 22∶0 and 24∶0 than clofibrate-decreased SM, which was significantly richer in 22∶1 and 24∶1.     

Nutritive value of marine oils. II. Effects ofin vivo antioxidants in feeding menhaden oil to swine

Five pair-groups of swine were fed diets composed of crude feed materials to which 10% of clay-bleached, light cold-pressed menhaden oil was added. The oil was allowed to oxidize under controlled conditions and aliquots of fresh and oxidized oil were removed at peroxide values (PV) of 2.6, 15.5, and 61—each of which was fed to one group of animals. Two additional animal groups received diets containing the highly oxidized oil (PV=61) plus either alpha-tocopherol acetate or ethoxyquin. All oils were stored frozen and were mixed with the diets daily. Lard was fed at a similar 10% level to a control group of pigs. Both feed intakes and weight gains were progressively reduced as the diet oil was more highly oxidized. As oxidation of the oil increased, intensity of “yellow fat” increased and hemoglobin and hematocrit levels were progressively decreased. Both alpha-tocopherol acetate and ethoxyquin actedin vivo to improve feed intake, rate of gain, and blood condition, and eliminated the incidence of steatitis. Paper I in this series appeared in the Journal of Nutrition79, 323–332 (1963). Carried out under Contract No. 14-17-0001-352, U.S.D.I. Bureau of Commercial Fisheries. Technical Paper 1615, Oregon Agricultural Experiment Station.     

Chemical properties and cytotoxicity of thermally oxidized oil

Heated frying oils with different chemical properties in terms of AV (acid value), POV (peroxide value), COV (carbonyl value), and contents of polar compounds (PC) and triacylglycerol (TG), as well as color and odor, were obtained. Male Wistar rats were fed ad libitum for 12 weeks a powdered diet (AIN93G; no fat) containing 7 wt% of fresh oil (control) or one of the frying oils described above. The rats were subjected to anthropometric measurements, hematological analyses, and observations of the liver and kidneys. All of the rats grew well, and no gross symptoms attributable to the experimental oils were observed. However, the rats fed a diet containing the heated oil developed apparent liver damage to different degrees regardless of the chemical properties of the ingested oils. Thus, it was suggested that the chemical properties evaluated here had little to do with the cytotoxicity of heated oil, although the properties express quality of oil. Volatile compounds seem to be major candidates for the toxic agents in heated oil because oils with rancid and deteriorated odor show strong toxicity.     

Effects of diets enriched in eicosapentaenoic or docosahexaenoic acids on prostanoid metabolism in the rat

To clarify the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on prostaglandin biosynthesis, diets supplemented with oils rich in one fatty acid or the other were fed to rats over a 4-wk period. Animals fed the Max EPA diet showed a significant decrease in plasma and tissue phospholipid arachidonic acid content. While plasma levels of DHA increased on a shark liver oil diet enriched in DHA, the liver and kidney phospholipid contents of DHA were not altered. In addiition, the DHA-enriched diet did not decrease the arachidonic acid content of either liver or kidney phospholipids. Whole blood thromboxane and vascular prostacyclin synthesis were decreased by 65% and 36%, respectively, in animals fed the Max EPA diet. No such decrease was seen in the rats fed DHA-enriched diets. We conclude from these results that in the rat DHA is not likely to have a significant effect on prostaglandin synthesis when given as a dietary supplement.     

Influence of lauroyl and myristoyl peroxides and oxidized cottonseed oil on depot fat and liver lipid composition

In view of the interest in the biological properties of products of fat oxidation, lauroyl and myristoyl peroxides were fed and their nutritional effects compared with those of autoxidized cottonseed oil, which had been analyzed for its composition. Purified diets containing no fat +2% of linoleic acid, 5% lauroyl or myristol peroxide, or 10% oxidized cottonseed oil were fed to weanling male albino rats for 73 to 98 days, after which they were killed and their organs weighed. Their sera, livers, and testicular fat bodies were used for lipid analysis. With peroxides, growth was significantly depressed but not as much as when oxidized cottonseed oil was fed. Analysis of organ weight data showed that peroxides and oxidized cottonseed oil differed in their effects. Animals fed the latter had significantly heavier livers, kidneys, and hearts. The rats fed peroxides were also different from those fed the fat-free diet and those kept on restricted food intake. Gas chromatographic analysis of the testicular fat bodies revealed a greater deposition of oleate in the animals fed oxidized cottonseed oil, which suggested that these animals were unable to use the oxidized oil for depot fat formation. In the anials fed lauroyl and myristoyl peroxides, appreciable amounts of laurate and myristate, respectively, were found. The composition of the liver neutral fat of the animals fed peroxides was similar to that of the animals fed the low-fat diet +2%, linoleic acid. Serum cholesterol levels of the rats fed peroxides were about 70 mg. %, and of those fed oxidized cottonseed oil, 53 mg. %. The groups fed peroxides also had significantly higher liver cholesterol levels, which suggests that peroxides and oxidized cottonseed oil differed in their effects on cholesterol formation and transport. Aided by Grant A-1654 from the United States Public Health Service. Presented at the 34th fall meeting of the American Oil Chemists’ Society.     

Influence of sources of dietary oils on the life span of stroke-prone spontaneously hypertensive rats

In recent studies, the life span of stroke-prone spontaneously hypertensive (SHRSP) rats was altered by a variety of dietary fats. It was relatively shorter in rats fed canola oil as the sole source of fat. The present study was performed to find out whether the fatty acid profile and the high content of sulfur compounds in canola oil could modulate the life span of SHRSP rats. SHRSP rats (47 d old, n=23/group) were matched by body weight and systolic blood pressure and fed semipurified diets containing 10% canola oil, high-palmitic canola oil, low-sulfur canola oil, soybean oil, high-oleic safflower oil, a fat blend that mimicked the fatty acid composition of canola oil, or a fat blend high in saturated fatty acids. A 1% sodium chloride solution was used as drinking water to induce hypertension. After consuming the diets for 37 d, five rats from each dietary group were killed for collection of blood and tissue samples for biochemical analysis. The 18 remaining animals from each group were used for determining their life span. The mean survival time of SHRSP rats fed canola oil (87.4±4.0 d) was not significantly different (P>0.05) from those fed low-sulfur canola oil (89.7±8.5 d), suggesting that content of sulfur in canola oil has no effect on the life span of SHRSP rats. The SHRSP rats fed the noncanola oil-based diets lived longer (mean survival time difference was 6–13 d, P<0.05) than those fed canola and low-sulfur canola oils. No marked differences in the survival times were observed among the noncanola oil-based groups. The fatty acid composition of the dietary oils and of red blood cells and liver of SHRSP rats killed after 37 d of treatment showed no relationship with the survival times. These results suggest that the fatty acid profile of vegetable oils plays no important role on the life span of SHRSP rat. However, phytosterols in the dietary oils and in liver and brain were inversely correlated with the mean survival times, indicating that the differential effects of vegetable oils might be ascribed, at least partly, to their different phytosterol contents.     

Dietary fats and properties of endoplasmic reticulum: I. Dietary lipid induced changes in composition of microsomal membranes in liver and gastroduodenal mucosa of rat

Rats were fed for four weeks with different lipid diets to determine the effects on the endoplasmic reticulum membranes of the liver and on the postmitochondrial supernatant fraction of the gastroduodenal mucosa. The diets contained cholesterol, cacao butter, olive oil, and these in combination. The results showed that dietary lipids were able to modify the composition of the hepatic endoplasmic reticulum and, to a lesser extent, that of postmitochondrial fraction of gastroduodenal mucosa. Cacao butter in the diet decreased the relative proportion of protein in hepatic microsomes. Cholesterol and olive oil were able to increase the cholesterol content of microsomes. The trypsin digestion of membranes revealed that cholesterol increased the solubility of microsomal protein and decreased the trypsin sensitive protein-lipid binding. The neutral fat diets increased the binding of proteins to the membrane, and cholesterol had no effect when it was given in combination. The low power photomicrographs revealed vacuolization of the cytoplasm of the hepatocytes when rats were fed on lipid rich diets. Also fatty degeneration was present. Cholesterol in combination with olive oil, however, did normalize the structure of the hepatocytes to a marked extent.     

Lipid peroxidation and antioxidant status is affected by different vitamin E levels when feeding fish oil

The protective role of vitamin E and changes in the status of several physiological antioxidants after feeding rats a fish oil diet were investigated. Six-week-old male Sprague-Dawley rats were divided into four groups and fed experimental diets for 8 wk. Three fish oil (FO) groups were fed a menhaden fish oil and soybean oil (SO) (9∶1) mixture as 10% (w/w) of the diet. These groups were provided with ≤3, 45 or 209 IU of vitamin E/kg diet. One SO group was used as control and was fed ≤45 IU of vitamin E/kg diet. Plasma vitamin E levels, when expressed as vitamin E per mL plasma, were extremely low in the group fed FO and ≤3 IU of vitamin E, and were lower in the groups fed FO than in the group fed SO. However, plasma vitamin E levels when expressed per mg plasma lipid were higher in the FO groups provided with ≤45 and 209 IU of vitamin E than in the SO group. Compared with the SO group, plasma levels of thiobarbituric acid reactive substances (TBARS), when expressed per mg lipid, were higher in the three FO groups, plasma retinol levels were lower in the FO groups provided with ≤3 and 45 IU of vitamin E, and ascorbic acid levels were lower only in the FO group provided with ≤3 IU of vitamin E. Blood glutathione (GSH) levels were lower in all three FO groups than in the SO group. Liver vitamin E levels increased as the dietary level of vitamin E increased, but all FO groups had higher liver levels of TBARS than the SO group. The dietary vitamin E levels were correlated positively with plasma vitamin E (r=0.71) and negatively with TBARS in both the plasma and liver of rats fed FO. Among the antioxidants measured, correlations were found between plasma retinol and vitamin C (r=0.64), and plasma vitamin C, uric acid (r=0.72) and blood GSH (r=0.60). Weaker correlations were found between plasma retinol, uric acid and blood GSH. It is concluded that vitamin E requirements are higher when feeding fish oil. Vitamin E seems necessary to prevent enhanced lipid peroxidation and to maintain appropriate levels of other physiological antioxidants.     

Observations on the role of vitamin E in the toxicity of oxidized fats

Studies are reported on the relative effects of in vivo oxidation produced by diets devoid of vitamin E and the consumption of oxidized fat. Rats of the Sprague-Dawley strain were raised from weaning on a sucrose-casein diet containing minerals and vitamins in the required amounts, supplemented with 10% of safflower oil, menhaden oil, hydrogenated coconut oil or no fat. Animals of ca. 185 g of the group fed the 10% safflower oil were then switched for 4 weeks to safflower or menhaden oil-supplemented diets that were allowed to oxidize by exposing them to room temperature in the dark for 2–8 days. For comparison with effects of in vivo oxidation, animals were raised from weaning on similar fresh diets devoid of vitamin E. Consumption of oxidized fat was accompanied by loss of weight, effects on the size of the organs, changes in triglyceride levels and production of TBA-reacting substances in the tissues. There was no effect on the induced swelling of liver mitochondria or the susceptibility of erythrocytes to hemolysis in these animals. Growth was also suppressed in the animals fed the vitamin E-free diets, and in vivo oxidation in these animals produced marked effects on the membrane properties of erythrocytes and liver mitochondria.     

Effects of oil heated with gluten on weight-loss dieting. II

We previously proposed that oil heated with gluten was suitable for use as a safe oil for weight-loss dieting. In the present paper, the properties of the oil were improved, and the weight-loss effect was compared with that of heated oil. Fresh oil was heated for 10 h at 180 degrees C with or without gluten and filtered using filter paper. A powdered diet (AIN93G; no fat) was mixed with 7 wt% of fresh oil (control) or filtrates of the heated oils described above, and the mixture was fed to male Wistar rats for 12 weeks. The gluten and heated oil groups showed no gross symptoms attributable to the experimental oils but had a slowed body weight increase; a significant difference was found in weight on and after 21 weeks of age as compared to rats consuming the control diet, and fecal excretion was increased as compared to the control group. Serum levels of triacylglycerol, phospholipids, cholesterol, and glucose of the gluten and heated oil groups were significantly lower than those of the control group. High aspartate aminotransferase (AST) levels occurred more frequently in the heated oil group than the gluten group. The number of rats with dark red patches on the surface of the liver, which are indicative of liver damage, was higher in the heated oil group. In conclusion, the weight-reducing effect of the oil heated with gluten was confirmed and improved by removing traces of heated gluten from the oil.     

Zur endogene Lipidperoxidation bei diätetischer Belastung des Masthuhns

Endogenous Lipid Peroxidation in Broiler Chickens under Dietary Loads Growing broiler chickens were fed a Vitamin E-deficient diet containing 10% reesterified triglyceride from soy-bean-oil. Six groups with day-old broiler chicken were supplemented with 0, 20 or 100 ppm of vitamin E. On each vitamin level one group was fed with the fresh fat, the other was supplied with the fat being oxidized. Clinical data and development of body weight were registered. The animals were euthanised after 3 weeks. Pentane production of liver mitochondria and microsomes was measured and tocopherol concentrations were determined as well as the GSH-PX-activity in liver cytosol and plasma. Deficiency of vitamin E together with a high level of dietary linoleic acid leads to an imbalance in peroxidative and antioxidative metabolism and finally to disease. It is discussed if the clinical signs after consumption of linoleic acid-rich oxidized oils are caused by specific toxic secundary products.     

Highly hydrogenated dietary soybean oil modifies the responses to polychlorinated biphenyls in rats

The effects of dietary highly hydrogenated soybean oil (HSO) upon the changes caused by dietary polychlorinated biphenyls (PCBs) were examined in rats. Six groups of rats were fed the following diets for 30 d: a 20% soybean oil-containing diet (control diet), a diet in which a half of soybean oil was substituted with HSO (HSO-A diet), a diet in which cellulose powder was replaced with HSO (HSO-B diet) and these diets supplemented with 100 ppm PCBs (control+PCBs, HSO-A+PCBs and HSO-B+PCBs diets). Hepatic concentration of PCBs and relative liver weight were markedly decreased in rats fed with the HSO-A+PCBs diet compared with those fed with the other diets containing PCBs. Liver lipids and liver cholesterol were considerably decreased with a reciprocal increase in fecal sterol excretion by rats fed the HSO-A+PCBs and the HSO-B+PCBs diets compared with those fed with the control+PCBs diet. The fatty acid composition in hepatic phospholipids showed an independent increase of the saturated fatty acid content induced by dietary HSO and PCBs. Dietary PCBs also caused decreases in the amounts of monounsaturated and n-3 polyunsaturated fatty acids. These results suggest that dietary HSO prevents accumulation of PCBs in the liver and promotes the excretion of lipids stimulated by PCBs, accompanied by a change in fatty acid metabolism.