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 reducion of Δ9-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 Δ6-desaturase activity with linoleic acid as substrate and lowered activity with α-linolenic acid as substrate. In contrast, zinc deficient rats on the linseed oil diet had increased Δ6-desaturase activity with linoleic acid as substrate and unchanged activity with α-linolenic acid. Because linoleic acid is the main substrate for Δ6-desaturase in the rats fed coconut oil diet, and α-linolenic acid is the main substrate in the rats fed linseed oil diet, it is concluded that in vivo Δ6-desaturation was not changed by zinc deficiency in the rats fed both types of dietary fat. Activity of Δ5-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 Δ4-, Δ5-, and Δ6-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 α-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 ofn-3 polyunsaturated fatty acids.     

Selective incorporation of n-3 and n-6 fatty acids in essential fatty acid deficient rats in response to short-term oil feeding

Essential fatty acid deficient male Sprague Dawley rats were fed for 7 days a fat-free semi-synthetic diet supplemented with 10% by weight of different oil supplements. The oil supplement was a mixture of olive, safflower and linseed oils prepared at different proportions so the dietary n-9/n-6/n-3 ratios were approximate 2/1/1, 1/2/1, 1/1/2, and 1/1/1. The fatty acid compositions of plasma and liver lipids were then examined. Our results show polyunsaturated n-6 and n-3 fatty acids were selectively incorporated into plasma and liver phospholipids, and also into plasma cholesteryl esters. A preferential incorporation of n-6 over n-3 fatty acids into plasma cholesteryl esters and phospholipids was also observed.     

Effect of long-term feeding olive and sunflower oils on fatty acid composition and desaturation activities of liver microsomes

Changes in microsomal fatty acid composition, delta 9- and delta 6-desaturase activities and cholesterol and phosphorus liver content were studied in dogs fed olive and sunflower oil diets. No changes were observed in the saturated fatty acids between dietary groups. The level of monounsaturated fatty acids was more elevated in animals fed the OO diet, because of its high relative content in this diet although the in vitro delta 9-desaturase activity was similar in microsomes from the two groups. The proportion of arachidonic acid was similar in SO and OO fed animals. This similar level occurred despite a significant increase in the level of linoleic acid in membrane lipids as a result of feeding the SO supplement. The in vitro delta 6-desaturase activity in liver microsomes showed no differences between dogs fed the two diets. Thus, the higher desaturation presented in vivo by microsomes from OO group may be related to the inhibition by linoleic acid of delta 6-desaturase in dogs fed the SO diet. The polyunsaturated fatty acids (PUFA) from the n-3 series were higher in microsomal phosphatidylcholine and phosphatidylethanolamine from animals fed the OO supplemented diet. The cholesterol/phosphorus molar ratio was higher in the SO group in which the unsaturation index was only slightly affected in phospholipids.     

Eritadenine-induced alterations of plasma lipoprotein lipid concentrations and phosphatidylcholine molecular species profile in rats fed cholesterol-free and cholesterol-enriched diets

The effects of dietary eritadenine on the concentration of plasma lipoprotein lipids and the molecular species profile of plasma lipoprotein phosphatidylcholine (PC) were investigated in rats fed cholesterol-free and cholesterol-enriched diets to obtain insights into the relationship between the changes in PC molecular species profile and the hypocholesterolemic action of eritadenine. The effect of eritadenine on the secretion rate of very low density lipoprotein (VLDL) from the liver was also estimated. Rats were fed the control or eritadenine-supplemented (50 mg/kg) diets with or without exogenous cholesterol for 14 d. Eritadenine supplementation significantly decreased the cholesterol of major plasma lipoproteins, high density lipoprotein and VLDL, in rats fed cholesterol-free and cholesterol-enriched diets, respectively. The ratio of PC to phosphatidylethanolamine, delta6-desaturase activity, and the ratio of arachidonic acid to linoleic acid in liver microsomes were markedly decreased by eritadenine irrespective of the presence or absence of exogenous cholesterol. Dietary eritadenine increased the proportion of 16:0-18:2 molecular species with a decrease in 18:0-20:4 in plasma lipoprotein PC in both rats fed cholesterol-free and cholesterol-enriched diets. Eritadenine did not depress the secretion rate of VLDL in rats fed a cholesterol-free diet containing a high level of choline. The results indicate that dietary eritadenine elicits its hypocholesterolemic action with modulations of the fatty acid and molecular species profiles of PC irrespective of the presence or absence of exogenous cholesterol. The eritadenine-induced alteration of PC molecular species profile is discussed in relation to the hypocholesterolemic action of eritadenine.     

Lipoprotein lipase and lipogenic enzyme activities in adipose tissue from rats fed different lipid sources

This work was designed to study the effect of different lipid sources on the activities of lipoprotein lipase and lipogenic enzymes in adipose tissue from rats fedad libitum or energy-controlled diets. Male Wistar rats were fed diets containing 40% of energy as fat (olive oil, sunflower oil, palm oil or beef tallow), for 4 wk. Underad libitum feeding no differences were found among dietary fat groups in final body weight, adipose tissue weights and total body fat. Under energy-controlled feeding, despite isoenergetic intake, rats fed the beef tallow diet gained significantly less weight than rats fed the other three diets. Beef tallow fed rats showed the lowest values for adipose tissue weights and total body fat. When rats had free access to food no effect of dietary lipid source on lipogenic enzyme activities was found. In contrast, under energy-controlled feeding rats fed the beef tallow diet showed significantly higher activities of glucose-6-phosphate dehydrogenase and fatty acid synthase than rats fed the other three diets. Heparin-releasable lipoprotein lipase activity in perirenal and subcutaneous adipose tissues was not different among rats fed olive oil, safflower oil, palm oil or beef tallow. When comparing both adipose tissue anatomical locations, significantly higher activities were found in subcutaneous than in perirenal fat pad independently of dietary fat. In conclusion, under our experimental protocol, lipogenesis in rat adipose tissue does not seem to be affected by dietary fat type.     

Interactions of saturated, n-6 and n-3 polyunsaturated fatty acids to modulate arachidonic acid metabolism

Anti-thrombotic effects of omega-3 (n-3) fatty acids are believed to be due to their ability to reduce arachidonic acid levels. Therefore, weanling rats were fed n-3 acids in the form of linseed oil (18:3n-3) or fish oil (containing 20:5n-3 and 22:6n-3) in diets containing high levels of either saturated fatty acids (hydrogenated beef tallow) or high levels of linoleic acid (safflower oil) for 4 weeks. The effect of diet on the rate-limiting enzyme of arachidonic acid biosynthesis (delta 6-desaturase) and on the lipid composition of hepatic microsomal membrane was determined. Both linseed oil- or fish oil-containing diets inhibited conversion of linoleic acid to gamma-linolenic acid. Inhibition was greater with fish oil than with linseed oil, only when fed with saturated fat. delta 6-Desaturase activity was not affected when n-3 fatty acids were fed with high levels of n-6 fatty acids. Arachidonic acid content of serum lipids and hepatic microsomal phospholipids was lower when n-3 fatty acids were fed in combination with beef tallow but not when fed with safflower oil. Similarly, n-3 fatty acids (18:3n-3, 20:5n-3, 22:5n-3, and 22:6n-3) accumulated to a greater extent when n-3 fatty acids were fed with beef tallow than with safflower oil. These observations indicate that the efficacy of n-3 fatty acids in reducing arachidonic acid level is dependent on the linoleic acid to saturated fatty acid ratio of the diet consumed.     

Effect of dietary alpha-linolenic acid on the activity and gene expression of hepatic fatty acid oxidation enzymes

The activities of hepatic fatty acid oxidation enzymes in rats fed linseed and perilla oils rich in alpha-linolenic acid (alpha-18:3) were compared with those in the animals fed safflower oil rich in linoleic acid (18:2) and saturated fats (coconut or palm oil). Mitochondrial and peroxisomal palmitoyl-CoA (16:0-CoA) oxidation rates in the liver homogenates were significantly higher in rats fed linseed and perilla oils than in those fed saturated fats and safflower oil. The fatty oxidation rates increased as dietary levels of alpha-18:3 increased. Dietary alpha-18:3 also increased the activity of fatty acid oxidation enzymes except for 3-hydroxyacyl-CoA dehydrogenase. Unexpectedly, dietary alpha-18:3 caused great reduction in the activity of 3-hydroxyacyl-CoA dehydrogenase measured with short- and medium-chain substrates but not with long-chain substrate. Dietary alpha-18:3 significantly increased the mRNA levels of hepatic fatty acid oxidation enzymes including carnitine palmitoyltransferase I and II, mitochondrial trifunctional protein, acyl-CoA oxidase, peroxisomal bifunctional protein, mitochondrial and peroxisomal 3-ketoacyl-CoA thiolases, 2, 4-dienoyl-CoA reductase and delta3, delta2-enoyl-CoA isomerase. Fish oil rich in very long-chain n-3 fatty acids caused similar changes in hepatic fatty acid oxidation. Regarding the substrate specificity of beta-oxidation pathway, mitochondrial and peroxisomal beta-oxidation rate of alpha-18:3-CoA, relative to 16:0- and 18:2-CoAs, was higher irrespective of the substrate/albumin ratios in the assay mixture or dietary fat sources. The substrate specificity of carnitine palmitoyltransferase I appeared to be responsible for the differential mitochondrial oxidation rates of these acyl-CoA substrates. Dietary fats rich in alpha-18:3-CoA relative to safflower oil did not affect the hepatic activity of fatty acid synthase and glucose 6-phosphate dehydrogenase. It was suggested that both substrate specificities and alterations in the activities of the enzymes in beta-oxidation pathway play a significant role in the regulation of the serum lipid concentrations in rats fed alpha-18:3.     

Comparative effects of perilla and fish oils on the activity and gene expression of fatty acid oxidation enzymes in rat liver

The activity and mRNA level of hepatic enzymes in fatty acid oxidation and synthesis were compared in rats fed diets containing either 15% saturated fat (palm oil), safflower oil rich in linoleic acid, perilla oil rich in α-linolenic acid or fish oil rich in eicosapentaenoic (EPA) and docosahexaenoic acids (DHA) for 15 days. The mitochondrial fatty acid oxidation rate was 50% higher in rats fed perilla and fish oils than in the other groups. Perilla and fish oils compared to palm and safflower oils approximately doubled and more than tripled, respectively, peroxisomal fatty acid oxidation rate. Compared to palm and safflower oil, both perilla and fish oils caused a 50% increase in carnitine palmitoyltransferase I activity. Dietary fats rich in n-3 fatty acids also increased the activity of other fatty acid oxidation enzymes except for 3-hydroxyacyl-CoA dehydrogenase. The extent of the increase was greater with fish oil than with perilla oil. Interestingly, both perilla and fish oils decreased the activity of 3-hydroxyacyl-CoA dehydrogenase measured using short- and medium-chain substrates. Compared to palm and safflower oils, perilla and fish oils increased the mRNA level of many mitochondrial and peroxisomal enzymes. Increases were generally greater with fish oil than with perilla oil. Fatty acid synthase, glucose-6-phosphate dehydrogenase, and pyruvate kinase activity and mRNA level were higher in rats fed palm oil than in the other groups. Among rats fed polyunsaturated fats, activities and mRNA levels of these enzymes were lower in rats fed fish oil than in the animals fed perilla and safflower oils. The values were comparable between the latter two groups. Safflower and fish oils but not perilla oil, compared to palm oil, also decreased malic enzyme activity and mRNA level. Examination of the fatty acid composition of hepatic phospholipid indicated that dietary α-linolenic acid is effectively desaturated and elongated to form EPA and DHA. Dietary perilla oil and fish oil therefore exert similar physiological activity in modulating hepatic fatty acid oxidation, but these dietary fats considerably differ in affecting fatty acid synthesis.     

Incorporation of dietary cis and trans isomers of octadecenoate in lipid classes of liver and hepatoma.

Groups of rats bearing Morris minimal deviation hepatoma 7288CTC were fed a fat-free diet supplemented with either 0.5% safflower oil (diet A), 15% safflower oil or free acids (diets Band C), or 15% safflower oil or free safflower fatty acids (diet D) for 4 weeks. A group of normal rats was also fed diet D. Triglycerides, cholesteryl esters, phosphatidylcholines, and phosphatidylethanolamines isolated from livers and hepatomas of animals on each diet were analyzed quantitatively for positional isomers in the cis- and trans-octadecenoate fractions. When sufficient samples could be obtained, the cis- and trans-hexadecenoate fractions were also analyzed. Plasma from normal rats on diet D was analyzed in the same manner. The octadecenoate fractions of all hepatoma and liver lipid classes from animals fed diets A, B, and C were greater than 95% the cis isomers. Trans isomers accounted for approximately 15, 30, 50, and 70% of the octadecenoate fractions isolated from liver triglycerides, cholesteryl esters, phosphatidylcholines, and phosphatidylethanolamines, respectively, of animals fed diet D. In contrast, all hepatoma lipid classes from animals on diet D contained the same approximate percentage of trans isomers (15 to 20%). Oleic and vaccenic acids were the major positional cis-octadecenoate isomers of all liver and hepatoma lipid classes from animals fed diets A, B, and C. The ratios of oleic to vaccenic, unaffected by diets A, B, and C, differed for each lipid class in liver, but the ratios were similar for the two hepatoma neutral lipid classes and for the two phospholipid classes. The cis-octadecenoate fractions from all liver and hepatoma lipid classes of animals fed diet D consisted predominantly of the delta9, delta11, and delta12 isomers. The cis delta10 isomer, which was a major isomer of the diet, was almost excluded from liver, hepatoma, and plasma lipids. The positional isomers of the trans-octadecenoate fractions from liver and hepatoma triglycerides and cholesteryl esters exhibited the same approximate distribution as the trans fatty acids of diet D. In contrast, the 10-trans-octadecenoate, like 10-cis-octadecenoate, was almost excluded from the phospholipids of liver and plasma. Unlike liver, the hepatoma phospholipids contained 10-trans-octadecenoate at approximately half the percentage of neutral lipids. Because diet D contained no hexadecenoic fatty acids, the occurrence of trans-hexadecenoate isomers in liver and plasma lipids indicated a chain shortening process. Predominance of the 8-trans-hexadecenoate isomer indicated a preference of the 10-trans-octadecenoate isomer for chain shortening.     

Changes in lipid composition and desaturase activities of duodenal mucosa induced by dietary fat

In the present work we have studied the effects of feeding either olive or sunflower oil on lipid composition and desaturase activities of duodenal mucosa microsomes. Duodenal microsomes prepared from dogs fed the sunflower oil diet showed higher percentages of saturated, of linoleic and of n - 3 polyunsaturated fatty acids as well as lower levels of oleic, dihomo-gamma-linolenic and arachidonic acids in phosphatidylcholine and phosphatidylethanolamine than those prepared from animals fed the olive oil diet. In sphingomyelin, the dietary supplementation did not produce significant differences between the two groups. The cholesterol/phospholipid molar ratio was higher in the sunflower oil group than in the olive oil group. The in vitro delta 9-desaturase activity was higher in microsomes from the olive oil dogs. The delta 6-desaturase activity was similar in microsomes from the two groups and lower than that found for delta 9-desaturase activity. Desaturase activities were higher in duodenal microsomes than those previously found for liver microsomes.     

Dietary mold oil rich in gamma linolenic acid increases insulin-dependent glucose utilization in isolated rat adipocytes

Effects of dietary fats differing in fatty acid composition on insulin-stimulated glucose metabolism in adipocytes isolated from rat white adipose tissue were compared. Rats were fed experimental diets containing various fats differing in fatty acid composition for 7 days. In the first experiment, rats were fed palm oil mainly consisting of palmitic (45.3%) and oleic acids (39.1%) or safflower oil rich in linoleic acid (71.6%). In the second trial, rats were fed palm oil, or a fat mixture rich in linoleic acid or mold oil rich in gamma-linolenic acid. Contents of fatty acids except for linoleic and gamma-linolenic acid were comparable between the fat mixture and mold oil. The former was devoid of gamma-linolenic acid and contained 42.0% linoleic acid, while the latter contained 25.9% gamma-linolenic and 15.7% linoleic acids. In the first experiment, the insulin-dependent increase in glucose oxidation and incorporation into lipids was higher in rats fed safflower oil compared to those fed palm oil. In the second experiment, the insulin-dependent increase in glucose oxidation and incorporation into lipids was higher in rats fed the fat mixture and mold oil than in those fed palm oil. However, the extent of the increase in these parameters was much greater in rats fed mold oil than in those fed the fat mixture. Therefore, dietary gamma-linolenic acid compared to linoleic acid increases glucose metabolism in response to insulin stimuli in isolated rat adipocytes.     

Isoproterenol-induced mortality and cardiac lipids of aspirin-pretreated rats with various fat intakes

The effect of altering cardiac concentrations of precursors and inhibitors of prostaglandin synthesis by varying fat intake was determined in rats injected with the cardiotoxic drug isoproterenol, following pretreatment with aspirin or potassium phosphate buffer solution. Prior to injection, four groups of rats were fed either a low-fat diet (3.7 energy percent coconut oil 3.7 energy percent safflower oil) or a high-fat diet (3.7 energy percent safflower oil-36.4 energy percent coconut oil mixture or 40.1 energy percent safflower oil.) Mortality as well as fatty acid composition of cardiac lipids changed in response to altered kinds and amounts of fats. Mortality and cardiac C20:4/C22:6 ratio were lowered by feeding 3.7 energy percent coconut oil, and increased by feeding 40.1 energy percent safflower oil. Aspirin reduced mortality in rats fed 40.1 energy percent safflower oil, but not in rats fed other diets. Results suggest that dietary manipulations which increase tissue content of polyunsaturated fatty acids of the n-6 type relative to those of the n-3 type may increase sensitivity to isoproterenol, and that effectiveness of aspirin in reducing isoproterenol-induced mortality depends upon the n-6/n-3 ratio of cardiac fatty acids.     

Short-term effect of dietary cholesterol on tissue n-6 fatty acids in fat-deficient rats

Weanling female rats raised on a fat-free diet for 8 weeks were then given the same diet supplemented with 0, 0.25, 0.5, or 1% by weight of cholesterol in addition to 10% of safflower oil for 3 days. Fatty acid compositions of cholesteryl esters (CE), triglycerides (TG), and phospholipids (PL) in liver and plasma were examined. Cholesterol feeding increased plasma and liver cholesterol contents and also affected the patterns of n-6 polyunsaturated fatty acids. There were no consistent changes in either plasma and liver TG which contained little 20:3n-6 and 20:4n-6. The levels of 20:3n-6 increased in plasma and liver PL, while proportions of 20:4n-6 decreased in liver and plasma CE. However, the absolute amount of 20:4n-6 in cholesteryl esters increased because of a threefold rise in cholesteryl ester levels. The changes might be attributable to an increased utilization of 20:4n-6 for cholesterol transport and/or an inhibition of delta 5-desaturation of n-6 fatty acids by cholesterol feeding.     

Interaction of dietary fat types and sesamin on hepatic fatty acid oxidation in rats

The interaction of sesamin, one of the most abundant lignans in sesame seed, and types of dietary fats affecting hepatic fatty acid oxidation was examined in rats. Rats were fed purified experimental diets supplemented with 0% or 0.2% sesamin (1:1 mixture of sesamin and episesamin), and containing 8% of either palm, safflower or fish oil for 15 days. Among the groups fed sesamin-free diets, the activity of various fatty acid oxidation enzymes was higher in rats fed fish oil than in those fed palm and safflower oils. Dietary sesamin increased enzyme activities in all groups of rats given different fats. The extent of the increase depended on dietary fat type, and a diet containing sesamin and fish oil in combination appeared to increase many of these parameters synergistically. In particular, the peroxisomal palmitoyl-CoA oxidation rate and acyl-CoA oxidase activity levels were much higher in rats fed sesamin and fish oil in combination than in animals fed sesamin and palm or safflower oil in combination. Analyses of mRNA levels revealed that a diet containing sesamin and fish oil increased the gene expression of various peroxisomal fatty acid oxidation enzymes and PEX11alpha, a peroxisomal membrane protein, in a synergistic manner while it increased the gene expression of mitochondrial fatty acid oxidation enzymes and microsomal cytochrome P-450 IV A1 in an additive manner. It was concluded that a diet containing sesamin and fish oil in combination synergistically increased hepatic fatty acid oxidation primarily through up-regulation of the gene expression of peroxisomal fatty acid oxidation enzymes.     

Activities of fatty acid desaturases and fatty acid composition of liver microsomes in rats fed beta-carotene and 13-cis-retinoic acid

The fatty acid composition of microsomal lipids and the activities of delta 9- and delta 6-desaturases in liver microsomes of rats fed diets supplemented with beta-carotene and two levels of 13-cis-retinoic acid were studied. Four groups of male, weanling rats were fed semipurified diets containing 0 or 100 mg beta-carotene per kg diet, and 20 or 100 mg 13-cis-retinoic acid per kg diet. After 11 weeks of feeding, the rats were killed, liver microsomes were prepared and assayed for delta 9-desaturase and delta 6-desaturase activities. The activity of delta 9-desaturase was lower in liver microsomes of rats fed beta-carotene-supplemented diet or the diet supplemented with the higher level of 13-cis-retinoic acid. Microsomal delta 6-desaturase activity was, however, higher in liver of rats fed 13-cis retinoic acid; there was no effect of beta-carotene on delta 6-desaturase activity. The fatty acid compositional data on total lipids of liver microsomes were consistent with the diet-induced changes in fatty acid desaturases. Phospholipid composition of liver microsomes was also altered as a result of feeding beta-carotene or 13-cis-retinoic acid-containing diets. The proportions of phosphatidylethanolamine were generally higher, whereas those of phosphatidylcholine were lower in the experimental groups as compared with the control.     

Iron utilization and liver mineral concentrations in rats fed safflower oil, flaxseed oil, olive oil, or beef tallow in combination with different concentrations of dietary iron

Diets with a higher proportion of polyunsaturated fatty acids (i.e., linoleic acid) have decreased iron absorption and utilization compared with diets containing a higher proportion of the saturated fatty acid stearic acid (e.g., beef tallow). However, less is known regarding the influence of other polyunsaturated or monounsaturated fatty acids, along with higher dietary iron, on iron absorption and utilization. The present study was conducted to compare the effects of dietary fat sources known to vary in (n-3), (n-6), and (n-9) fatty acids on iron utilization and liver mineral concentrations. Male weanling rats were fed a diet containing 10, 35, or 100 μg/g iron in combination with saffower oil, flaxseed oil, olive oil, or beef tallow for 8 wk. Indicators of iron status, iron utilization, and liver iron concentrations were unaffected by an interaction between the fat source and iron concentration. Plasma copper was the only variable affected by an interaction between the fat source and dietary iron. Findings of this study demonstrate that flaxseed oil and olive oil may alter tissue minerals and affect iron utilization. Further studies should be conducted to establish the effect of varying (n-3), (n-6), and (n-9) fatty acids on trace mineral status and iron utilization. Data were presented in part at Experimental Biology 2000 as a poster session. A. D. Shotton and E. A. Droke, Dietary fat and iron modify immune function, FASEB J. 14, A239 (2000).     

Effects of dietary eritadenine on the liver microsomal Delta6-desaturase activity and its mRNA in rats

Eritadenine, a hypocholesterolemic factor of Lentinus edodes mushroom, has a wide range of effects on lipid metabolism such as an increase in the liver microsomal phosphatidylethanolamine (PE) concentration, a decrease in the liver microsomal Delta6-desaturase activity, and an alteration of the fatty acid and molecular species profile of liver and plasma lipids. In this study, the time-dependent effects of dietary eritadenine on several variables concerning lipid metabolism were investigated in rats to clarify the sequence of metabolic changes caused by eritadenine, with special interest in the association of the liver microsomal phospholipid profile and the activity of Delta6-desaturase. The effect of dietary eritadenine on the abundance of mRNA for Delta6-desaturase was also investigated. When the time required for a half-change of variables was estimated during the first 5 days after the change from the control diet to the eritadenine-supplemented (50 mg/kg) diet, the change rates of the variables were fastest in the following order: alteration of the liver microsomal phospholipid profile>decrease in liver microsomal Delta6-desaturase activity>alteration of the fatty acid and molecular species profiles of microsomal and plasma phosphatidylcholine (PC)>decrease in the plasma cholesterol concentration. There was a significant correlation between the Delta6-desaturase activity and liver microsomal PE concentration, but not PC concentration, or the proportion of PC and PE or the PC/PE ratio. The suppression of Delta6-desaturase activity by dietary eritadenine was accompanied by a significant reduction in the abundance of mRNA for the enzyme. These results suggest that dietary eritadenine might suppress the activity of liver microsomal Delta6-desaturase by altering the microsomal phospholipid profile, as represented by an increase in PE concentration, and that the effect of eritadenine is mediated by the regulation of gene expression.     

Preparation and Regeneration of Chalara paradoxa Protoplasts

A lignan mixture from sesame salad oil containing episesamin and sesamin as major components was fed to rats. Lignans at the dietary level of approximately 0.2% tended to decrease plasma and liver cholesterol levels with an accompanying increase in the fecal excretion of neutral steroids, particularly when the dietary fat source was evening primrose oil containing γ-linolenic acid. There was a decreasing trend in the specific activity of Δ5-desaturase in liver microsomes whereas that of Δ6-desaturase tended to increase, in particular in rats fed with safflower oil. The proportion of dihomo-γ-linolenate increased in response to the reduction of Δ5-desaturation activity, and that of docosapentaenoate (n-6) decreased in liver phosphatidylcholine in both groups of rats, suggesting that lignans interfered with various steps of linoleate metabolism. However, the production by the aorta of prostacyclin and by platelets of thromboxane A₂ was not influenced by lignans. Thus, episesamin and/or sesamin functioned as a regulator of cholesterol and linoleate metabolism in rats.     

Dietary fish oil administration retards the development of hypertension and influences vascular neuroeffector function in the stroke prone spontaneously hypertensive rat (SHRSP).

An influence of fish oils (rich in eicosapentaenoic acid, EPA) in modulating (a) the development of hypertension in the stroke prone spontaneously hypertensive rat (SHRSP) and (b) vascular neuroeffector mechanisms in the SHRSP was explored. Rats (SHRSP) were placed on a series of diets for a period of 13 weeks from 4 weeks of age. The fatty acid composition of the diets was derived from fish oil, olive oil, safflower oil or beef fat. After 13 weeks, rats fed diets containing fish oil (at a total dietary fat level of either 5% or 15%) had mean blood pressures approximately 20-25 mmHg lower than other SHRSP rats maintained on diets containing either olive oil, safflower oil or beef fat. The dietary schedules providing fish oil depressed the contractile responses mediated by sympathetic nerve stimulation in the mesenteric vascular bed preparation. The results suggest that the n-3 polyunsaturated fatty acids retard the development of hypertension in the SHRSP rat and modulate the contractile responses of blood vessels mediated by sympathetic nerves in the isolated perfused mesenteric vascular bed preparation.     

Influence of amount and type of dietary fat on plasma cholesterol concentrations in goats

Adult, non-pregnant, dry goats were fed diets differing in the amount and type of fat. To modulate the type of dietary fat, rations containing either palm oil or olive oil were used, the amount of fat being 86 g/kg dry matter (DM). To modulate the amount of dietary fat, the oils were replaced by an isoenergetic amount of native corn starch so that the dietary fat concentration dropped to 26 g/kg DM. The high fat diets, when compared with the low fat diet, significantly raised plasma total cholesterol by 91%, high-density lipoprotein (HDL) cholesterol by 100%, triglycerides by 47% and phospholipids by 57%. On an average, dietary palm oil versus olive oil significantly increased plasma total cholesterol by 6%, HDL cholesterol by 9% and phospholipids by 4%, but left plasma triglycerides unchanged. This study shows that plasma lipid concentrations in goats respond to the amount and type of fat in the diet.