An interaction of DDT in the metabolism of essential fatty acids

The growth of female rats was depressed further by the incorporation of DDT into a ration deficient in essential fatty acids (EFA). With female rats fed a ration supplemented with EFA, DDT produced a slight stimulation in growth. DDT also produced an increase in the 20∶3ω9/20∶4ω6 ratio in liver lipids of male rats fed a ration deficient in EFA. These data indicate an effect in EFA nutrition. Substantial changes in the fatty acid composition of liver lipids resulted from the feeding of DDT. The proportion of 16∶0 was decreased, while that of 18∶0 was increased. With rats on the supplemented rations an increase in the proportion of 20∶4ω6 was observed, while in the deficient rats a comparable increase was observed in the proportion of 20∶3ω9. These changes in fatty acid composition have been related to the proliferation of hepatic smooth endoplasmic reticulum induced by the DDT, and it is suggested that this effect could increase the demand for EFA by the liver, thus influencing EFA nutrition. Technical Paper No. 3156, Oregon Agricultural Experiment Station.     

Isolated brain capillary endothelia: Influence of various levels of essential fatty acids on the acyl group composition of glycerophospholipids

On day seven of gestation, Wistar rats were assigned to a high essential fatty acid (EFA), low EFA, or a fat free diet. The same diets were continued during lactation. On weaning, the offspring were fed the same diets as their mother. Rats were killed at 222 days, brain capillary endothelia isolated, and total lipids extracted from the purified capillaries. The composition of the constituent fatty acids of ethanolamine glycerophospholipid (EGP), choline glycerophospholipid (CGP), and the alk-1-eny EGP composition from each diet is reported. A decrease in dietary EFA led to reduced proportions of total saturated acyl groups in EGP with no change observed in the total saturated acyl groups from CGP, and an increase in monoenoic fatty acids, particularly 18∶1n−9 for each phospholipid class. The proportions of 20∶4n−6 in alk-1-enyl EGP were reduced in fat-free fed animals. In addition, the relationship between 20∶3n−9 and 20∶4n−6 fatty acids in brain capillary endothelia were markedly increased with a reduction in dietary fat. Low EFA and fat deficient animals showed a tendency to sequester 22∶6n−3.     

Reduction of essential fatty acid deficiency in rats fed a low iron fat free diet

Young male rats were fed ad libitum for 8 weeks a low iron fat-free (FF-Fe) diet or a fat-free diet supplemented with iron (FF+Fe). The relative levels of 16∶1 to 16∶0 and 18∶1 to 18∶0 in the total fatty acids of liver and other tissues (plasma, erythrocytes and intestinal mucosa) were considerably decreased because of a lack of dietary iron. In rats fed the FF-Fe diet, the levels of essential fatty acids (18∶2ω6+20∶4ω6) in tissues were 2-to 3-fold greater than in the corresponding tissues of rats fed the FF+Fe diet. Eicosatrienoic acid (20∶3ω9) levels in tissue lipids from rats fed the FF+Fe diet were high (8–16%), whereas they were low (2–5%) in the case of animals fed the FF-Fe diet. The proportion of 20∶4 in total fatty acids of tissues was 2-to 3-fold greater in rats fed the FF-Fe diet than when they were fed the FF+Fe diet. Therefore, the relative levels of 20∶3ω9/20∶4ω6 varied from 1-2.9 in tissue lipids of rats fed the FF+Fe diet, while it varied only from 0.2–0.3 in animals fed the FF-Fe diet. These results suggest that a lack of dietary iron may reduce the synthesis of 16∶1, 18∶1, 20∶3 and 20∶4 and the metabolism of 20∶4.     

Effects of dietary saturated andtrans fatty acids on cholesteryl ester synthesis and hydrolysis in the testes of rats

Studies were made of the enzymic synthesis and hydrolysis of cholesteryl esters in rat testes. Weanling rats were fed for 14 weeks diets containing 5% by wt of hydrogenated coconut oil (HCO), a concentrate of ethyl elaidate and linolelaidate (TRANS), devoid of essential fatty acids (EFA), or safflower oil (SAFF). Cholesterol esterifying activity was localized in the soluble fraction, and cholesteryl ester hydrolase activity was distributed in both particulate and soluble fractions obtained from tissue homogenates. The optimum pH was 6.0 for esterification and 6.9–7.0 for hydrolysis. Neither esterifying nor hydrolytic activity was affected by freezing and thawing, but both reactions were inhibited by heat or sonication. The animals of both the HCO and TRANS groups had developed an EFA deficiency before they were sacrificed. The EFA deficiency produced upon feeding the HCO diet had no apparent effect on the synthesis and hydrolysis of cholesteryl esters in rat testes. The TRANS diet influenced the development of the testes as judged by their size, and cholesterol esterifying and cholesteryl ester hydrolyzing activities were suppressed in the testes of the animals of this group. A major difference in the effects of the HCO and TRANS diets on the lipids of the testes was the relatively minor amount of eicosatrienoic acid (20∶3) and the elevated level of docosapentaenoic acid (22∶5) in the cholesteryl esters of the testicular lipids of the TRANS group.     

A relationship between essential fatty acid and vitamin E deficiency

To test whether vitamin E deficiency might influence the course of essential fatty acid (EFA) deficiency, Long Evans rats were fed diets containing a marginal amount (1.5% of calories) of 18∶2ω6 or 18∶3ω3 fatty acid with complete absence of the other and with or without vitamin E. Vitamin E contents decreased continuously in serum and liver in all rats fed the E-free diets but in the brains of only the rats fed the marginal 18∶3ω3, E-free diet. It is considered that the vitamin E is cooxidized in the liver with 22∶6ω3, since this fatty acid is very low in livers of the rats fed the marginal 18∶2ω6 diet but much higher in livers of the rats fed the marginal 18∶3ω3 diet. Brain 22∶6ω3 values are comparable for both groups. The source of 22∶6ω3 is evidently in the mother's milk, since following weaning there is a precipitous drop in 22∶6ω3 in serum, liver and carcass of rats on the 18∶2ω6-containing diet. No significant signs of EFA deficiency were seen in the E-deficient rats. Operated for the U.S. Department of Energy by the University of California under contract no. DE-AC03-76-SF00012.     

Interrelationship between dietarytrans fatty acids and the 6- and 9-desaturases in the rat

Studies are reported on the effects of dietarytrans fatty acids on the 6- and 9-acyl desaturase activities in the liver microsomes of rats fed essential fatty acid (EFA)-deficient and non-FFA-deficient diets. In experiment I, weanling male rats were fed a semisynthetic diet with either 10% safflower oil (SAF) or 10% hydrogenated coconut oil (HCO). At the age of one year, half of the dietary fat was replaced by a supplement containing elaidate, linolelaidate andcis,trans-trans,cis-18∶2 (TRANS) for 12 weeks. In experiment II, male rats which were kept from weaning on a 10% SAF diet for one year received one of the following fat supplements for a 12-week period: 10% HCO, 9% HCO+1% TRANS, or 5% HCO+5% TRANS. Feeding TRANS depressed the 6-desaturase activity in the liver microsomes, especially in the EFA-deficient rats (HCO+TRANS group of experiment I). Unlike the 6-deaturase activity, the 9-desaturase activity was not inhibited by the dietarytrans fatty acids and was significantly stimulated in the non-EFA-deficient rats (SAF+TRANS group of experiment I and HCO+TRANS groups of experiment II). This was evidenced by incubation reactions and by comparisons of fatty acid consumptions and microsomal fatty acid levels, showing extra biosynthesis of 16∶1 and 18∶1 when TRANS was fed. The biosynthesis of essential (n−6) fatty acids was depressed by the TRANS supplement in EFA-deficient as well as in non-EFA-deficient animals.     

Rat testicular lipids and dietary isomeric fatty acids in essential fatty acid deficiency

Weanling rats were fed essential fatty acid-deficient diets, either completely fat-free, or with partially hydrogenated fish oil (PHFO, 28 wt %), or with fractions derived from PHFO containing primarily positional isomers oftrans-eicosenoate (20∶1, 3 wt %) ortrans-docosenoate (22∶1, 3 wt %). Control animals were fed a peanut oil-containing diet (28 wt %). After 5 or 15 weeks on the diet, the content of neutral and phosphorus-containing lipids in the testes was determined. The fatty acid distribution in major lipid classes was analyzed for animals fed the diets for 15 weeks. The testicular stage of maturation or degeneration was assessed by histology. The group fed PHFO exhibited signs of complete testicular degeneration, or lack of maturation, already after 5 weeks, whereas the animals on the diets with the very long chain monoenoic acids suffered severe degenerations only after 15 weeks. In the PHFO-fed rats, a sharp decline in the concentration of testicular triacylglycerols was observed. In all of the essential fatty acid-deficient groups, an increase in testicular sphingomyelin was observed. Cholesterol levels were fairly similar among all dietary groups. The total testicular fatty acids of the PHFO-fed animals contained somewhat more eicosadienoic acid than found in the other groups, and somewhat less (n−9)-acids. In all EFA-deficient groups, (n−6)-acids were lowered, in particular in triacylglycerols and phosphatidyl cholines. The PHFO group did not show a lower (n−6)-concentration than the other deficient groups, in spite of the more severe symptoms of deficiency. There was no evidence of a major accumulation of long chain isomeric fatty acids in the degenerated testes of the PHFO-, 20∶1, and 22∶1-fed groups.     

Effect of dietary fatty acid composition on the biosynthesis of unsaturated fatty acids in rat liver microsomes

A study was made of the influence of semisynthetic diets of low and high unsaturation on the fatty acid composition and desaturation-chain elongation enzymatic activity of the liver microsomal fractions of male Sprague-Dawley rats of different ages. Groups of rats were fed 5 or 20% coconut oil (CO), or a 5 or 20% mixture of corn and menhaden oils (3∶7) (CME) from weaning to 100 wk of age. Growth rate and food consumption were measured during this period in which animals were sacrificed at 36, 57, 77 and 100 wk of age. Both the level and composition of the dietary fat supplements produced marked effects on the fatty acid composition of the liver microsomal lipids. In general, the fatty acid composition of the microsomal fractions reflected that of the dietary fat and was more unsaturated with the higher level of fat fed. The rate of conversion of linoleic to arachidonic acid in assays performed in vitro with liver microsomal preparations from animals of the different groups also showed marked differences. The 6-desaturase-chain elongation activity was higher in the 5% than 20% group and corresponded to the essential fatty acid (EFA) status of the animals in these groups as represented by the triene-tetraene ratio of the microsomal lipid. The relationship of the 6-desaturase activity to fatty acid composition of the microsomal lipid indicated that if varied directly with the level of 20∶3ω9, 18∶1 and 16∶1 and was inhibited by arachidonic acid. The activity of the 6-desaturase enzyme system was lowest in the liver microsomal fraction obtained from the animals fed the CME diets and appeared to be suppressed by the high levels of 20∶5 and 22∶6 that accumulated in the microsomal lipid. Accordingly, the levels of arachidonic acid were lower in the microsomal lipid of these groups than those of the corresponding CO groups in spite of a greater abundance of linoleic acid in the diet. The data suggest that the activity of the 6-desaturase-chain elongation system is regulated by the fatty acid composition of the microsomal lipid as influenced by the composition of the dietary fat.     

Specific inhibition of hepatic fatty acid synthesis exerted by dietary linoleate and linolenate in essential fatty acid adequate rats

Dietary linoleate and linolenate were investigated for their ability to specifically inhibit liver and adipose tissue lipogenesis in meal-fed (access to food 900-1,200 hr), essential fatty acid (EFA) adequate rats. Supplementing a high carbohydrate diet containing 2.5% safflower oil with 3% palmitate 16∶0, oleate 18∶1, or linoleate 18∶2 did not affect in vivo liver or adipose tissue fatty acid synthesis. However, 18∶2 addition to the basal diet did result in a significant (P<0.05) decline of liver fatty acid synthetase (FAS) and glucose-6-phosphate dehydrogenase (G6PD) activities. When the safflower oil content of the basal diet was reduced to 1%, the addition of 3% 18∶2 or linolenate 18∶3 significantly (P<0.05) depressed hepatic FAS, G6PD, and in vivo fatty acid synthesis by 50%. Addition of 18∶1 caused no depression in hepatic FAS activity but did result in a significant (P<0.05) decline in liver G6PD activity and fatty acid synthesis which was intermediate between basal and basal +18∶2-or+18∶3-fed animals. Adipose tissue rates of lipogenesis were completely unaffected by dietary fatty acid supplementation. Similarly, the addition of 3 or 5% 18∶3 to a basal diet for only one meal resulted in no change in lipogenesis relative to that in animals fed the basal diet. The data indicate that, like rats fed EFA-deficient diets, dietary 18∶2 and 18∶3 exert a specific capacity to depress rat liver FAS and G6PD activities and rate of fatty acid synthesis. Michigan Agricultural Experiment station Journal Article No. 7581. D.R. Romsos is the recipient of Career Development Award K04 AM 00112     

Effect of essential fatty acid depletion on tissue phospholipid fatty acids in spontaneously hypertensive and normotensive rats

Weanling male spontaneously hypertensive (SHR) and normotensive (WKY) rats were maintained on a fat-free semisynthetic diet and killed at various intervals. The effects of fat-depletion on the appearance of essential fatty acid (EFA) deficiency symptoms, the progressive changes of major fatty acids in plasma, liver, heart, and kidney phospholipids (PL), and in skin total lipids were compared between these two strains. After five weeks on the diet, the slower growth and the appearance of EFA deficiency symptoms became evident in SHR. In general, fat-depletion reduced the levels of n−6 fatty acids, whereas it increased those of 20∶3n−9. However, the fat-depletion induced reduction of 18∶2n−6 in heart PL and 20∶4n−6 in kidney, while the elevation of 20∶3n−9 in plasma, heart, and kidney PL were greater in WKY than in SHR. As a result, the elevation of biochemical EFA deficiency index—20∶3n−9/20∶4n−6 ratio—was greater in WKY than in SHR. In comparison with WKY, the concentrations of liver triacylglycerols and the weights of adipose tissues in SHR were reduced to a greater extent, indicating an active catabolism of triacylglycerols in SHR. This study suggests that the earlier appearance of morphological symptoms of EFA deficiency in SHR was not associated with the reducing n−6 EFA levels or with an elevation of triene/tetraene ratio, but possibly to a reduced supply of n−6 EFA for skin prostaglandin synthesis.     

Effects of an essential fatty acid deficiency on serum lipoproteins in the rat

Studies are reported on the effect of an essential fatty acid (EFA) deficiency in male Sprague-Dawley rats and its exacerbation by inclusion oftrans fatty acids in the diet on the level and composition of serum lipoproteins. Weanling male Sprague-Dawley rats were fed diets containing all essential nutritients and a 5% fat supplement of safflower oil (SAFF) or hydrogenated coconut oil (HCO) in 2 experiments, one for 31 wk and the other for 17 wk. For the final 3 wk of each experiment, animals were switched from each group to a 5% supplement of a concentrate of ethyl linolelaidate (TRANS). In addition, a group of animals fed the HCO diet in the first experiment were also switched to the SAFF Diet. With the development of an EFA deficiency in the HCO group, there was a decrease in the high density lipoprotein (HDL) and an increase in the very low density plus the low density (VL-LDL) lipoprotein fractions separated by heparin-manganese precipitation. Switching animals of the HCO group to the TRANS supplement exaggerated this effect and produced a very low ratio of HDL-to-VL-LDL. Analysis of the serum lipoproteins by polyacrylamide disc gel electrophoresis showed that an EFA deficiency produced a marked alternation of the HDL fraction. Changes also appeared to be produced in the VL-LDL fraction by an EFA deficiency and particularly upon switching EFA-deficient animals to the TRANS supplemented diet. Switching animals of the SAFF group to the TRANS supplement brough about an immediate reduction in HDL with a corresponding decrease in serum arachidonic acid. The data suggested a general relationship between arachidonic acid and the level and composition of HDL on the one hand, and 18∶1 and VL-LDL on the other. Accordingly, the ratio of HDL-to-VL-LDL appears to provide a sensitive biochemical index of the EFA status of the rat.     

Effects of dietary linolenate on the fatty acid composition of brain lipids in rats

Weanling male rats were fed hydrogenated coconut oil to induce essential fatty acid (EFA) deficiency. After 15 weeks, the rats were divided into six groups. Five groups were fed graded amounts of purified linolenate (18∶3ω3) with a constant amount of linoleate (18∶2ω6) for six weeks. Fatty acid composition was determined in brain lipids. Increasing dietary 18∶3ω3 resulted in a decrease in arachidonic acid (20∶4ω6), docosatetraenoic acid (22∶4ω6) and docosapentaenoic acid (22∶5ω6), whereas 18∶2ω6 and eicosatrienoic acid (20∶3ω6) were increased both in total lipids and phospholipids. These results suggest that dietary 18∶3ω3 exerts its inhibitory effect mainly on the desaturation of 20∶ω6 to 20∶4ω6 in brain lipids. Linolenate was undetectable in brain lipids from any dietary treatments. The levels of eicosapentaenoic acid (20∶5ω3) in groups receiving dietary 18∶3ω3 were not different from that of the group receiving no 18∶3ω3. These results indicate that, in the brain, 18∶3ω3 is rapidly converted mainly to 22∶6ω3 without being accumulated and imply that dietary 18∶3ω3 can modulate the level of precursor of diene prostaglandins (PG) but not that of triene PG in the rat brain.     

Cholesteryl ester hydrolase activity in adrenal homogenates from normal and essential fatty acid-deficient female rats

Cholesteryl ester hydrolase was assayed in adrenal homogenates from mature female rats fed a control (corn oil-containing) or essential fatty acid (EFA)-deficient diet. Cholesteryl ester of 16∶0, 18∶0, 18∶1, 18∶2(n−6), 20∶4(n−6) and 22∶4(n−6) were used as substrates. In control rats, the unsaturated esters were hydrolyzed more rapidly than the saturated esters and cholesteryl arachidonate was the preferred substrate of the six investigated; cholesteryl oleate elicited the highest activity in the deficient group. Polyunsaturated esters were hydrolyzed at a significantly lower rate by homogenates from EFA-deficient rats than by those from control animals. The esters of 18∶1, 18∶2(n−6) and 20∶4(n−6) were hydrolyzed more extenstively in relation to their concentrations in adrenal tissue than were cholesteryl esters of 16∶0, 18∶0 and 22∶4(n−6). This difference was more pronounced in control than in EFA-deficient rats. No simple relationship of adrenal cholesteryl ester hydrolase activity to ester fatty acid structure or to nutritional essentiality was evident.     

Effect of low levels of dietary fish oil on fatty acid desaturation and tissue fatty acids in obese and lean rats

The effect of very low levels of dietary long-chain n−3 fatty acids on Δ6 desaturation of linoleic acid (18∶2n−6) and α-linolenic acid (18∶3n−3), and on Δ5 desaturation of dihomo-γ-linolenic acid (20∶3n−6), in liver microsomes and its influence on tissue fatty acids were examined in obese and lean Zucker rats and in Wistar rats. Animals fed for 12 wk a balanced diet containing ca. 200 mg of long-chain polyunsaturated n−3 fatty acids per 100 g of diet were compared to those fed the same amount of α-linoleic acid. Low amounts of long-chain n−3 fatty acids greatly inhibited Δ6 desaturation of 18∶2n−6 and Δ5 desaturation of 20∶3n−6, while Δ6 desaturation of 18∶3n−3 was not inhibited in Zucker rats and was even stimulated in Wistar rats. Inhibition of the biosynthesis of long-chain n−6 fatty acids was reflected in a decrease in arachidonic acid (20∶4n−6) content of serum lipids when fasting, and also in the phospholipid fatty acids of liver microsomes. On the contrary, heart and kidney phospholipids did not develop any decrease in 20∶4n−6 during fish oil ingestion. Docosahexaenoic acid (22∶6n−3), present in the dietary fish oil, was increased in serum lipids and in liver microsome, heart, and kidney phospholipids.     

Slow recovery of the fatty acid composition of sciatic nerve in rats fed a diet initially low in n−3 fatty acids

The sciatic nerve of rats fed sunflower oil (6 mg 18∶3n−3/100 g of diet) presented dramatic alterations in the long chain polyunsaturated fatty acids in comparison with those fed soy oil (130 mg 18∶3n−3/100 g of diet). In both 15-day-old and 60-day-old animals fed sunflower oil, 22∶6n−3 (cervonic acid) was fourfold less, 22∶5n−6 was 10-fold greater; adrenic acid (22∶4n−6) was slightly greater and arachidonic acid (20∶4n−6) was close to that in rats fed soy oil. The percentage distribution of total polyunsaturated fatty acids as well as the individual saturated and monounsaturated fatty acids were the same in both groups. When the sunflower oil-fed animals were switched to a soy oil-containing diet for either 15 or 60 days, the percentage distribution of 22∶6n−3 increased slowly to reach the control value 2.5 months later. Conversely 22∶5n−6 decreased slowly. The decay of 22∶5n−6 was more rapid than the increase of 22∶6n−3.     

The prevention of alcoholic fatty liver using dietary supplements: Dihydroxyacetone,pyruvate and riboflavin compared to arachidonic acid in pair-fed rats

Male Sprague-Dawley rats were fed for 30 days a high-fat liquid ethanol diet with dihydroxyacetone, pyruvate and riboflavin added as supplements (AMA-). Plasma triglyceride (TG) levels were 6-fold greater in these rats than in those fed and alcohol with without the supplements (AA-). The liver TG content in rats fed the AMA-diet was similar to that of rats fed a control diet (CA-) in which alcohol was replaced with isocaloric amounts of dextrose. Livers of rats fed the AA- diet had 3 times more TG than controls. Alcohol ingestion also enhanced the hepatic content of cholesteryl esters (CE) and phospholipids (PL). These lipids were reduced to levels found in livers of rats fed the control diet (CA-) when dihydroxyacetone, pyruvate and riboflavin were included in the alcohol diet. The fatty acid compositions of TG, CE and PL from livers of rats fed the AMA-diet were similar to those of corresponding lipids from rats fed the control diet (CA-) but differed from compositions when fed the alcohol diet (AA-). Regardless of the diet fed, TG had the same fatty acid composition in plasma and liver. The same was true of PL fatty acid composition. However, the fatty acid composition of CE differed between liver and plasma. The major fatty acid in liver CE was 18∶1 whereas in plasma it was arachidonic acid (20∶4). Reduced fatty liver was observed in an earlier study when rats were fed ad libitum an ethanol diet containing 20∶4. In the present study, we pair-fed the same diet and fatty liver was not reduced. Dihydroxyacetone, pyruvate and riboflavin did not prevent alcohol-induced fatty liver when 20∶4 was included in the AMA-diet. Our results confirm that dietary dihydroxyacetone, pyruvate and riboflavin prevent alcohol-induced fatty liver, and show that this effect may result from increased mobilization of fat from liver.     

Maternal diet and brain fatty acids in young rats

In order to determine to what extent maternal diet influenced the brain lipids of young rats, female rats were maintained on diets differing in fatty acid composition. Fatty acid determinations on the total brain lipids of the young from these dams indicated that the maternal dietary lipids influence the polyunsaturated fatty acid composition of these animals. A maternal diet with a high linoleic-linolenic acid ratio (corn oil) resulted in lower levels of 22∶6ω3 and higher levels of 22∶5ω6 than one with a low linoleic-linolenic acid ratio (grain). Transfer of young rats at birth to a foster mother, which was fed a diet differing from that of the natural dam, resulted in brain polyunsaturated fatty acid patterns at weaning similar to those of the natural young, and suckling, of the foster mother, thus indicating that the maternal diet in the immediate postnatal period can modify the brain lipids of young rats prior to weaning. The brain lipids of young rats from dams which were fed corn oil exhibited a marked tendency to incorporate 22∶6ω3 in the immediate postnatal period in spite of a relatively high linoleic-linolenic acid ratio in the milk.     

The use of essential fatty acid deficient rats to study pathophysiological roles of prostaglandins. Comparison of prostaglandin production with some parameters of deficiency

In a retrospective study on essential fatty acid deficient, (EFAD) rats used to study pathophysiological roles of prostaglandins (PGs) slight increases in the linoleic acid content of the diet were found to gradually restore the depressed growth rate and to increase the reduced endogenous PG production. These apparently poorly deficient animals had a serum triene tetraene (ω9:ω6) ratio much higher than the value of 0.4 used as a criterion for EFA deficiency by nutritionists. Changes in body weight, serum ω9∶ω6 and platelet PG production were not correlated with each other. Feeding rats on a diet containing <0.1 mg/g/linoleic acid led to decreasing platelet PG production as the degree of EFA deficiency increased. At this high level of deficiency, a serum ω9∶ω6 ratio of 6 or over was achieved. This high ratio may be taken as anindicator of the degree of EFA deficiency required for studies of PG deprivation, but PG production by the tissue investigated or by plalets should preferentially be measured.     

The effects of dietary cholesterol on blood and liver polyunsaturated fatty acids and on plasma cholesterol in rats fed various types of fatty acid diet

Male rats were fed on a fat-free diet for 8 weeks and then switched to diets containing 10% hydrogenated coconut oil (HCO), safflower oil (SFO) or evening primrose oil (EPO). Half of each group was also given 1% of cholesterol in the diet. After 5 further weeks, plama, red cell and liver fatty acids were measured in the various lipid fractions. Plasma and liver cholesterol also were estimated. In almost all fractions and on all three diets, feeding cholesterol led to accumulation of the substrates of desaturation reactions and to deficits of the products of these reactions. The results were consistent with inhibition of Δ-6, Δ-5 and Δ-4 desaturation of n−6 essential fatty acids. Since the diets were deficient in n−3 fatty acids, levels were very low but were also consistent with inhibition of desaturation. In contrast, cholesterol had relatively less consistent effects on 20∶3n−9, suggesting that desaturation of n−9 fatty acids was less inhibited. Plasma cholesterol levels rose sharply in the HCO and SFO groups but not at all in the EPO group. EPO contains the product of Δ-6 desaturation, 18∶3n−6, suggesting that conversion of linoleic acid to 18∶3n−6 and possibly to further metabolites may be important for the cholesterol-lowering effect of polyunsaturates.     

The effect of dietary fat on the fatty acid composition of lipids secreted in rats' milk

During pregnancy and lactation, female rats were fed diets containing either 28% partially hydrogenated marine oil (28MO), 2% arachis oil (2AO), or no fat (FF). Milk lipid composition was examined by gas chromatographic analysis of the gastric content of 10-day-old suckling pups. An increase to 45% in the milk content of long chain monoenoic acids, 18∶1, 20∶1 and 22∶1, reflects the fatty acid composition of the marine oil. Milk fatty acids of medium chain length comprised 6%, 31% and 24% of total fatty acids in the (28MO), (2AO) and (FF) groups, respectively, suggesting that a high-fat diet (28MO) inhibits the lipid synthetic activity of mammary glands. The amount of dienoic C₁₈-acids (6%) in the group fed (28MO) containing no essential fatty acids (EFA) was similar to the amount of 18∶2 in the group receiving a low-fat, EFA-rich diet (2AO). However, only half the dienoic acid from the milk of the (28MO)-fed animals was linoleic acid, which was most likely mobilized from fat depots.