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.     

Severe fatty liver in rats fed a fat-free ethanol diet,and its prevention by small amounts of dietary arachidonate

Rats were fed ethanol and a fat-free diet for 30 days to determine whether dietary fat is needed for the development of fatty liver. The severity of fatty liver was similar to that of rats fed an isocaloric diet with 35% fat. Small amounts (29 mg/day) of dietary arachidonic acid prevented alcoholic fatty liver. Rats fed either the alcohol (AF) or control (CF) fat-free diets developed essential fatty acid deficiency (EFAD) as measured by the triene/tetraene ratio of liver and plasma lipids. Rats fed arachidonic acid (AA, alcohol and CA, control diets) did not develop EFAD. Although EFAD alone did not cause the development of fatty liver, the combination of dietary ethanol and EFAD did. The ratios of 16∶1/16∶0 and 18∶1/18∶0 in liver lipids indicated that desaturase enzymes were less active and lipogenesis was reduced in rats fed the AA diet compared to those fed the AF diet. In contrast, stimulated lipogenesis appears to have been the cause of fatty liver in rats fed the AF diet. Presented at the XII International Congress of Nutrition, San Diego, CA, August 1981. Abbreviations: Diets are indicated as fat-free with ethanol (AF), fat-free without ethanol (CF), or similar diets with 0.9% of the calories as arachidonic acid with (AA) or without (CA) ethanol. The composition of these diets is discribed in the text and Table 1.     

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.     

Liver subcellular fatty acid profiles of chicks fed diets containing hydrogenated fats and varying linoleate levels

Day-old male broiler chickens were fed semipurified diets containing 5% lipid from one of four different lipid sources: corn oil (CO), partially hydrogenated soybean oil (HSBO), a spent restaurant grease (SRG) and a purified mixture of triolein, tripalmitin and tristearin (OPS). Diets CO and HSBO contained adequate amounts of linoleic acid, but diets SRG and OPS were deficient in linoleate. In addition, SRG and HSBO containedtrans isomers of 16∶1 and 18∶1. The diets were fed for 3 wk to determine the effects of low linoleate levels andtrans isomers on fatty acid profiles in liver microsomes, mitochondria and cytosol. Chicks fed HSBO had the highest body weights, while those fed SRG and OPS had the lowest. The incidence and severity of dermatitis were similar for all treatments. The proportions of linoleate and arachidonate in lipids from liver subcecullar fractions were reduced significantly in chicks fed OPS and SRG; however levels of 20∶3ω9 were not increased. Feeding HSBO, which is high in both linoleate and linolenate, resulted in higher levels of 18∶3ω3 and 20∶5ω3 in liver subcellular fractions and lower levels of 20∶4ω6 than those seen in chicks fed CO. The isomeric forms of 18∶1 present in the partially hydrogenated fats (HSBO and SRG) appeared to be incorporated into the lipids of liver fractions. The results of this study show that dietary lipids influence fatty acid, profiles of chick liver microsomes, mitochondria and cytosol. Decreases in linoleate and arachidonate in these organelles occur before overt essential fatty acid (EFA) deficiency signs in chicks fed EFA-deficient diets. Published as Scientific Paper No. 7512, College of Agriculture and Home Economics Research Center, Project No. 4723, Washington State University, Pullman, WA.     

Fatty acid pattern of tissue phospholipids in copper and iron deficiencies

Because copper and iron have been reported to be essential cofactors in Δ9 desaturation of fatty acids, the effects of different dietary intakes of copper and iron on tissue fatty acids were studied. Male Long-Evans rats (ten per group) were fed diets containing adequate, deficient or excess copper or iron. On day 42 of the dietary regimen, the animals were killed and tissues and blood were removed for analysis of metals and fatty acids of phospholipids. Compared with the copper-adequate rats, the copper-deficient rats showed increased 18∶0 in liver and decreased 16∶1ω7 in liver, heart and serum. There were no differences for 16∶0 or 18∶1ω9. Intake of excess copper did not cause an increase in products of Δ9 desaturation. Comparisons between iron-deficient and iron-adequate rats showed that iron deficiency increased 18∶2ω6 in liver and serum and decreased 20∶4ω6 in serum only. Relative percentages of 16∶0, 18∶0, 16∶1ω7 and 18∶1ω9 in liver and serum phospholipids were similar for both groups. Intake of excess iron caused a decrease in 18∶2ω6; and 16∶0 and 18∶1ω9 were higher in the liver of the iron-excess group than the iron-deficient group. This study did not support the requirement for copper or iron in the Δ9 desaturation of fatty acids as expressed in phospholipids of liver, heart and serum.     

Dietary saturated fat level alters the competition between α-linolenic and linoleic acid

Male weanling rats were fed semi-synthetic diets high in saturated fat (beef tallow) vs high in linoleic acid (safflower oil) with or without high levels of α-linolenic acid (linseed oil) for a period of 28 days. The effect of feeding these diets on cholesterol content and fatty acid composition of serum and liver lipids was examined. Feeding linseed oil with beef tallow or safflower oil had no significant effect on serum levels of cholesterol. Serum cholesterol concentration was higher in animals fed the safflower oil diet than in animals fed the beef tallow diet without linseed oil. Feeding linseed oil lowered the cholesterol content in liver tissue for all dietary treatments tested. Consumption of linseed oil reduced the arachidonic acid content with concomitant increase in linoleic acid in serum and liver lipid fractions only when fed in combination with beef tallow, but not when fed with safflower oil. Similarly, ω3 fatty acids (18∶3ω3, 20∶5ω3, 22∶5ω3, 22∶6ω3) replaced ω6 fatty acids (20∶4ω6, 22∶4ω6) in serum and liver lipid fractions to a greater extent when linseed oil was fed with beef tallow than with safflower oil. The results suggest that the dietary ratio of linoleic acid to saturated fatty acids or of 18∶3ω3 to 18∶2ω6 may be important to determine the cholesterol and arachidonic acid lowering effect of dietary α-linolenic acid.     

Fatty acid patterns in iron-deficient maternal and neonatal rats

To determine the effects of maternal iron deficiency on lipid composition and fatty acid patterns in offspring, rats were fed ad libitum diets containing 5 ppm iron (deficient) (n=8) or 320 ppm iron (control) (n=7) and deionized water from day-1 of gestation through day-18 of lactation. On day-2 of lactation, litters were standardized to three male and three female pups. On day-18, pups were fasted for 4 hr before tissue and blood collection. Significant changes in serum and liver lipid concentrations and fatty acid patterns were observed in deficient pups. Serum triglycerides, cholesterol and phospholipids and liver triglycerides, cholesterol, and cholesteryl esters were increased. In deficient pups, percentage total fatty acids of 14∶0, 16∶1, 18∶1, 18∶2 from serum lipids were increased; in liver, 14∶0, 18∶2, 18∶3 were increased; 18∶0 and 20∶4 were decreased in both serum and liver. Dam serum lipid levels did not differ between groups. Lipid changes observed in iron-deficient pups did not consistently reflect the milk, serum or liver lipid patterns observed in dams. Altered lipid composition and fatty acid patterns of iron-deficient pups thus appear to be of endogenous origin.     

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.     

Modulation of tissue prostaglandin synthesizing capacity by increased ratios of dietary alpha-linolenic acid to linoleic acid

Semipurified diets containing ratios of α-linolenic acid (18∶3ω3) to linoleic acid (18∶2ω6) of 1/32, 1/7, 1/1, and 3.5/1 in the form of corn oil, soybean oil, soybean/linseed oil mix and linseed oil were fed to rats for 2 months. The first 3 diets were fed to another group of rats for 4 months and to a group through the second generation. Fatty acid analysis of liver and spleen ethanolamine glycerophosphatide revealed that, as the level of 18∶3ω3 in the diet increased, the elongated, desaturated metabolites of the ω6 series decreased and the ω3 series increased. Noteworthy was the depression in the amount of the precursor of the 2-series prostaglandins (PG) as the ω3 levels increased. Synthesis of PG by liver of rats fed 2 or 4 months markedly decreased, but at 2 months in thymus and spleen, it showed a trend toward decreasing only. Brain slices showed no decrease in PGF_2α synthesis after 4 months, but did decrease significantly after feeding the diets to the second generation. Synthesis of PGE₂ by spleen homogenate from the second generation also significantly decreased. The replacement of ω6 series fatty acids by ω3 series is explained by the effective competition of 18∶3ω3 over 18∶2ω6 for the Δ6 desaturase. Depressions in PG synthesis by high dietary 18∶3ω3 is explained by the competitive inhibition of the PG synthetase complex by 20∶5ω3 as well as by the decreased levels of 20∶4ω6. Part of a dissertation submitted by Lisa A. Marshall in partial fulfillment of requirements for the Ph.D. degree in Nutritional Sciences. Presented in part at the 72nd AOCS annual meeting, New Orleans, May 1981.     

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     

Effects of parenteral nutrition with high doses of linoleate on the developing human liver and brain

The developmental changes in the fatty acid composition of ethanolamine phosphoglycerides (EPG) and choline phosphoglycerides (CPG) were studied in the liver and brain of 18 newborn infants with gestational ages ranging from 20 to 44 wk. A small group of five newborns receiving total parenteral nutrition (TPN) with high doses of linoleic acid (18∶2ω6) was also studied and compared to controls of the same gestational age to look for effects on the developmental fatty acid patterns of liver and brain EPG and CPG. TPN with Intralipid 20% was given for 4–12 days, the total fat intake being 14.7–90 g (mean ±S.D.=47.1±29.8 g). The main developmental changes in the liver and brain of the control group were an increase in 22∶6ω3 (docosahexaenoic acid) at the end of gestation and a linear decrease in 20∶4ω6 (arachidonic acid) and 18∶1ω9 (oleic acid) in EPG and CPG. A very good correlation in the percent values of these fatty acids in the brain and liver tissues was obtained. Very significant changes in the fatty acid composition of liver EPG and CPG could be found in the infants receiving TPN with Intralipidmainly an increase in 18∶2ω6, a decrease in the linoleate elongation/desaturation to longer members of the series and a decrease in the 22∶6ω3 levels of liver EPG and CPG. In the brain, only an increase in the 18∶2ω6 value of CPG, not accompanied by any increase in the longer ω6 fatty acids, could be detected. Possible adverse effects of high doses of 18∶2ω6 on the tissue levels of long chain polyunsaturated fatty acids (PUFA), especially of 22∶6ω3, are discussed.     

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.     

Effect of dietary linolenic acid and docosahexaenoic acid on growth and fatty acid composition of rainbow trout (Salmo gairdneri)

Methyl linolenate 18∶3ω3 and docosahexaenoate 22∶6ω3 were incorporated in semipurified diets at several levels and fed to trout previously maintained on a fat-free diet. After 14 weeks, the weight gain and feed conversion of the fish on each diet were determined. The fatty acid composition of the lipid from each group of fish was analyzed by gas liquid chromatography. Both 18∶3ω3 and 22∶6ω3 fed at the 1% level supported maximum growth of the fish. The control group, which were fed no ω3 fatty acids, exhibited a shock syndrome, poor appetite and a very slow growth rate. Tissue fatty acid analysis revealed eicosatrienoic acid 20∶3ω9 accumulated in the phospholipid fraction of this group. The 20∶3ω9 level was lowered when either 18∶3ω3 or 22∶6ω3 was included in the diet. Analysis showed that the dietary 18∶3ω3 was rapidly converted by the fish into 22∶6ω3 with a high concentration in the phospholipid. However 22∶6ω3 fed to the fish remained unchanged and little or no retroconversion of this fatty acid was observed. Presented in part at the AOCS Meeting, Atlantic City, October 1971. Technical paper no. 3247, Oregon Agricultural Experiment Station.     

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.     

Polyunsaturated fatty acid changes suggesting a new enzymatic defect in Zellweger Syndrome

The fatty acid composition of red blood cells, fibroblasts, forebrain, liver and kidney were studied in a 3-month-old infant who died from Zellweger Syndrome, and the results were compared with those of age-matched controls. Besides a typical increase in the very long chain fatty acids 26∶0 and 26∶1 and a great reduction in the plasmalogen levels, confirming the diagnosis of Zellweger Syndrome, some striking changes in the polyunsaturated fatty acid patterns were discovered. The most important was a very drastic decrease in the values of 22∶6ω3 and 22∶5ω6, the two products of Δ4-desaturation. In the kidney, the level of 22∶6ω3 fell below that of 26∶0. Consequently, the ratio 26∶0/22∶6ω3 (and 26∶1/22∶6ω3) was most useful in emphasizing the fatty acid anomalies, especially in renal tissue, where the 26∶0/22∶6ω3 ratio increased to almost 200 times the normal values. Other significant, although less consistent fatty acid alterations were increases in 18∶2ω6, 18∶3ω6, 20∶3ω6, 18∶4ω3 and 20∶4ω3, and a decrease in 20∶4ω6 in some tissues. The existence is proposed of a new enzyme defect in peroxisomal disorders, involving the desaturase system of long chain polyunsaturated fatty acids.     

Effects of essential fatty acid deficiency on prostaglandin synthesis and fatty acid composition in rat renal medulla

Studies are reported on the capacity of isolated rat renal papilla (inner medulla) to synthesize and release prostaglandin (PG) E from endogenous and exogenous precursor(s) during development of an essential fatty acid (EFA) deficiency in the rat. Weanling (21-day-old) male Sprague-Dawley rats were fed a fat-free diet supplemented with either 5% hydrogenated coconut oil (HCO) or 5% safflower oil (SO). At approximately 3, 6 and 7 weeks (6, 9 and 10 weeks of age), groups of animals fed each diet were killed for studies of PGE synthesis in the renal papillae. Differences in the fatty acid composition of the papillae lipids of the animals of each group were also determined. The in vitro production of PGE from endogenous precursor(s) was significantly reduced in the papillae from the 6-week-old rats fed the HCO diet compared to the control (SO) rats, and appeared to be near maximally depressed in the 10-week-old animals compared to that of animals fed an EFA deficient diet for over a year in an accessory experiment. Analyses of the fatty acids of the papillae lipids of the HCO groups showed that the levels of 18∶2 and 20∶4 were markedly reduced, and those of 16∶1, 18∶1 and 20∶3 were elevated compared to the controls even in the 6-week-old animals, typical of an EFA deficiency. The papillae lipids of the animals fed the HCO diet were also depleted of their stores of 22∶4ω6. A fatty acid believed to be derived by chain elongation of 20∶3ω9, 22∶3, was found in large concentrations in the papillae triglycerides of the EFA deficient rats. Incubations of exogenous arachidonic acid (20∶4) in homogenates and tissue slices of the papillae of the HCO dietary groups showed that the PG synthetase was not impaired by an EFA deficiency. The rate of PGE synthesis in the papillae of the EFA deficient animals was generally enhanced when exogenous 20∶4 was added, indicating that the concentration of available precursor(s) is a primary factor in the control of PGE synthesis in the papilla of the rat.     

Fatty acid composition of selected organs of gerbils maintained on a fat-deficient or fat-supplemented diet

The fatty acid composition of liver, heart, and testes was determined in gerbils maintained on a fat-deficient or fatsupplemented diet since the age of twenty-eight days and in gerbil pups, the mothers of which were placed on the respective diets on the day of delivery. Pups born to these mothers were killed at 11 to 19 days at which time increased concentrations of 16∶1, 18∶1, and 20∶3ω9 and decreased concentrations of 18∶2 and 20∶4 (and 22∶5ω6 in testes) were apparent in organs of fat-deficient compared to fat-supplemented gerbils. Similar but more marked changes occurred in organs of gerbils placed on the fat-deficient diet at twenty-eight days of age and examined at intervals of time up to two months later. In these animals, minimal changes were seen also in fatty acids of the brain. The concentration of 22∶6ω3 was resistant to change with the fat-deficient diet. Deficient gerbils had hair loss, decreased quantities of spermatids and spermatozoa in the testis, and most but not all had decreased body weight compared to the fat-supplemented controls. Extremely high concentrations of oleic acid were present in carcass fatty acids of deficient compared to supplemented gerbils, indicating an extremely dynamic fatty acid metabolism in these animals.     

Fish oil prevents change in arachidonic acid and cholesterol content in rat caused by dietary cholesterol

Rats were fed diets high in either saturated fat (beef tallow) or α-linolenic acid (linseed oil) or eicosapentaenoic and docosahexaenoic acids (fish oil) with or without 2% cholesterol supplementation. Consumption of linseed oil and fish oil diets for 28 days lowered arachidonic acid content of plasma, liver and heart phospholipids. Addition of 2% cholesterol to diets containing beef tallow or linseed oil lowered 20∶4ω6 levels but failed to reduce 20∶4ω6 levels when fed in combination with fish oil. Feeding ω3 fatty acids lowered plasma cholesterol levels. Addition of 2% cholesterol to the beef tallow or linseed oil diet increased plasma cholesterol concentrations but not when fish oil was fed. Feeding the fish oil diet reduced the cholesterol content of liver, whereas feeding the linseed oil diet did not. Dietary cholesterol supplementation elevated the cholesterol concentration in liver in the order: linseed oil > beef tallow > fish oil (8.6-, 5.5-, 2.6-fold, respectively). Feeding fish oil and cholesterol apparently reduced 20∶4ω6 levels in plasma and tissue lipids. Fish oil accentuates the 20∶4ω6 lowering effect of dietary cholesterol and appears to prevent accumulation of cholesterol in plasma and tissue lipids under a high dietary load of cholesterol.     

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.     

The circadian cycles of plasma corticosterone and adrenal cholesteryl esters in the normal and EFA-deficient female rat

In female rats subjected to a 12 hr light-12 hr darkness schedule and fed a semipurified diet containing 10% corn oil, plasma corticosterone concentration showed a monophasic circadian cycle with minimum and maximum concentrations at the start of the light and dark periods, respectively. Adrenal total cholesteryl ester concentration was inversely related to plasma corticosterone, as were those of several of the individual esters; changes in cholesteryl ester concentration appeared to follow rather than precede changes in plasma corticosterone. There was preferential depletion of the cholesteryl esters of 18∶1, 18∶2ω6, and 20∶4ω6 during glucocorticoid secretion. [Abbreviations: EFA, essential fatty acid (s);X:YωZ, fatty acid with X carbon atoms and Y olefinic bonds with the terminal double bond Z carbon atoms from the methyl group.] In female rats fed hydrogenated coconut oil (EFA-deficient), a monophasic cycle for plasma corticosterone was also observed, but the peak was much broader than that recorded for rats fed corn oil, although minima and maxima occurred at similar times for the two groups. No significant cycle of adrenal total cholesteryl esters was evident in the deficient rats, but the 20∶3ω9 and 22∶3ω9 esters did decrease significantly during the period of high plasma corticosterone concentration. Preferential net decreases in adrenal cholesteryl esters during corticosteroidogenesis were more apparent in normal than in EFA-deficient rats.