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.     

Fatty acid composition of liver lipids during development of rat

The fatty acid composition of triglycerides and phospholipids from rat liver was determined throughout the period of growth in the rat. Major changes in the triglyceride fatty acid composition were observed during the period studied. The triglycerides from fetal and newborn rats contained only a small percentage of polyunsaturated acids compared with suckling and weanling rats. During the suckling phase the liver triglycerides were rich in long chain polyunsaturated acids such as 20∶4, 20∶5, 22∶5, and 22∶6; once the pups were weaned, the percentage of these acids in the liver triglycerides fell. In these experiments, 18∶2 and 18∶3 were the only polyunsaturated acids in the maternal diet. However, the stomach contents of the suckling pups contained 18∶2 and 18∶3, as well as the long chain polyunsaturated acids. Radioactive 18∶3 and 22∶6 were fed to suckling pups, and the results suggested that the LCP in the rat liver triglycerides during the suckling period were derived from the long chain polyunsaturated acids in the dam's milk, rather than by synthesis from either 18∶2 or 18∶3 within the pups.     

Serum lipids in suckling and post-weanling iron-deficient rats

Serum lipids were studied in iron-deficient and control rats during suckling and after weaning at 21, 30, and 60 days of age. Diets providing 5 or 307 ppm iron were fed to dams and their offspring during gestation, lactation, and after weaning. Rats on the deficient diet throughout the experimental period developed a hyperlipidemia characterized by elevated triglycerides, cholesterol, and phospholipids which was present at 21, 30, and 60 days. Control pups weaned to the deficient diet developed anemia at 30 days of age and hypertriglyceridemia at 60 days of age. Repletion of deficient rats with iron after weaning caused a rapid decline in serum lipid levels after only 9 days on the control diet. The hyperlipidemia of iron deficiency thus appears to be reversible with iron supplementation. The time required to develop hypertriglyceridemia in iron deficiency is longer postweaning than during suckling.     

Different degrees of moderate iron deficiency modulate lipid metabolism of rats

Severe iron deficiency affects lipid metabolism. To investigate whether moderate iron depletion also alters lipid variables—including lipid levels in serum and liver, hepatic lipogenesis, and fatty acid composition indicative of an impaired desaturation—we carried out experiments with rats fed 9, 13, and 18 mg iron/kg diet over a total of 5 wk. The study also included three pair-fed control groups and an ad libitum control group, fed with 50 mg iron/kg diet. The iron-depleted rats were classified as iron-deficient on the basis of reduced serum iron, hemoglobin concentration, and hematocrit. All moderately iron-deficient rats had significantly lower cholesterol concentrations in liver and serum lipoproteins than their pair-fed controls. Rats with the lowest dietary iron supply had higher concentrations of hepatic phosphatidylcholine (PC) and phosphatidylethanolamine (PE), lower activities of glucose-6-phosphate dehydrogenase, malic enzyme and fatty acid synthase, and higher triacylglycerol concentrations in serum lipoproteins than the corresponding pair-fed control rats. Moderate iron deficiency also depressed the serum phospholipid level. Moreover, several consistent significant differences in fatty acid composition of hepatic PC and PE occurred within moderate iron deficiency, which indicate impaired desaturation by Δ-9 and Δ-6 desaturases of saturated and essential fatty acids. We conclude that lipid variables, including cholesterol in liver and serum lipoproteins as well as fatty acid desaturation, reflect the gradations of iron status best and can be used as an indicator of the degree of moderate iron deficiency.     

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.     

Effect of chronic ingestion of DDT on physiological and biochemical aspects of essential fatty acid deficiency

Male weanling rats were fed semipurified diets with and without essential fatty acid (EFA) and DDT (150 ppm) for 14 weeks to determine the effects of the pesticide on physiological and biochemical aspects of EFA deficiency (EFAD). DDT did not affect EFAD-induced reduction in growth rate or final body weight, nor did the pesticide affect EFAD-induced changes in feed efficiency or skin dermatitis. The pesticide did increase liver/body mass ratios, but did not interact with EFAD, which also increased this ratio. The pesticide produced complex changes in total fatty acid composition of liver and tail skin: liver levels of 18∶0, 18∶2 and 20∶3ω9 were increased, whereas levels of 12∶0, 14∶0 and 16∶0 were decreased. In both tissues, DDT interacted with EFA to increase 18∶2 levels. DDT did not change the total fatty acid 20∶3ω9/20∶4ω6 ratio in either tissue. In this study, although DDT did not exacerbate the physiological aspects of EFAD, DDT-induced changes in fatty acid composition of liver and tail skin indicated that 150 ppm DDT in the diets did alter lipid metabolism of the rats in an unexplained manner. Scientific contribution No. 811, Storrs Agricultural Experimental Station, University of Connecticut, Storrs, CT 06268.     

Black currant seed oil feeding and fatty acids in liver lipid classes of guinea pigs

Guinea pigs were fed one of three diets containing 10% black currant seed oil (a source of gamma-linolenic (18∶3 n−6) and stearidonic (18∶4 n−3) acids), walnut oil or lard for 40 days. The fatty acid composition of liver triglycerides, free fatty acids, cholesteryl esters, phosphatidylinositol, phosphatidylserine, cardiolipin, phosphatidylcholine and phosphatidylethanolamine were determined. Dietary n−3 fatty acids found esterified in liver lipids had been desaturated and elongated to longer chain analogues, notably docosapentaenoic acid (22∶5 n−3) and docosahexaenoic acid (22∶6 n−3). When the diet contained low amounts of n−6 fatty acids, proportionately more of the n−3 fatty acids were transformed. Significantly more eicosapentaenoic acid (EPA) (20∶5 n−3) was incorporated into triglycerides, cholesteryl esters, phosphatidylcholine and phosphatidylethanolamine of the black currant seed oil group compared with the walnut oil group. Feeding black currant seed oil resulted in significant increases of dihomogamma-linolenic acid (20∶3 n−6) in all liver lipid classes examined, whereas the levels of arachidonic acid (20∶4 n−6) remained relatively stable. The ratio dihomo-gamma-linolenic acid/arachidonic acid was significantly (2.5-fold in PI to 17-fold in cholesteryl esters) higher in all lipid classes from the black currant seed oil fed group.     

Lymphatic absorption of structured glycerolipids containing medium-chain fatty acids and linoleic acid,and their effect on cholesterol absorption in rats

The effects of various structured triglycerides containing medium-chain (caprylic or capric acids) and long-chain (linoleic acid) fatty acids on fatty acid and cholesterol absorption were studied in lymph-cannulated rats. A considerable portion of capric and caprylic acid was absorbed through the lymph duct, although to a lesser extent than was linoleic acid. Capric and linoleic acid located at the 2-position of 2-decanoyl-1,3-dilinoleoyl-glycerol (18∶2/10∶0/18∶2) and 2-linoleoyl-1,3-didecanoyl-glycerol (10∶0/18∶2/10∶0), respectively, tended to be absorbed more efficiently than those located at the 1- and 3-position or those from tricaprin (10∶0/10∶0/10∶0) or trilinolein (18∶2/18∶2/18∶2). A similar trend was observed when the medium-chain fatty acid was caprylic acid instead of capric acid. Caprylic acid absorption from 2-octanoyl-1,3-dilinoleoylglycerol (18∶2/8∶0/18∶2) was significantly greater (p<0.05) than from 2-linoleoyl-1,3-dioctanoyl-glycerol (8∶0/18∶2/8∶0) or tricaprylin (8∶0/8∶0/8∶0). Preferential absorption of caprylic and linoleic acid was not observed when the 1 to 2 and the 2 to 1 mixtures of 8∶0/8∶0/8∶0 and 18∶2/18∶2/18∶2, respectively, were administered. The structured lipids did not affect the lymphatic absorption of cholesterol. The results suggest that structured triglycerides composed of medium-chain fatty acids and linoleic acid may be more useful for the treatment of lipid malabsorption than are mixtures of medium-chain triglyceride (MCT) and long-chain triglycride (LCT).     

Lipids of cultured hepatoma cells: IV. Effect of serum and lipid upon cellular and media neutral lipids

Minimal deviation hepatoma 7288C cells were cultured in a modified Swim's medium supplemented with decreasing levels of serum, lipid-free serum, lipid-free serum plus fatty acids, and other additives. Cellular and media neutral lipid classes were quantitated, the fatty acids of triglycerides and sterol esters analyzed, and the carbon number distribution of triglycerides determined. Cellular triglyceride biosynthesis virtually was inhibited when the medium was supplemented with bovine serum alone. This inhibition was not observed when the medium was supplemented with fetal calf serum alone or mixtures of fetal calf serum and bovine serum. Cells cultivated on medium supplemented with lipid-free serum plus palmitic or linoleic acids had much lower levels of free and esterified cholesterol. The fatty acid composition of cellular triglycerides and cholesterol esters differed dramatically from the corresponding media lipid classes. Except when linoleic acid was added to the medium, changes in the media serum and lipid levels had only marginal effects upon the fatty acid composition of cellular triglycerides and cholesterol esters. These data, in conjunction with earlier data that showed the media neutral lipid levels did not decrease during cell growth, indicate that these hepatoma cells utilize little or no serum triglycerides and cholesterol esters. Linoleic acid added to the medium dramatically reduced the level of 18∶1 acids in cellular triglycerides and cholesterol esters. Palmitic acid added to the medium did not change the fatty acid compositions significantly. Comparison of experimentally determined and calculated triglyceride carbon number percentages indicated a random distribution of fatty acids in this glyceride. The fatty acid composition of cellular triglycerides was similar to the composition of the cholesterol esters. The lack of characteristic and distinguishable compositions of these two classes that occur in most normal tissues suggests a loss of specificity in the lipid metabolism of this neoplasm at the class level.     

High dietary 18∶3n−3 increases the 18∶3n−3 but not the 22∶6n−3 content in the whole body, brain, skin, epididymal fat pads, and muscles of suckling rat pups

The objective of this study was to test the hypothesis that increasing maternal dietary 18∶3n−3 by decreasing the 18∶2n−6/18∶3n−3 ratio will increase the 18∶3n−3 and 22∶6n−3 content of the whole body, liver, skin (epidermis, dermis, and subcutaneous tissue), epididymal fat pads, and muscles (arms and legs) of 2-wk-old rat pups. Sprague-Dawley dams at parturition were fed semipurified diets containing either a low (18∶2n−6 to 18∶3n−3 ratio of 24.7∶1) or a high (18∶2n−6 to 18∶3n−3 ratio of 1.0∶1) 18∶3n−3 fatty acid content. During the first 2 wk of life, rat pups received only their dams' milk. Fatty acid composition of the pups' stomach contents (dams' milk), whole body, brain, liver, skin, epididymal fat pads, and muscles was determined. The stomach fatty acid composition of 18∶3n−3 reflected the dams' diet. The content of 18∶3n−3 in whole body, brain, liver, skin, epididymal fat pads, and muscles was significantly (P<0.05) greater in rat pups fed the high compared with the low 18∶3n−3 fatty acid diet. The 22∶6n−3 content of the whole body, brain, skin, epididymal fat pads, and muscles was not quantitatively different in rat pups fed either the low or high 18∶3n−3 fatty acid diet. The 20∶5n−3 and 22∶5n−3 content of the whole body, skin, and epididymal fat pads was significantly increased in rat pups fed the high compared with the low 18∶3n−3 fatty acid diet. High content of 18∶3n−3 was found in the skin of rat pups fed either a low or high 18∶3n−3 fatty acid diet. These findings demonstrate that high maternal dietary 18∶3n−3 significantly increases the 18∶3n−3 but not the 22∶6n−3 content of the whole body, brain, skin, epididymal fat pads, and muscles with approximately 39 and 41% of the whole body 18∶3n−3 content being deposited in the skin of suckling rat pups fed either the low or high 18∶3n−3 diet, respectively.     

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.     

Kidney lipids: Changes caused by dietary 9-Trans, 12-Trans-octadecadienoate

Trans, trans-linoleate at 50 and 100% of dietary fat decreased kidney size and altered its composition.Trans, trans-linoleate as the sole source of dietary fat imparied growth and caused more severe symptoms of essential fatty acid deficiency than was observed with hydrogenated coconut oil (HCO). The concentration of renal cholesterol, phospholipids (PL), triglycerides (TG) and cholesteryl esters (CE) were also decreased. Linoleic (18∶2), homo-γ-linolenic acid (20∶3n6) and arachidonic acid (20∶4n6) were significantly depressed in lipid classes, especially in PL and CE, by dietarytrans, trans-linoleate. The increase in eicosatrienoate (20∶3n9), especially in PL and CE of kidneys of rats fed HCO (essential fatty acid deficient), was slight in rats fed 100%trans, trans-linoleate, indicating that thetrans, trans acid probably inhibited acyl elongation and desaturation.     

A diet containing myristoleic plus palmitoleic acids elevates plasma cholesterol in young growing swine

The objective of this study was to test the effect of a novel fatty acid mixture, enriched with myristoleic and palmitoleic acids, on plasma lipoprotein cholesterol concentrations. Weanling pigs were assigned to one of six groups and each group received a diet differing in fatty acid composition. Diets were fed for 35 days and contained 10 g added cornstarch/100 g (to provide baseline data) or 10 g added fatty acids/100 g. For those diets containing added fatty acids, extracted lipids contained 36% myristoleic plus palmitoleic acid combined (14∶1/16∶1 diet), 52% palmitic acid (16∶0 diet), 51% stearic acid (18∶0 diet), 47% oleic acid (18∶1 diet), or 38% linoleic acid (18∶2 diet). Witht the exception of the cornstarch diet, all diets contained approximately 30% myristic acid. There were no significant differences in weight gain across treatment groups (P=0.22). All diets caused a significant increase in triglycerides and in total, low density lipoprotein, high density lipoprotein, and very low density lipoprotein cholesterol. The increase in total plasma cholesterol from pretreatment values was greatest in pigs fed the 14∶1/16∶1 and 18∶1 diets. However, the increase in low density lipoprotein cholesterol from the pretreatment concentration was greatest in the 14∶1/16∶1-fed pigs. Increases in very low density lipoprotein cholesterol above pretreatment concentrations were lowest in 16∶0-fed pigs and greatest in 18∶1-fed pigs. Dietary fatty acids elicited changes in plasma fatty acids which generally were reflective of the diets, although the 18∶0 diet did not alter plasma fatty acid concentrations and the 16∶0 diet increased plasma 16∶0 only at the end of the study. These results demonstrated that the combination of myristoleic plus palmitoleic acids increased plasma cholesterol in young pigs, suggesting that fatty acid chain length, rather than degree of unsaturation, is primarily responsible for the effects of fatty acids on circulating lipoprotein cholesterol concentrations.     

Effect of reproductive states on lipid mobilization and linoleic acid metabolism in mammary glands

Effects of pregnancy and lactation on lipid metabolism in mouse mammary fat pads and nonmammary adipose tissues have been studied. In order to address the question whether the influence of hormonal milieu on lipid metabolism in mammary epithelial cells during pregnancy and lactation is the same as in fat cells, we have studied the mobilization of lipids and metabolism of fatty acids in the intact mammary glands, parenchyma-free mammary fat pads and in the perimetrial fat tissues of virgin, pregnant and lactating mice. Compared to parenchyma-free mammary fat pads, the perimetrial adipose tissues accumulated 5-fold higher levels of triglycerides during pregnancy. Mammary fat cells maintained overall lipid levels during pregnancy and lactation (16–20 μg/fat pad). In contrast, lactation depleted total lipid stores from 108 ± 5 to 24 ± 4.5 μg/fat pad in perimetrial fat pads. Results of comparative analysis of fatty acid composition of mammary fat pads, with and without epithelial tissue, from virgin and lactating mice showed stimulation of 18∶2ω6 metabolism leading to 130% increase in the ratio 20∶4ω6 to 18∶2ω6 in the epithelial compartment. Pregnancy and lactation resulted in the elevation of 20∶4ω6 levels probably due to a 4-fold increase in Δ5 desaturase activity and a decrease in oxidative degradation of 18∶2ω6. These results suggest that, unlike other adipose tissues, the metabolic pathways in mammary fat cells are not dedicated to sequestration and accumulation of dietary lipids during pregnancy. Lactation favors mammary epithelial cell-stimulated production of precursors of eicosanoids which are known to have agonist-like effect on mammary epithelial cells.     

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.     

Effects of oleic,arachidonic and 5,8,11,14-nonadecatetraenoic acids on lipid secretion and ketogenesis in perfused rat liver

The effects of perfused oleic (18∶1n−9), arachidonic (20∶4n−6) and 5,8,11,14-nonadecatetraenoic (19∶4n−5) acids on triglyceride and cholesterol secretion and ketone body production were studied in isolated rat liver. As compared to oleic and 19∶4n−5 acids, both ketone body production and triglyceride secretion were significantly lowered when arachidonic acid was perfused. The concentration of triglyceride in the post-perfused liver was lower upon perfusion with arachidonic acid than upon perfusion with oleic acid or 19∶4n−5 acid. Cholesterol secretion in the liver perfused with arachidonic acid or 19∶4n−5 acid was significantly higher than with oleic acid. The concentration of cholesterol in the post-perfused liver was slightly but significantly higher with 19∶4n−5 acid than with the other fatty acids. The results suggest that 19∶4n−5 acid when compared with arachidonic acid affects lipid metabolism in liver differently.     

Fatty acid interrelationships in plasma,liver, muscle and adipose tissues of cattle fed safflower oil protected from ruminal hydrogenation

Steers were given diets containing formaldehyde-treated casein-safflower oil supplements, in which the constituent 18∶2 was protected from ruminal hydrogenation. A similar group was given unsupplemented diets. The fatty acid compositions of plasma, liver, muscle and adipose tissue lipids were determined in both groups of cattle after 0, 2, 4 and 8 weeks of experimentation. The proportion of 18∶2 in the triglycerides was markedly increased on feeding the supplement and the rate of incorporation into the plasma triglycerides was higher than that in the triglycerides of muscle and adipose tissue. Associated with this increase there were compensatory decreases in the proportions of 16∶0 and 18∶1 but no consistent change in the proportion of 18∶0. The proportion of 18∶2 in the plasma phospholipids and cholesteryl esters was initially much higher than in the triglycerides and this was further increased by feeding the safflower oil supplement. A linear relationship existed between the proportion of 18∶2 in the phospholipids and cholesteryl esters of plasma. The supplement also caused substantial increases in the proportion of 18∶2, both in phospholipids from liver and muscle and in cholesteryl esters from liver, and there were compensatory decreases in the proportions of other unsaturated fatty acids, e.g., 18∶1, 18∶3, 22∶6. These studies demonstrate that when ruminal hydrogenation was circumvented by feeding formaldehyde-treated casein-safflower oil particles, the linoleic acid was absorbed and the pattern of incorporation into plasma and tissue lipids was similar to that in nonruminants.     

Influence of dietary fat composition on intestinal absorption in the rat

Omega-3 fatty acids influence the function of the intestinal brush border membrane. For example, the omega-3 fatty acid eicosapentaenoic acid (20∶5ω3) has an antiabsorptive effect on jejunal uptake of glucose. This study was undertaken to determine whether the effect of feeding α-linolenic acid (18∶3ω3) or EPA plus docosahexaenoic acid (22∶6ω3) on intestinal absorption of nutrients was influenced by the major source of dietary lipid, hydrogenated beef tallow or safflower oil. Thein vitro intestinal uptake of glucose, fatty acids and cholesterol was examined in rats fed isocaloric diets for 2 weeks: beef tallow, beef tallow + linolenic acid, beef tallow + eicosapentaenoic acid/docosahexaenoic acid, safflower oil, safflower oil + linolenic acid, or safflower oil + eicosapentaenic acid/docosahexaenoic acid. Eicosapentaenoic acid/docosahexaenoic acid reduced jejunal uptake of 10 and 20 mM glucose only when fed with beef tallow, and not when fed with safflower oil. Linolenic acid had no effect on glucose uptake, regardless of whether it was fed with beef tallow or safflower oil. The jejunal uptake a long-chain fatty acids (18∶0, 18∶2ω6, 18∶3ω3, 20∶4ω6, 20∶5ω3 and 22∶6ω3) and cholesterol was lower in salfflower oil than with beef tallow. When eicosapentaenoic acid/docosahexaenoic acid was given with beef tallow (but not with safflower oil), there was lower uptake of 18∶0, 20∶5ω3 and cholesterol. The demonstration of the inhibitory effect of linolenic acid or eicosapentaenoic acid/docosahexaenoic acid on cholesterol uptake required the feeding of a saturated fatty acid diet (beef tallow). These changes in uptake were not explained by differences in the animals’ food intake, body weight gain or intestinal weight. Feeding safflower oil was associated with an approximately 25% increase in the jejunal and ileal mucosal surface area, but this increase was prevented by combining linolenic acid or eicosapentaenoic acid/docosahexaenoic acid with safflower oil. Different inhibitory patterns were observed when mixtures of fatty acids were present together in the incubation medium, rather than in the diet: for example, when 18∶0 was in the incubation medium with 20∶4ω6, the uptake of 20∶4ω6 was reduced, whereas the uptake was unaffected by 18∶2ω6 or 20∶5ω3. Thus, (1) the inhibitory effect of eicosapentaenoic acid/docosahexaenoic acid on jejunal uptake of glucose, fatty acids and cholesterol was influenced by the major dietary lipid, saturated (beef tallow) or polyunsaturated fatty acid (safflower oil); and (2) different omega-3 fatty acids (linolenic acid versus eicosapentaenoic acid/docosahexaenoic acid) have a variable influence on the intestinal absorption of nutrients.     

Effects of dietary protein and cholesterol on phosphatidylcholine and phosphatidylethanolamine molecular species in mouse liver

The present study examined the effects of two atherogenic factors, animal protein and cholesterol, on the distribution of fatty acids and the molecular species of major liver phospholipids in mice. Weanling mice were fed a semisynthetic diet supplemented with either casein or soy protein (20%, w/w) in the presence or absence of 0.5% cholesterol for 4 wk. Results from mouse liver showed that animal protein and, more so, dietary cholesterol modified the fatty acid profiles of the phospholipids. Animal protein had no significant effect on the concentration of lipids, but it altered the relative distribution and fatty acid profiles of the phospholipids, phosphatidylcholine and phosphatidylethanolamine. Dietary cholesterol, on the other hand, significantly increased the concentration of liver lipids, but it did not alter the relative distribution of phosphatidylcholine and phosphatidylethanolamine. In cholesterol-fed mice, the proportions of molecular species containing 18∶2n−6 were increased, whereas those containing 20∶4n−6 were decreased, indicating that dietary cholesterol suppressed linoleic acid metabolism. Since cholesterol feeding selectively decreased the ratio of 18∶0/20∶4n−6 in phosphatidylcholine, whereas it increased the 18∶0/18∶2n−6 ratio in phosphatidylethanolamine, this finding suggests that dietary cholesterol may affect the incorporation of fatty acids but not the rate of synthesis of phosphatidylcholine and phosphatidylethanolamine.     

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.